heat-induced-antigen-retrieval-an-effective-method-to-detect-identify

Heat-Induced Antigen Retrieval: An Effective Method to Detect and Identify Progenitor Cell Types during Adult Hippocampal Neurogenesis

Traditional  methods of immunohistochemistry (IHC) following tissue fixation allow visualization  of various cell types. These typically proceed with the ...

Mayo Clinic College of Medicine

Alpha7 nicotinic acetylcholine receptors (nAChRs) modulate network activity in the CNS. Thus, functional regulation of alpha7 nAChRs could influence the flow of information through various brain nuclei. It is hypothesized here that these receptors are amenable to modulation by tyrosine phosphorylation. In both Xenopus oocytes and rat hippocampal interneurons, brief exposure to a broad-spectrum protein tyrosine kinase inhibitor, genistein, specifically and reversibly potentiated alpha7 nAChR-mediated responses, whereas a protein tyrosine phosphatase inhibitor, pervanadate, caused depression. Potentiation was associated with an increased expression of surface alpha7 subunits and was not accompanied by detectable changes in receptor open probability, implying that the increased function results from an increased number of alpha7 nAChRs. Soluble N-ethylmaleimide-sensitive factor attachment protein receptor-mediated exocytosis was shown to be a plausible mechanism for the rapid delivery of additional alpha7 nAChRs to the plasma membrane. Direct phosphorylation/dephosphorylation of alpha7 subunits was unlikely because mutation of all three cytoplasmic tyrosine residues did not prevent the genistein-mediated facilitation. Overall, these data are consistent with the hypothesis that the number of functional cell surface alpha7 nAChRs is controlled indirectly via processes involving tyrosine phosphorylation.

Rapid upregulation of alpha7 nicotinic acetylcholine receptors by tyrosine dephosphorylation.

&#x77ED;&#x6682;&#x8111;&#x7F3A;&#x8840;&#x662F;&#x795E;&#x7ECF;&#x5143;&#x7684;&#x4FAE;&#x8FB1;&#xFF0C;&#x8BF1;&#x5BFC;&#x8FDF;&#x53D1;&#x6027;&#x7684;&#x7EC6;&#x80DE;&#x6B7B;&#x4EA1;&#x3002;&#x65E9;&#x671F;&#x7F3A;&#x8840;&#x540E;&#x65F6;&#x671F;&#x7684;&#x6807;&#x5FD7;&#x6027;&#x4E8B;&#x4EF6;&#x662F;&#x589E;&#x5F3A;&#x7EBF;&#x7C92;&#x4F53;&#x819C;&#x7684;&#x6E17;&#x900F;&#x3002;&#x7EBF;&#x7C92;&#x4F53;&#x529F;&#x80FD;&#x53D7;&#x5230;&#x5E72;&#x6270;&#x7684;&#x786E;&#x5207;&#x673A;&#x5236;&#x5C1A;&#x4E0D;&#x6E05;&#x695A;&#x3002;&#x5728;&#x8FD9;&#x91CC;&#x6211;&#x4EEC;&#x663E;&#x793A;&#x8BE5;&#x5168;&#x7403;&#x7F3A;&#x8840;&#x4FC3;&#x8FDB;&#x6539;&#x5EFA;&#x4E2D;&#x7EBF;&#x7C92;&#x4F53;&#x819C;&#x8054;&#x7CFB;&#x70B9;&#x3001; &#x4E0A;&#x5347; intramitochondrial Zn2 +&#xFF0C;&#x548C;&#x5927;&#x578B;&#x7684; multi-conductance &#x901A;&#x9053;&#x5728;&#x7EBF;&#x7C92;&#x4F53;&#x5916;&#x819C;&#x4E2D;&#x7684;&#x6FC0;&#x6D3B;&#x7684; 1 h &#x540E;&#x7684;&#x4FAE;&#x8FB1;&#x3002;&#x7EBF;&#x7C92;&#x4F53;&#x901A;&#x9053;&#x6D3B;&#x52A8;&#x662F;&#x4E0E;&#x589E;&#x5F3A;&#x7684;&#x86CB;&#x767D;&#x9176;&#x6D3B;&#x6027;&#x548C; Bcl-xl &#x751F;&#x6210; deltaN Bcl-xl &#x503E;&#x5411;&#x4E8E;&#x5BF9;&#x53E3;&#x7684;&#x86CB;&#x767D;&#x6C34;&#x89E3;&#x88C2;&#x89E3;&#x76F8;&#x5173;&#x8054;&#x3002;&#x7ED3;&#x679C;&#x7275;&#x8FDE; deltaN Bcl-xl &#x5728;&#x5927;&#x578B;&#x3001; multi-conductance &#x901A;&#x9053;&#x6D3B;&#x52A8;&#x3002;&#x4E00;&#x81F4;&#x8FD9;&#x4E00;&#x70B9;&#xFF0C;&#x5927;&#x901A;&#x9053;&#x6D3B;&#x52A8;&#x662F;&#x901A;&#x8FC7;&#x5B9E;&#x884C;&#x91CD;&#x7EC4; deltaN-Bcl-xl &#x63A7;&#x5236;&#x7EBF;&#x7C92;&#x4F53;&#x6A21;&#x4EFF;&#x548C;&#x901A;&#x8FC7;&#x4FEE;&#x8865;&#x7A0B;&#x5E8F;&#x5438;&#x7BA1;&#x7F3A;&#x8840;&#x540E;&#x7EBF;&#x7C92;&#x4F53;&#x529F;&#x80FD;&#x7684; Bcl-xl &#x6297;&#x4F53;&#x7B80;&#x4ECB;&#x88AB;&#x963B;&#x6B62;&#x3002;&#x901A;&#x9053;&#x6D3B;&#x52A8;&#x8FD8;&#x884C;&#x52A8;&#x70DF;&#x9170;&#x80FA;&#x817A;&#x560C;&#x5464;&#x4E8C;&#x6838;&#x82F7;&#x9178;&#xFF0C;&#x6307;&#x793A;&#x7EBF;&#x7C92;&#x4F53;&#x5916;&#x819C;&#x7535;&#x538B;&#x4F9D;&#x8D56;&#x6027;&#x9634;&#x79BB;&#x5B50;&#x901A;&#x9053; (VDAC) &#x7684;&#x4F5C;&#x7528;&#x53D7;&#x5230;&#x6291;&#x5236;&#x3002;&#x819C; impermeant Zn2 + &#x87AF; CaEDTA &#x4E4B;&#x524D;&#x5FC3;&#x808C;&#x7F3A;&#x8840;&#x6216;&#x4F53;&#x5916;&#x819C; permeant Zn2 + &#x87AF;&#x5408;&#x5242; tetrakis-(2-pyridylmethyl) &#x4E59;&#x4E8C;&#x80FA;&#x5E94;&#x7528;&#x51CF;&#x6BD2;&#x901A;&#x9053;&#x6D3B;&#x52A8;&#xFF0C;&#x63D0;&#x51FA;&#x4E00;&#x9879;&#x8981;&#x6C42;&#x4E3A; Zn2 + &#x4F53;&#x5185;&#x7BA1;&#x7406;&#x3002;&#x8FD9;&#x4E9B;&#x7814;&#x7A76;&#x7ED3;&#x679C;&#x63ED;&#x793A;&#x5176;&#x4E2D;&#x7F3A;&#x8840;&#x6027;&#x4FAE;&#x8FB1;&#x6270;&#x4E71;&#x529F;&#x80FD;&#x5B8C;&#x6574;&#x6027;&#x7684;&#x7EBF;&#x7C92;&#x4F53;&#x5916;&#x819C;&#xFF0C;&#x5E76;&#x7275;&#x8FDE; deltaN Bcl-xl &#x4E0E; VDAC &#x4E2D;&#x7684;&#x5927;&#xFF0C;Zn2 + &#x7684;&#x65B0;&#x673A;&#x5236;-&#x4F9D;&#x8D56;&#x7EBF;&#x7C92;&#x4F53;&#x901A;&#x9053;&#x5728;&#x7F3A;&#x8840;&#x540E;&#x6D77;&#x9A6C;&#x7EBF;&#x7C92;&#x4F53;&#x4E2D;&#x89C2;&#x5BDF;&#x5230;&#x3002;

&#x5728;&#x7F3A;&#x8840;&#x6027;&#x8111;&#x7EBF;&#x7C92;&#x4F53;&#x4E2D;&#x542B;&#x950C; multi-conductance &#x901A;&#x9053;&#x6D3B;&#x52A8;&#x3002;

Transient global ischemia is a neuronal insult that induces delayed cell death. A hallmark event in the early post-ischemic period is enhanced permeability of mitochondrial membranes. The precise mechanisms by which mitochondrial function is disrupted are, as yet, unclear. Here we show that global ischemia promotes alterations in mitochondrial membrane contact points, a rise in intramitochondrial Zn2+, and activation of large, multi-conductance channels in mitochondrial outer membranes by 1 h after insult. Mitochondrial channel activity was associated with enhanced protease activity and proteolytic cleavage of BCL-xL to generate its pro-death counterpart, deltaN-BCL-xL. The findings implicate deltaN-BCL-xL in large, multi-conductance channel activity. Consistent with this, large channel activity was mimicked by introduction of recombinant deltaN-BCL-xL to control mitochondria and blocked by introduction of a functional BCL-xL antibody to post-ischemic mitochondria via the patch pipette. Channel activity was also inhibited by nicotinamide adenine dinucleotide, indicative of a role for the voltage-dependent anion channel (VDAC) of the outer mitochondrial membrane. In vivo administration of the membrane-impermeant Zn2+ chelator CaEDTA before ischemia or in vitro application of the membrane-permeant Zn2+ chelator tetrakis-(2-pyridylmethyl) ethylenediamine attenuated channel activity, suggesting a requirement for Zn2+. These findings reveal a novel mechanism by which ischemic insults disrupt the functional integrity of the outer mitochondrial membrane and implicate deltaN-BCL-xL and VDAC in the large, Zn2+-dependent mitochondrial channels observed in post-ischemic hippocampal mitochondria.

Zinc-dependent multi-conductance channel activity in mitochondria isolated from ischemic brain.

Isch&eacute;mie globale transitoire est une insulte neuronale qui induit la mort cellulaire retard&eacute;e. Un &eacute;v&eacute;nement de marque distinctive dans le d&eacute;but de la p&eacute;riode post-isch&eacute;mique est la perm&eacute;abilit&eacute; des membranes mitochondriales. Les m&eacute;canismes pr&eacute;cis par lesquels la fonction mitochondriale est perturb&eacute;e sont, pour l&#39;instant, pas clairs. Nous d&eacute;montrons que cette isch&eacute;mie globale favorise des alt&eacute;rations dans les points de contact de la membrane mitochondriale, une &eacute;l&eacute;vation d&#39;intramitochondrial Zn2 + et l&#39;activation des canaux grands, multi-conductance dans la membrane externe mitochondriale de 1 h apr&egrave;s l&#39;insulte. L&#39;activit&eacute; mitochondriale a &eacute;t&eacute; associ&eacute;e &agrave; une activit&eacute; prot&eacute;ase am&eacute;lior&eacute;e et le clivage prot&eacute;olytique de BCL-xL pour g&eacute;n&eacute;rer son homologue Pro-mort, deltaN-BCL-xL. Les r&eacute;sultats indiquent que deltaN-BCL-xL dans l&#39;activit&eacute; du canal grande, multi-conductance. Compatible avec cela, activit&eacute; du grand canal a &eacute;t&eacute; imit&eacute;e par l&#39;introduction de recombinant deltaN-BCL-xL pour contr&ocirc;ler des mitochondries et bloqu&eacute;e par l&#39;introduction d&#39;un anticorps de BCL-xL fonctionnelle aux mitochondries post-isch&eacute;mique via la pipette. Activit&eacute; des canaux est aussi inhib&eacute;e par le nicotinamide ad&eacute;nine dinucl&eacute;otide, indicatif d&#39;un r&ocirc;le pour le canal anionique voltage-d&eacute;pendants (CAVD) de la membrane mitochondriale externe. Administration in vivo de la membrane-imperm&eacute;ants Zn2 + ch&eacute;lateur CaEDTA avant une isch&eacute;mie ou une application in vitro de l&#39;&eacute;thyl&egrave;nediamine tetrakis-(2-pyridylmethyl) membrane perm&eacute;able Zn2 + ch&eacute;lateur a att&eacute;nu&eacute; l&#39;activit&eacute;, ce qui sugg&egrave;re une n&eacute;cessit&eacute; pour Zn2 +. Ces r&eacute;sultats r&eacute;v&egrave;lent un nouveau m&eacute;canisme par lequel les insultes isch&eacute;miques perturbent l&#39;int&eacute;grit&eacute; fonctionnelle de la membrane mitochondriale externe et impliquent le deltaN-BCL-xL et CAVD dans les grands, Zn2 +-canaux mitochondrial d&eacute;pendants observ&eacute;s dans les mitochondries hippocampe post-isch&eacute;mique.

Activit&eacute; du canal multi-conductance zinc-d&eacute;pendant dans les mitochondries isol&eacute;es du cerveau isch&eacute;mique.

Transiente globale Isch&auml;mie ist eine neuronale Beleidigung, die verz&ouml;gerte Zelltod bedingt. Ein Markenzeichen-Ereignis in der Fr&uuml;hzeit der post-ischemic ist erh&ouml;hte Durchl&auml;ssigkeit der mitochondrialen Membranen. Die genauen Mechanismen, die durch die mitochondriale Funktion gest&ouml;rt ist, sind noch unklar. Hier zeigen wir, dass dieser globale Isch&auml;mie Umbauten in mitochondrialen Membran Kontaktstellen, einen Anstieg der intramitochondrial Zn2 + und Aktivierung von gro&szlig;en, multi-conductance Kan&auml;le in mitochondrialen &auml;u&szlig;eren Membranen von 1 h nach Beleidigung f&ouml;rdert. Mitochondriale Channel-Aktivit&auml;ten war verbunden mit verbesserten Protease-Aktivit&auml;t und proteolytische Spaltung von BCL-xL pro Gegenst&uuml;ck, Deltaner-BCL-xL zu generieren. Die Ergebnisse implizieren Deltaner-BCL-xL in gro&szlig;en, multi-conductance Channel-Aktivit&auml;ten. Einklang mit diesem gro&szlig;en Kanal Aktivit&auml;t nachgeahmt durch Einf&uuml;hrung von rekombinantem Deltaner-BCL-xL Mitochondrien steuern und durch Einf&uuml;hrung eines funktionalen BCL-xL-Antik&ouml;rpers in post-ischemic Mitochondrien &uuml;ber die Patch-Pipette blockiert wurde. Channel-Aktivit&auml;ten wurde auch durch Nicotinamid-adenin-dinucleotid, bezeichnend f&uuml;r eine Rolle f&uuml;r den Spannung-abh&auml;ngigen Anion Channel (VDAC) der &auml;u&szlig;eren mitochondrischen Membrane gehemmt. In-vivo-Administration von der Membran-impermeant Zn2 + Chelatbildner CaEDTA bevor Isch&auml;mie oder in-vitro Anwendung der Membran-permeant Zn2 + Chelatbildner tetrakis-(2-pyridylmethyl) Ethylendiamin abgeschw&auml;cht Channel-Aktivit&auml;ten, was auf eine Anforderung f&uuml;r Zn2 +. Diese Ergebnisse zeigen einen neuen Mechanismus, durch den isch&auml;mische Beleidigungen st&ouml;ren die funktionelle Integrit&auml;t der mitochondrialen Au&szlig;enmembran und implizieren Deltaner-BCL-xL und VDAC in den gro&szlig;en, Zn2 +-abh&auml;ngige mitochondriale Kan&auml;le im post-ischemic hippocampal Mitochondrien beobachtet.

Zink-abh&auml;ngige multi-conductance Channel-Aktivit&auml;ten in den Mitochondrien von isch&auml;mischen Gehirn isoliert.

Ischemia transitoria globale &egrave; un insulto neuronale che induce la morte cellulare ritardata. Un evento segno distintivo nel breve periodo il &egrave; una maggiore permeabilit&agrave; delle membrane mitocondriali. I meccanismi precisi di quale funzione mitocondriale &egrave; perturbato sono ancora poco chiari. Qui vi mostriamo che ischemia globale promuove alterazioni nei punti di contatto di membrana mitocondriale, un aumento della intramitochondrial Zn2 + e l&#39;attivazione di canali grandi, multi-conductance nella membrana mitocondriale esterna da 1 h dopo insulto. Attivit&agrave; del canale mitocondriale &egrave; stato associato con attivit&agrave; proteasica rafforzata e clivaggio proteolitico di BCL-xL per generare la sua controparte pro-death, Deltana-BCL-xL. I risultati coinvolgono Deltana-BCL-xL in attivit&agrave; del canale grande, multi-conductance. Coerenti con questo, attivit&agrave; del grande canale fu imitato da introduzione di ricombinanti Deltana-BCL-xL per controllare i mitocondri e bloccato dall&#39;introduzione di un anticorpo di BCL-xL funzionale ai mitocondri i via la pipetta di patch. Attivit&agrave; del canale &egrave; stato inibito anche da nicotinamide adenina dinucleotide, indicativo di un ruolo per il canale voltaggio-dipendente anione (VDAC) della membrana mitocondriale esterna. Somministrazione in vivo di membrana-impermeant Zn2 + chelante CaEDTA prima di ischemia o applicazione in vitro della membrana permeant etilendiammina tetrakis-(2-pyridylmethyl) di chelante Zn2 + attenuato attivit&agrave; del canale, suggerendo un requisito per Zn2 +. Questi risultati rivelano un meccanismo romanzo da cui insulti ischemici perturbare l&#39;integrit&agrave; funzionale della membrana mitocondriale esterna e coinvolgono Deltana-BCL-xL e VDAC nel grande, Zn2 +-dipendente canali mitocondriale osservano nei mitocondri hippocampal i.

Attivit&agrave; del canale multi-conductance zinco-dipendente in mitocondri isolati da ischemico cerebrale.

&#x4E00;&#x6642;&#x7684;&#x306A;&#x30B0;&#x30ED;&#x30FC;&#x30D0;&#x30EB;&#x865A;&#x8840;&#x9045;&#x5EF6;&#x7D30;&#x80DE;&#x6B7B;&#x3092;&#x8A98;&#x5C0E;&#x3059;&#x308B;&#x795E;&#x7D4C;&#x4FAE;&#x8FB1;&#x3067;&#x3059;&#x3002;&#x7279;&#x5FB4;&#x30A4;&#x30D9;&#x30F3;&#x30C8;&#x963B;&#x8840;&#x5F8C;&#x521D;&#x671F;&#x306B;&#x304A;&#x3051;&#x308B;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x819C;&#x306E;&#x5F37;&#x5316;&#x3055;&#x308C;&#x305F;&#x900F;&#x904E;&#x6027;&#x3067;&#x3059;&#x3002;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x306E;&#x6A5F;&#x80FD;&#x304C;&#x4E2D;&#x65AD;&#x3055;&#x308C;&#x308B;&#x6B63;&#x78BA;&#x306A;&#x30E1;&#x30AB;&#x30CB;&#x30BA;&#x30E0;&#x306F;&#x307E;&#x3060;&#x4E0D;&#x660E;&#x3067;&#x3042;&#x308A;&#x307E;&#x3059;&#x3002;&#x3053;&#x3053;&#x3067;&#x306F;&#x30B0;&#x30ED;&#x30FC;&#x30D0;&#x30EB;&#x306E;&#x865A;&#x8840;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x819C;&#x306E;&#x63A5;&#x89E6;&#x30DD;&#x30A4;&#x30F3;&#x30C8;&#x306E;&#x5909;&#x66F4;&#x306B;&#x3064;&#x3044;&#x3066;&#x3001;1 h &#x306B;&#x3088;&#x308B;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x5185; zn 2 +&#x3001;&#x304A;&#x3088;&#x3073;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x5916;&#x819C;&#x3067;&#x5927;&#x898F;&#x6A21;&#x306A; multi-conductance &#x30C1;&#x30E3;&#x30CD;&#x30EB;&#x306E;&#x6D3B;&#x6027;&#x5316;&#x306E;&#x4E0A;&#x6607;&#x5F8C;&#x4FAE;&#x8FB1;&#x3092;&#x4FC3;&#x9032;&#x3059;&#x308B;&#x3092;&#x793A;&#x3057;&#x307E;&#x3059;&#x3002;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2; &#x30C1;&#x30E3;&#x30CD;&#x30EB;&#x306E;&#x5229;&#x7528;&#x72B6;&#x6CC1;&#x306F;&#x3001;&#x5F37;&#x5316;&#x3055;&#x308C;&#x305F;&#x30D7;&#x30ED;&#x30C6;&#x30A2;&#x30FC;&#x30BC;&#x6D3B;&#x6027;&#x3068;&#x30D7;&#x30ED;&#x5BFE;&#x5FDC; deltaN Bcl-xl &#x3092;&#x751F;&#x6210;&#x3059;&#x308B; bcl-xl &#x86CB;&#x767D;&#x8CEA;&#x5206;&#x89E3;&#x958B;&#x88C2;&#x306B;&#x95A2;&#x9023;&#x4ED8;&#x3051;&#x3089;&#x308C;&#x3066;&#x3060;&#x3063;&#x305F;&#x3002;&#x8ABF;&#x67FB;&#x7D50;&#x679C; deltaN Bcl-xl &#x5927;&#x3001;multi-conductance &#x30C1;&#x30E3;&#x30CD;&#x30EB;&#x306E;&#x6D3B;&#x52D5;&#x306B;&#x5DFB;&#x304D;&#x8FBC;&#x307F;&#x307E;&#x3059;&#x3002;&#x4E00;&#x8CAB;&#x6027;&#x306E;&#x3042;&#x308B;&#x3053;&#x308C;&#x3067;&#x591A;&#x30C1;&#x30E3;&#x30F3;&#x30CD;&#x30EB;&#x6D3B;&#x52D5;&#x3055;&#x308C;&#x305F;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x3092;&#x5236;&#x5FA1;&#x3059;&#x308B;&#x907A;&#x4F1D;&#x5B50;&#x7D44;&#x63DB;&#x3048; deltaN BCL xL &#x306E;&#x5C0E;&#x5165;&#x306B;&#x3088;&#x3063;&#x3066;&#x3092;&#x307E;&#x306D;&#x3057;&#x3066;&#x30D1;&#x30C3;&#x30C1; &#x30D4;&#x30DA;&#x30C3;&#x30C8;&#x306B;&#x3088;&#x308B;&#x865A;&#x8840;&#x5F8C;&#x306E;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x6A5F;&#x80FD; Bcl-xl &#x6297;&#x4F53;&#x306E;&#x5C0E;&#x5165;&#x306B;&#x3088;&#x3063;&#x3066;&#x30D6;&#x30ED;&#x30C3;&#x30AF;&#x3057;&#x307E;&#x3059;&#x3002;&#x30C1;&#x30E3;&#x30CD;&#x30EB;&#x306E;&#x5229;&#x7528;&#x72B6;&#x6CC1;&#x306F;&#x3001;&#x30CB;&#x30B3;&#x30C1;&#x30F3;&#x9178;&#x30A2;&#x30DF;&#x30C9;&#x30A2;&#x30C7;&#x30CB;&#x30F3;&#x30B8;&#x30CC;&#x30AF;&#x30EC;&#x30AA;&#x30C1;&#x30C9;&#x3001;&#x5916;&#x306E;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x819C;&#x96FB;&#x4F4D;&#x4F9D;&#x5B58;&#x6027;&#x30A4;&#x30AA;&#x30F3; &#x30C1;&#x30E3;&#x30CD;&#x30EB; (VDAC) &#x306E;&#x5F79;&#x5272;&#x3092;&#x793A;&#x3059;&#x3082;&#x306E;&#x3067;&#x3082;&#x6291;&#x5236;&#x3055;&#x308C;&#x307E;&#x3057;&#x305F;&#x3002;In vivo &#x6295;&#x4E0E;&#x3001;&#x819C;&#x975E;&#x900F;&#x904E;&#x6027;&#x306E; zn 2 + &#x30AD;&#x30EC;&#x30FC;&#x30C8;&#x865A;&#x8840;&#x304A;&#x3088;&#x3073; in vitro &#x3067;&#x306E;&#x30A2;&#x30D7;&#x30EA;&#x30B1;&#x30FC;&#x30B7;&#x30E7;&#x30F3;&#x306E;&#x819C;&#x4E0B;&#x6D41; zn 2 + &#x30AD;&#x30EC;&#x30FC;&#x30C8;&#x5264; tetrakis-(2-pyridylmethyl) &#x30A8;&#x30C1;&#x30EC;&#x30F3;&#x30B8;&#x30A2;&#x30DF;&#x30F3;&#x306E;&#x30C1;&#x30E3;&#x30CD;&#x30EB;&#x306E;&#x5229;&#x7528;&#x72B6;&#x6CC1;&#x3092;&#x6E1B;&#x8870;&#x3059;&#x308B;&#x524D;&#x306B; CaEDTA &#x8981;&#x4EF6; zn 2 + &#x3092;&#x793A;&#x5506;&#x3057;&#x3066;&#x3044;&#x308B;&#x306E;&#x3002;&#x3053;&#x308C;&#x3089;&#x306E;&#x8ABF;&#x67FB;&#x7D50;&#x679C;&#x306F;&#x865A;&#x8840;&#x6027;&#x306F;&#x5916;&#x306E;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x819C;&#x306E;&#x6A5F;&#x80FD;&#x306E;&#x6574;&#x5408;&#x6027;&#x3092;&#x6DF7;&#x4E71;&#x3055;&#x305B;&#x308B;&#x3057;&#x3001;&#x3059;&#x308B;&#x5927;&#x898F;&#x6A21;&#x306A; zn 2 + deltaN Bcl-xl &#x3068; VDAC &#x3092;&#x5DFB;&#x304D;&#x8FBC;&#x3080;&#x65B0;&#x3057;&#x3044;&#x30E1;&#x30AB;&#x30CB;&#x30BA;&#x30E0;&#x3092;&#x660E;&#x3089;&#x304B;&#x306B;-&#x4F9D;&#x5B58;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2; &#x30C1;&#x30E3;&#x30F3;&#x30CD;&#x30EB;&#x89B3;&#x6E2C;&#x306B;&#x304A;&#x3051;&#x308B;&#x865A;&#x8840;&#x5F8C;&#x306E;&#x6D77;&#x99AC;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x3002;

&#x4E9C;&#x925B;&#x4F9D;&#x5B58;&#x6027; multi-conductance &#x30C1;&#x30E3;&#x30CD;&#x30EB;&#x6D3B;&#x6027;&#x865A;&#x8840;&#x6027;&#x8133;&#x304B;&#x3089;&#x5206;&#x96E2;&#x3055;&#x308C;&#x307E;&#x3057;&#x305F;&#x3002;

&#xC784;&#xC2DC; &#xAE00;&#xB85C;&#xBC8C; &#xD5C8; &#xD608; &#xC9C0;&#xC5F0;&#xB41C; &#xC138;&#xD3EC; &#xC8FD;&#xC74C;&#xC744; &#xC720;&#xB3C4; &#xD558;&#xB294; &#xC2E0;&#xACBD; &#xBAA8;&#xC695; &#xC774;&#xB2E4;. Post-ischemic &#xC2DC;&#xB300; &#xCD08;&#xAE30;&#xC5D0; &#xAC01; &#xC778; &#xC774;&#xBCA4;&#xD2B8;&#xB294; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xB9C9;&#xC758; &#xCE68;&#xD22C;&#xC131;&#xC744; &#xAC15;&#xD654;. &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xAE30;&#xB2A5; &#xC911;&#xB2E8; &#xB418;&#xB294; &#xC815;&#xD655;&#xD55C; &#xBA54;&#xCEE4;&#xB2C8;&#xC998;&#xC740;, &#xC544;&#xC9C1;, &#xBD84;&#xBA85;. &#xC5EC;&#xAE30; &#xC6B0;&#xB9AC;&#xB294; &#xAE00;&#xB85C;&#xBC8C; &#xD5C8; &#xD608; &#xBAA8;&#xC695; &#xD6C4; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC; &#xB9AC;&#xC544; &#xBA64;&#xBE0C;&#xB808;&#xC778; &#xC811;&#xC810;&#xC73C;&#xB85C; &#xBCC0;&#xACBD;, 1 h intramitochondrial Zn2 + &#xBC0F; &#xC678;&#xBD80; &#xC138;&#xD3EC; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xB9C9;&#xC5D0; &#xD070;, multi-conductance &#xCC44;&#xB110;&#xC758; &#xD65C;&#xC131;&#xD654;&#xC758; &#xC0C1;&#xC2B9;&#xC744; &#xCD09;&#xC9C4;&#xC744; &#xBCF4;&#xC5EC;&#xC90D;&#xB2C8;&#xB2E4;. &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xCC44;&#xB110; &#xD65C;&#xB3D9; &#xD5A5;&#xC0C1; &#xB41C; &#xD504;&#xB85C; &#xD14C;&#xC544; &#xC81C; &#xD65C;&#xB3D9; &#xBC0F; BCL-xL &#xC2F1;&#xD06C;&#xB300; &#xD30C;&#xD2F0;&#xC158;&#xCC98;&#xB7FC; deltaN BCL xL &#xC0DD;&#xC131;&#xC758; &#xB2E8;&#xBC31;&#xC9C8; &#xBD84;&#xC5F4;&#xC640; &#xC5F0;&#xAD00; &#xB418;&#xC5C8;&#xB2E4;. &#xC5F0;&#xAD6C; &#xACB0;&#xACFC;, multi-conductance &#xCC44;&#xB110; &#xD65C;&#xB3D9;&#xC5D0;&#xC11C; deltaN BCL xL &#xC5F0;&#xB8E8;. &#xC77C;&#xAD00; &#xB41C; &#xD070; &#xCC44;&#xB110; &#xD65C;&#xB3D9;&#xC774;, &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544;&#xB97C; &#xC81C;&#xC5B4; &#xD558;&#xB824;&#xBA74; deltaN-BCL-xL &#xC7AC;&#xC870;&#xD569;&#xC758; &#xB3C4;&#xC785;&#xC5D0; &#xC758;&#xD574; &#xC720;&#xC0AC; &#xD558; &#xACE0; &#xD328;&#xCE58; &#xD53C; &#xD3AB;&#xC744; &#xD1B5;&#xD574; post-ischemic &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xAE30;&#xB2A5; BCL-xl&#xC5D0; &#xD56D; &#xCCB4;&#xC758; &#xB3C4;&#xC785;&#xC5D0; &#xC758;&#xD574; &#xCC28;&#xB2E8; &#xD588;&#xB2E4;. &#xCC44;&#xB110; &#xD65C;&#xB3D9; &#xB610;&#xD55C; &#xB2C8;&#xCF54;&#xD2F4;&#xC544;&#xBBF8;&#xB4DC; &#xC544;&#xB370;&#xB2CC; &#xB514;&#xB274;&#xD074;&#xB808;&#xC624;&#xD2F0;&#xB4DC;, &#xC678;&#xBD80; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC; &#xB9AC;&#xC544; &#xBA64;&#xBE0C;&#xB808;&#xC778;&#xC758; &#xC804;&#xC555; &#xC885;&#xC18D; &#xC74C;&#xC774;&#xC628; &#xCC44;&#xB110; (VDAC)&#xC5D0; &#xB300; &#xD55C; &#xC5ED;&#xD560;&#xC758; &#xC9C0;&#xD45C;&#xC5D0; &#xC758;&#xD574; &#xC800;&#xD574; &#xB418;&#xC5C8;&#xB2E4;. &#xBA64;&#xBE0C;&#xB808;&#xC778; impermeant Zn2 + chelator CaEDTA &#xAD6D; &#xC18C; &#xBE48; &#xD608; &#xB610;&#xB294; &#xCCB4; &#xC678; &#xC751;&#xC6A9; &#xD504;&#xB85C;&#xADF8;&#xB7A8; &#xB9C9; permeant Zn2 + chelator tetrakis-(2-pyridylmethyl) ethylenediamine&#xC758; &#xAC10;&#xC1E0; &#xCC44;&#xB110; &#xD65C;&#xB3D9; &#xC804;&#xC5D0; Zn2 +&#xC5D0; &#xB300; &#xD55C; &#xC694;&#xAD6C; &#xC0AC;&#xD56D;&#xC740; &#xC81C;&#xC548;&#xC758; vivo&#xC5D0;&#xC11C; &#xAD00;&#xB9AC;. &#xC774;&#xB7EC;&#xD55C; &#xC5F0;&#xAD6C; &#xACB0;&#xACFC; &#xACF5;&#xAC1C;&#xB294; &#xD5C8; &#xD608; &#xC131; &#xBAA8;&#xC695;&#xACFC; &#xC678;&#xBD80; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xB9C9;&#xC758; &#xAE30;&#xB2A5;&#xC801; &#xBB34;&#xACB0;&#xC131;&#xC744; &#xC911;&#xB2E8; &#xC2DC;&#xD0AC; &#xB300;&#xADDC;&#xBAA8;, Zn2 + deltaN-BCL-Xl&#xACFC; VDAC&#xC744; &#xC62D; &#xC544; &#xB9E4;&#xAE30; &#xC18C;&#xC124; &#xBA54;&#xCEE4;&#xB2C8;&#xC998;-&#xC885;&#xC18D; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC; &#xB9AC;&#xC544; &#xCC44;&#xB110; post-ischemic hippocampal &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544;&#xC5D0;&#xC11C; &#xAD00;&#xCC30;.

&#xD5C8; &#xD608; &#xC131; &#xB1CC;&#xC5D0;&#xC11C; &#xACE0;&#xB9BD; &#xB41C; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544;&#xC5D0;&#xC11C; &#xC544;&#xC5F0; &#xC885;&#xC18D; multi-conductance &#xCC44;&#xB110; &#xD65C;&#xB3D9;.

Isquemia global transitoria es un insulto neuronal que induce muerte celular retardada. Un evento distintivo en el per&iacute;odo temprano de la post-ischemic es mayor permeabilidad de las membranas mitocondriales. Los mecanismos precisos por los cuales se interrumpe la funci&oacute;n mitocondrial son, todav&iacute;a, claros. Aqu&iacute; mostramos que la isquemia global promueve alteraciones en puntos de contacto de membrana mitocondrial, un aumento de intramitochondrial Zn2 + y la activaci&oacute;n de canales grandes, multi-conductance en las membranas mitocondriales del exteriores por 1 h despu&eacute;s de insulto. Actividad del canal mitocondrial se asoci&oacute; con actividad prote&aacute;sica mejorada y clivaje proteol&iacute;tico de BCL-xL para generar a su hom&oacute;logo partidarios, deltaN-BCL-xL. Los resultados implican deltaN-BCL-xL en la actividad del canal grande, multi-conductance. Consecuente con esto, actividad del canal grande fue imitado por introducci&oacute;n de recombinante deltaN-BCL-xL para controlar las mitocondrias y bloqueado por la introducci&oacute;n de un anticuerpo funcional de BCL-xL post-ischemic mitocondria mediante la pipeta de parche. Actividad del canal tambi&eacute;n fue inhibida por nicotinamida adenina dinucle&oacute;tido, indicativo de un papel para el canal ani&oacute;nico dependiente de voltaje (VDAC) de la membrana mitocondrial externa. Administraci&oacute;n en vivo de la membrana-impermeant Zn2 + quelante CaEDTA antes de isquemia o aplicaci&oacute;n in vitro de la membrana-Florescente Zn2 + quelante tetrakis-(2-pyridylmethyl) etilendiamina aten&uacute;a la actividad del canal, lo que sugiere un requisito para Zn2 +. Estos resultados revelan un nuevo mecanismo por el cual isqu&eacute;micas insultos interrumpen la integridad funcional de la membrana mitocondrial externa e implican deltaN-BCL-xL y VDAC en el grande, Zn2 +-dependientes canales mitocondriales observaron en las mitocondrias hippocampal post-ischemic.

Actividad de canal multi-conductance dependientes de zinc en las mitocondrias aisladas de cerebro isqu&eacute;mico.

Role of c-Src in muscle differentiation has been controversial. Here, we investigated if c-Src positively or negatively regulates muscle differentiation, using H9c2 and C2C12 cell lines. Inhibition of c-Src by treatment with PP1 and SU6656, pharmacologic inhibitors of Src family kinases, or by expression of a dominant negative c-Src, all induced muscle differentiation in proliferation medium (PM). In differentiating cells in differentiation medium (DM), c-Src activity gradually decreased and reached basal level 3 days after induction of differentiation. Inhibition of c-Src suppressed Raf/MEK/ERK pathway but activated p38 MAPK. Inhibition of p38 MAPK did not affect c-Src activity in PM. However, it reactivated Raf/MEK/ERK pathway in c-Src-inhibited cells regardless of PM or DM. Concomitant inhibition of c-Src and p38 MAPK activities blocked muscle differentiation in both media. In conclusion, suppression of c-Src activity stimulates muscle differentiation by activating p38 MAPK uni-directionally.

Suppression of c-Src activity stimulates muscle differentiation via p38 MAPK activation.

Transmembrane AMPA receptor regulatory proteins (TARPs) are auxiliary AMPA receptor subunits that regulate both the trafficking and gating properties of AMPA receptors, and different TARP isoforms display distinct expression patterns in brain. Here, we compared the effects of four TARP isoforms on the kinetics of AMPA receptor currents. Each isoform slowed the deactivation of GluR1 currents, but the slowing was greatest with gamma-4 and gamma-8. Isoform-specific differences in desensitization were also observed that correlated with effects on deactivation. TARP isoforms also differentially modulated responses to trains of glutamate applications designed to mimic high-frequency presynaptic firing. Importantly, whereas both stargazin and gamma-4 rescued excitatory synaptic transmission in cerebellar granule cells from stargazer mice, the decay of miniature EPSCs was 2-fold slower in neurons expressing gamma-4. The results show that heterogeneity in the composition of AMPA receptor/TARP complexes contributes to synapse-specific differences in EPSC decays and frequency-dependent modulation of neurotransmission.

Two families of TARP isoforms that have distinct effects on the kinetic properties of AMPA receptors and synaptic currents.

Neuronal AMPA receptors autoinactivate at high concentrations of glutamate, i.e., the current declines at glutamate concentrations above 10-100 microM. The mechanisms underlying this phenomenon are unclear. Stargazin-like TARPs are AMPA receptor auxiliary subunits that modulate receptor trafficking and channel properties. Here, we found that neuronal AMPA receptors and recombinant AMPA receptors coexpressed with stargazin autoinactivate at high concentrations of glutamate, whereas recombinant AMPA receptors expressed alone do not. The reduction of currents at high glutamate concentrations is not associated with a reduction of AMPA receptor number, but rather with the loss of stargazin-associated allosteric modulation of channel gating. We show that receptor desensitization promotes the dissociation of TARP-AMPA receptor complexes in a few milliseconds. This dissociation mechanism contributes to synaptic short-term modulation. The results demonstrate a mechanism for dynamic regulation of AMPA receptor activity to tune synaptic strength.

Autoinactivation of neuronal AMPA receptors via glutamate-regulated TARP interaction.

Studies of epilepsy have mainly focused on the membrane proteins that control neuronal excitability. Recently, attention has been shifting to intracellular proteins and their interactions, signaling cascades and feedback regulation as they relate to epilepsy. The mTOR (mammalian target of rapamycin) signal transduction pathway, especially, has been suggested to play an important role in this regard. These pathways are involved in major physiological processes as well as in numerous pathological conditions. Here, involvement of the mTOR pathway in epilepsy will be reviewed by presenting; an overview of the pathway, a brief description of key signaling molecules, a summary of independent reports and possible implications of abnormalities of those molecules in epilepsy, a discussion of the lack of experimental data, and questions raised for the understanding its epileptogenic mechanism.

Frontier of epilepsy research - mTOR signaling pathway.

The pathogenesis of osteonecrosis of the femoral head (ONFH) has been implicated in hypofibrinolysis and blood supply interruption. Previous studies have demonstrated that decreased fibrinolytic activity due to elevated plasminogen activator inhibitor-1 (PAI-1) levels correlates with ONFH pathogenesis. The -675 4G/5G single nucleotide polymorphism (SNP rs1799889) in the PAI-1 gene promoter is associated with PAI-1 plasma level. We investigated whether rs1799889 and two other SNPs of the PAI-1 gene (rs2227631, -844 G/A in the promoter; rs11178, +10700 C/T in the 3'UTR) are associated with increased ONFH risk.

Significant associations of PAI-1 genetic polymorphisms with osteonecrosis of the femoral head.

Unstable carotid atherosclerotic plaques are characterized by cap rupture, leading to thromboembolism and stroke. Matrix metalloproteinases (MMPs) have been implicated in the progression of atherosclerosis and plaque rupture. The aim of this study was to assess the relationship between the expressions of MMP-2 and MMP-9 and carotid plaque instability.

Plaque rupture is a determinant of vascular events in carotid artery atherosclerotic disease: involvement of matrix metalloproteinases 2 and 9.

The apoptosis of cancer cells is associated with changes in the important cell properties including morphology, surface roughness and stiffness. Therefore, the changes in morphology and biophysical properties can be a good way of evaluating the anticancer activity of a drug. This study examined the effect of paclitaxel on the properties of Ishikawa and HeLa cells using atomic force microscopy (AFM), and the relationship between the changes in morphology and the biophysical properties and apoptosis was discussed. The viability and proliferation of the cells were analyzed using the methylthiazol tetrazolium (MTT) method and a TUNEL assay to confirm cellular apoptosis due to a paclitaxel treatment. AFM observations clearly showed the apoptotic morphological and biophysical changes in Ishikawa and HeLa cells. After the paclitaxel treatment, the cell membrane was torn and holed, the surface roughness was increased, and the stiffness was decreased. These changes were observed more apparently after a 24 h treatment and in Ishikawa cells compared to HeLa cells. The MTT and TUNEL assays results revealed the Ishikawa cells to be more sensitive to paclitaxel than HeLa cells and definite apoptosis occurred after a 24 h treatment. These results showed good agreement with the AFM results. Therefore, research on the morphological and biophysical changes by AFM in cancer cells will help to evaluate the anticancer activities of the drugs.

AFM-detected apoptotic changes in morphology and biophysical property caused by paclitaxel in Ishikawa and HeLa cells.

Because the cell membrane is an important regulator of cell function, its morphological changes are important markers of cell apoptosis. These changes can differ for each cell type, and depend on the treatment conditions, including the drug, doses, and treatment time. To quantify morphological changes, HeLa and Ishikawa cells were investigated with atomic force microscopy. Both cells were treated with cisplatin (1 mM) for 24 hours. The viability and proliferation of the cells were analyzed with methylthiazol tetrazolium method. The proliferation rates of both cells treated with cisplatin decreased more than 50%. The morphological changes induced by cisplatin were dependent on the cell type, and the results were determined quantitatively. The surface of HeLa cells became rougher with cisplatin treatment, whereas cisplatin-treated Ishikawa cells were smoother than untreated cells. In both cases, cell height was decreased with cisplatin treatment. These results suggest that atomic force microscopy can be used to analyze anticancer drug activity in cancer cells.

Quantitative analysis with atomic force microscopy of cisplatin-induced morphological changes in HeLa and Ishikawa cells.

DNA DSBs are induced by IR or radiomimetic drugs such as doxorubicin. It has been indicated that cells from ataxia-telangiectasia patients are highly sensitive to radiation due to defects in DNA repair, but whether they have impairment in apoptosis has not been fully elucidated. A-T cells showed increased sensitivity to high levels of DNA damage, however, they were more resistant to low doses. Normal cells treated with combination of KU55933, a specific ATM kinase inhibitor, and doxorubicin showed increased resistance as they do in a similar manner to A-T cells. A-T cells have higher viability but more DNA breaks, in addition, the activations of p53 and apoptotic proteins (Bax and caspase-3) were deficient, but Akt expression was enhanced. A-T cells subsequently underwent premature senescence after treatment with a low dose of doxorubicin, which was confirmed by G2 accumulation, senescent morphology, and SA-Î²-gal positive until 15 days repair incubation. Finally, A-T cells are radio-resistant at low doses due to its defectiveness in detecting DNA damage and apoptosis, but the accumulation of DNA damage leads cells to premature senescence.

ATM-deficient human fibroblast cells are resistant to low levels of DNA double-strand break induced apoptosis and subsequently undergo drug-induced premature senescence.

The circadian pattern of seizures in people with epilepsy (PWE) was first described two millennia ago. However, these phenomena have not received enough scientific attention, possibly due to the lack of promising hypotheses to address the interaction between seizure generation and a physiological clock. To propose testable hypotheses at the molecular level, interactions between circadian rhythm, especially transcription factors governing clock genes expression, and the mTOR (mammalian target of rapamycin) signaling pathway, the major signaling pathway in epilepsy, will be reviewed. Then, two closely related hypotheses will be proposed: (1) Rhythmic activity of hyperactivated mTOR signaling molecules results in rhythmic increases in neuronal excitability. These rhythmic increases in excitability periodically exceed the seizure threshold, displaying the behavioral seizures. (2) Oscillation of neuronal excitability in SCN modulates the rhythmic excitability in the hippocampus through subiculum via long-range projections. Findings from published results, their implications, and proposals for new experiments will be discussed. These attempts may ignite further discussion on what we still need to learn about the rhythmicity of spontaneous seizures.

Molecular mechanism of circadian rhythmicity of seizures in temporal lobe epilepsy.

Microcephalin 1 (MCPH1) has a crucial role in the DNA damage response by promoting the expression of checkpoint kinase 1 (CHK1) and breast cancer susceptibility gene 1 (BRCA1). MCPH1 containing BRCT domain has been suggested as a tumor suppressor in breast and ovarian cancers. We analyzed the effect of both protein expression and MCPH1 polymorphisms in breast cancer patients. Low nuclear expression of microcephalin was present in 52.4% of breast cancers and was associated with allele T in rs2912010 (p=0.046). However, cytoplasmic microcephalin expression increased with increasing grade (p=0.010). An association between low nucleus microcephalin expression and allele T was identified in rs2912010 (p=0.046). After data analysis, allele distribution of the MCPH1 polymorphisms was not different between breast cancer patients and healthy controls. But the polymorphism was associated with negative status for ER (rs2912010/C2302T; p=0.032, rs1057090/C2358T; p=0.027, rs2912016/C2494A; p=0.024), and allele T in both rs2912010 and rs1057090 was associated with increasing tumor grade (rs2912010; p=0.040, rs1057090; p=0.043) in breast cancer. We are first to report that association of MCPH1 protein expression and its polymorphisms in breast cancer. The MCPH1 polymorphisms and protein expression were associated with tumorigenesis in breast cancer and may be a useful biomarker for identification of the aggressive types of breast cancer.

MCPH1 protein expression and polymorphisms are associated with risk of breast cancer.

The structural and morphological properties of the teratoma membrane were investigated to better understand the pathogenesis of ovarian teratomas. A mature cystic teratoma and amnion were obtained from patients who underwent laparoscopic cystectomy and uncomplicated delivery, respectively. The teratoma membrane was divided into three layers according to the results of the histological analysis. Each layer showed distinct morphological properties, including an outer layer that was uniformly arranged, a middle layer with an irregular pattern of fibers, and an inner layer that was structurally dense with a wavy pattern of fibers. The morphology of the layers of the amniotic membrane was the reverse that of the teratoma membrane. In the teratoma membrane, the outer layer was primarily composed of type III collagen and the inner layer had a large amount of type III and IV collagen. The amniotic membrane showed a small amount of type III collagen in the outer layer, whereas the inner layer had large amounts of type I, III, and IV collagen. In the teratoma membrane, the collagen fibrils were arranged regularly in the outer layer, but irregularly in the inner layer. In the amniotic membrane, the arrangement of collagen fibrils was the reverse that of the teratoma membrane. Additionally, the collagen fibrils in the teratoma membrane were thinner than those of the amniotic membrane and had slightly shorter d-spacing. Two membranes showed the differences in collagen fibril arrangement, which may caused by the different functional roles.

Article	Year
Rapid upregulation of alpha7 nicotinic acetylcholine receptors by tyrosine dephosphorylation. The Journal of neuroscience : the official journal of the Society for Neuroscience\| PubMed ID: 15814802	2005
Zinc-dependent multi-conductance channel activity in mitochondria isolated from ischemic brain. The Journal of neuroscience : the official journal of the Society for Neuroscience\| PubMed ID: 16793892	2006
Suppression of c-Src activity stimulates muscle differentiation via p38 MAPK activation. Archives of biochemistry and biophysics\| PubMed ID: 17612500	2007
Two families of TARP isoforms that have distinct effects on the kinetic properties of AMPA receptors and synaptic currents. Neuron\| PubMed ID: 17880893	2007
Autoinactivation of neuronal AMPA receptors via glutamate-regulated TARP interaction. Neuron\| PubMed ID: 19146816	2009
Frontier of epilepsy research - mTOR signaling pathway. Experimental & molecular medicine\| PubMed ID: 21467839	2011
Significant associations of PAI-1 genetic polymorphisms with osteonecrosis of the femoral head. BMC musculoskeletal disorders\| PubMed ID: 21752301	2011
Plaque rupture is a determinant of vascular events in carotid artery atherosclerotic disease: involvement of matrix metalloproteinases 2 and 9. Journal of clinical neurology (Seoul, Korea)\| PubMed ID: 21779294	2011
AFM-detected apoptotic changes in morphology and biophysical property caused by paclitaxel in Ishikawa and HeLa cells. PloS one\| PubMed ID: 22272274	2012
Quantitative analysis with atomic force microscopy of cisplatin-induced morphological changes in HeLa and Ishikawa cells. Journal of Nippon Medical School = Nippon Ika Daigaku zasshi\| PubMed ID: 23123387	2012
ATM-deficient human fibroblast cells are resistant to low levels of DNA double-strand break induced apoptosis and subsequently undergo drug-induced premature senescence. Biochemical and biophysical research communications\| PubMed ID: 23178571	2013
Molecular mechanism of circadian rhythmicity of seizures in temporal lobe epilepsy. Frontiers in cellular neuroscience\| PubMed ID: 23189039	2012
MCPH1 protein expression and polymorphisms are associated with risk of breast cancer. Gene\| PubMed ID: 23296058	2013
Characterization of ultrastructure and collagen composition of the teratoma membrane: comparison to the amniotic membrane. Microscopy research and technique\| PubMed ID: 23401282	2013
New mechanism for glutamate hypothesis in epilepsy. Frontiers in cellular neuroscience\| PubMed ID: 23964202	2013

Chang Hoon Cho

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