RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing

Small interfering RNA (siRNA) is among the most widely used RNA interference methods for the short-term silencing of protein-coding genes. siRNA is a ...

Asan Medical Center

A cDNA, PHCC-TPx, specifying a protein highly homologous to known phospholipid hydroperoxide glutathione peroxidases was isolated from a Chinese cabbage cDNA library. PHCC-TPx encodes a preprotein of 232 amino acids containing a putative N-terminal chloroplast targeting sequence and three conserved Cys residues (Cys(107), Cys(136), and Cys(155)). The mature form of enzyme without the signal peptide was expressed in Escherichia coli, and the recombinant protein was found to utilize thioredoxin (Trx) but not GSH as an electron donor. In the presence of a Trx system, the protein efficiently reduces H(2)O(2) and organic hydroperoxides. Complementation analysis shows that overexpression of the PHCC-TPx restores resistance to oxidative stress in yeast mutants lacking GSH but fails to complement mutant lacking Trx, suggesting that the reducing agent of PHCC-TPx in vivo is not GSH but is Trx. Mutational analysis of the three Cys residues individually replaced with Ser shows that Cys(107) is the primary attacking site by peroxide, and oxidized Cys(107) reacts with Cys(155)-SH to make an intramolecular disulfide bond, which is reduced eventually by Trx. Tryptic peptide analysis by matrix-assisted laser desorption and ionization time of flight mass spectrometry shows that Cys(155) can form a disulfide bond with either Cys(107) or Cys(136).

A Chinese cabbage cDNA with high sequence identity to phospholipid hydroperoxide glutathione peroxidases encodes a novel isoform of thioredoxin-dependent peroxidase.

Rheumatoid arthritis (RA) synoviocytes are resistant to apoptosis and exhibit a transformed phenotype, which might be caused by chronic exposure to genotoxic stimuli including reactive oxygen species and growth factors. In this study, we investigated the role of vascular endothelial growth factor165 (VEGF165), a potent angiogenic factor, and its receptor in the apoptosis of synoviocytes. We demonstrated here that neuropilin-1, rather than fms-like tyrosine kinase-1 and kinase insert domain-containing receptor, is the major VEGF165 receptor in the fibroblast-like synoviocytes. Neuropilin-1 was highly expressed in the lining layer, infiltrating leukocytes, and endothelial cells of rheumatoid synovium. The production of VEGF165, a ligand for neuropilin, was significantly higher in the RA synoviocytes than in the osteoarthritis synoviocytes. The ligation of recombinant VEGF165 to its receptor prevented the apoptosis of synoviocytes induced by serum starvation or sodium nitroprusside (SNP). VEGF165 rapidly triggered phospho-Akt and phospho-ERK activity and then induced Bcl-2 expression in the rheumatoid synoviocytes. The Akt or ERK inhibitor cancelled the protective effect of VEGF165 on SNP-induced synoviocyte apoptosis. Moreover, VEGF165 blocks SNP-induced Bcl-2 down-regulation as well as SNP-induced Bax translocation from the cytosol to the mitochondria. The down-regulation of the neuropilin-1 transcripts by short interfering RNA caused spontaneous synoviocyte apoptosis, which was associated with both the decrease in Bcl-2 expression and the increase in Bax translocation to mitochondria. Collectively, our data suggest that the interaction of VEGF165 with neuropilin-1 is crucial to the survival of rheumatoid synoviocytes and provide important implications for the abnormal growth of synoviocytes and therapeutic intervention in RA.

Interaction of vascular endothelial growth factor 165 with neuropilin-1 protects rheumatoid synoviocytes from apoptotic death by regulating Bcl-2 expression and Bax translocation.

We investigated the mechanism by which cannabinoid receptors-1 (CB1) and -2 (CB2) modulate inflammatory activities of macrophages.

CB1 and CB2 cannabinoid receptors differentially regulate the production of reactive oxygen species by macrophages.

Tumor necrosis factor receptor-associated factor 2 (TRAF2) is an adaptor protein which involves in the activation of the transcription factor, nuclear factor kappaB (NF-κB), in the tumor necrosis factor (TNF) receptor pathway. This signaling is modulated by proteins that interact with tumor necrosis factor receptor-associated factor 2. In this study, we identified the zinc-finger protein AWP1 as a tumor necrosis factor receptor-associated factor 2-interacting protein through yeast two-hybrid screening. We found that AWP1 directly interacted with the C-terminal tumor necrosis factor receptor-associated factor (TRAF) domain of tumor necrosis factor receptor-associated factor 2. Knockdown of AWP1 using small hairpin RNA significantly decreased nuclear factor kappaB activity but increased tumor necrosis factor alpha (TNFα)-induced apoptosis, presumably by decreasing the induction of nuclear factor kappaB-responsive anti-apoptotic molecules, including FICE-like inhibitory protein (FLIP), X-linked inhibitor of apoptosis protein (XIAP), Bcl-2, and Bcl-xL. In contrast, overexpression of wild-type AWP1 inhibited nuclear factor kappaB activation. Detailed domain mapping experiments showed that the AN1 domain of AWP1 mediated the functional interaction with tumor necrosis factor receptor-associated factor 2, and the A20 domain was responsible for the negative regulation of nuclear factor kappaB activation. Importantly, ectopic AWP1 overexpression led to an A20 domain-dependent increase in K-48 ubiquitination of tumor necrosis factor receptor-associated factor 2. These data indicate that AWP1 binds to tumor necrosis factor receptor-associated factor 2 and that regulates tumor necrosis factor alpha-induced nuclear factor kappaB activation through two distinct domains.

AWP1 binds to tumor necrosis factor receptor-associated factor 2 (TRAF2) and is involved in TRAF2-mediated nuclear factor-kappaB signaling.

&#x6458;&#x8981;&#xFF1A; &#x7B80;&#x4ECB;&#xFF1A; &#x767D;&#x7EC6;&#x80DE;&#x4ECB;&#x7D20;-34 (IL-34) &#x662F;&#x6700;&#x8FD1;&#x5B9A;&#x4E49;&#x7684;&#x7EC6;&#x80DE;&#x56E0;&#x5B50;&#xFF0C;&#x4E0E;&#x5DE8;&#x566C;&#x7EC6;&#x80DE;&#x96C6;&#x843D;&#x523A;&#x6FC0;&#x56E0;&#x5B50; (M-CSF) &#x663E;&#x793A;&#x529F;&#x80FD;&#x91CD;&#x53E0;&#x3002;&#x8FD9;&#x9879;&#x7814;&#x7A76;&#x8FDB;&#x884C;&#x4E86;&#x5E76;&#x89E3;&#x51B3;&#x5728;&#x7C7B;&#x98CE;&#x6E7F;&#x5173;&#x8282;&#x708E; (RA) &#x60A3;&#x8005;&#x7684;&#x767D;&#x7EC6;&#x80DE;&#x4ECB;&#x7D20;-34 &#x8868;&#x8FBE;&#x8C03;&#x67E5;&#x4E2D;&#x98CE;&#x6E7F;&#x53D1;&#x75C5;&#x4E2D;&#x7684;&#x4F5C;&#x7528;&#x53CA;&#x5176;&#x8C03;&#x63A7;&#x65B9;&#x6CD5;&#xFF1A; IL 34 &#x7EA7;&#x522B;&#x786E;&#x5B9A; RA &#x6ED1;&#x819C;&#x7EC4;&#x7EC7;&#xFF0C;&#x6ED1;&#x6DB2; (SF) &#x548C;&#x6210;&#x7EA4;&#x7EF4;&#x6837;&#x6ED1;&#x819C;&#x7EC6;&#x80DE; (FLS) &#x514D;&#x75AB;&#x7EC4;&#x5316;&#x3001; &#x5B9E;&#x65F6;&#x805A;&#x5408;&#x9176;&#x94FE;&#x53CD;&#x5E94;&#x3001; &#x9176;&#x8054;&#x9176;&#x8054;&#x514D;&#x75AB;&#x5438;&#x9644;&#x6CD5;&#x548C;&#x514D;&#x75AB;&#x5370;&#x8FF9;&#x6CD5;&#x3002;RA &#x6D3B;&#x52A8;&#x8BC4;&#x4F30;&#x6CBB;&#x7597;&#x540E;&#x8840;&#x6D46;&#x6536;&#x96C6;&#x5728;&#x57FA;&#x7EBF;&#x548C; 1 &#x5E74;&#x4F7F;&#x7528;&#x75BE;&#x75C5;&#x6D3B;&#x52A8;&#x5F97;&#x5206; 28 &#xFF08;DAS28&#xFF09; &#x6D3B;&#x52A8;&#x3002;&#x57F9;&#x517B;&#x6DB2; &#xFF08;&#x5398;&#x7C73;&#xFF09; &#x4E3A; 24 h &#x4ECE; RA FLS &#x6587;&#x5316;&#x4E0E;&#x80BF;&#x7624;&#x574F;&#x6B7B;&#x56E0;&#x5B50; &alpha; (&#x80BF;&#x7624;&#x574F;&#x6B7B;&#x56E0;&#x5B50;) &#x7F16;&#x5199;&#xFF0C;&#x5E76;&#x7528;&#x4E8E;&#x529F;&#x80FD;&#x6D4B;&#x5B9A;&#x3002;&#x7ED3;&#x679C;: &#x767D;&#x7EC6;&#x80DE;&#x4ECB;&#x7D20;-34 &#x4E2D;&#x6709;&#x4EBA;&#x6ED1;&#x819C;&#x3001; SF &#x548C;&#x8D22;&#x52A1;&#x548C;&#x540E;&#x52E4;&#x7CFB;&#x7EDF;&#x4ECE;&#x7C7B;&#x98CE;&#x6E7F;&#x5173;&#x8282;&#x708E;&#x60A3;&#x8005;&#x3002;&#x751F;&#x4EA7;&#x7684; IL-34 &#x5728;&#x8D22;&#x52A1;&#x548C;&#x540E;&#x52E4;&#x7CFB;&#x7EDF;&#x662F;&#x4E0A;&#x8C03;&#x80BF;&#x7624;&#x574F;&#x6B7B;&#x56E0;&#x5B50;&#x4E0E;&#x9AA8;&#x5173;&#x8282;&#x708E; (OA) &#x60A3;&#x8005;&#x76F8;&#x6BD4; RA &#x6837;&#x54C1;&#x4E2D;&#x3002;&#x91CD;&#x8981;&#x7684;&#x662F;&#xFF0C;IL-34 &#x62E9;&#x4F18;&#x4E0A;&#x5C97;&#xFF0C;&#x800C;&#x4E0D;&#x662F; M &#x8111;&#x810A;&#x6DB2;&#x7684;&#x80BF;&#x7624;&#x574F;&#x6B7B;&#x56E0;&#x5B50;&#x5728; RA FLS &#x4ECB;&#x5BFC;&#x8F6C;&#x5F55;&#x56E0;&#x5B50;&#x6838;&#x56E0;&#x5B50; kappa B (NF-&#x6D3B;&#x5316;&#xFF09; &#x548C; c C-jun &#x6C28;&#x57FA;&#x672B;&#x7AEF;&#x6FC0;&#x9176; (JNK) &#x6FC0;&#x6D3B;&#x3002;&#x4ECE;&#x7C7B;&#x98CE;&#x6E7F;&#x5173;&#x8282;&#x708E;&#x60A3;&#x8005;&#x8840;&#x6D46;&#x4E2D;&#x7684;&#x767D;&#x7EC6;&#x80DE;&#x4ECB;&#x7D20;-34 &#x9AD8;&#x7A0B;&#x88AB;&#x4E0B;&#x8DCC;&#x540E;&#x75BE;&#x75C5;&#x4FEE;&#x6539; anti-rheumatic &#x836F; &#xFF08;DMARDs&#xFF09; &#x653F;&#x5E9C;&#x6839;&#x636E; DAS28 &#x7684;&#x8DCC;&#x5E45;&#x3002;&#x5398;&#x7C73;&#x4ECE; RA FLS &#x7EC6;&#x80DE;&#x80BF;&#x7624;&#x574F;&#x6B7B;&#x56E0;&#x5B50;&#x4FC3;&#x8FDB;&#x4EBA;&#x7C7B;&#x5916;&#x5468;&#x8840;&#x5355;&#x4E2A;&#x6838;&#x7EC6;&#x80DE; (&#x5916;&#x5468;&#x8840;&#xFF09; &#x548C;&#x968F;&#x540E;&#x7834;&#x9AA8;&#x7EC6;&#x80DE; (OC) &#x5F62;&#x6210;&#x4E86;&#x51CF;&#x6BD2;&#x6297;-IL-34 &#x6297;&#x4F53;&#x7684;&#x5F71;&#x54CD;&#x8D8B;&#x5316;&#x8FC1;&#x79FB;&#x3002;&#x7ED3;&#x8BBA;&#xFF1A; &#x8FD9;&#x4E9B;&#x6570;&#x636E;&#x63D0;&#x4F9B;&#x6709;&#x5173;&#x751F;&#x4EA7;&#x7684; IL-34 &#x5728; RA FLS &#x65B0;&#x578B;&#x4FE1;&#x606F;&#x5E76;&#x8BF4;&#x660E; IL-34 &#x662F;&#x989D;&#x5916; osteoclastogenic &#x56E0;&#x5B50;&#x80BF;&#x7624;&#x574F;&#x6B7B;&#x56E0;&#x5B50;&#x5728; RA&#xFF0C;&#x6697;&#x793A; IL-34 &#x5728; RA &#x708E;&#x75C7;&#x79BB;&#x6563;&#x4F5C;&#x7528;&#x53D7;&#x89C4;&#x7BA1;&#x3002;

&#x4EA7;&#x751F;&#x7684;&#x7C7B;&#x98CE;&#x6E7F;&#x6027;&#x5173;&#x8282;&#x708E;&#x7684;&#x4EBA;&#x78B1;&#x6027;&#x6210;&#x7EA4;&#x7EF4;&#x7EC6;&#x80DE;&#x6837;&#x6ED1;&#x819C;&#x7EC6;&#x80DE;&#x7684;&#x767D;&#x7EC6;&#x80DE;&#x4ECB;&#x7D20;-34 &#x652F;&#x6301;&#x7834;&#x9AA8;&#x7EC6;&#x80DE;&#x5F62;&#x6210;&#x3002;

ABSTRACT: INTRODUCTION: Interleukin-34 (IL-34) is a recently defined cytokine, showing a functional overlap with macrophage colony stimulating factor (M-CSF). This study was undertaken to address the expression of IL-34 in rheumatoid arthritis (RA) patients and to investigate its regulation and pathogenic role in RA. METHODS: IL-34 levels were determined in the RA synovium, synovial fluid (SF) and fibroblast-like synovial cells (FLS) by immunohistochemistry, real-time PCR, enzyme-linked immunosorbent assay and immunoblotting. RA activity was assessed using Disease Activity Score 28 (DAS28) activity in the plasma collected at baseline and 1-yr after treatment. Conditioned media (CM) was prepared from RA FLS culture with tumor necrosis factor alpha (TNFa) for 24 h and used for functional assay. RESULTS: IL-34 was expressed in the synovium, SF, and FLS from RA patients. The production of IL-34 in FLS was up-regulated by TNFa in RA samples compared with osteoarthritis (OA) patients. Importantly, the preferential induction of IL-34 rather than M-CSF by TNFa in RA-FLS was mediated by the transcription factor nuclear factor kappa B (NF-kappaB) and activation of c-Jun N-terminal kinase (JNK). IL-34 elevation in plasma from RA patients was decreased after disease-modifying anti-rheumatic drugs (DMARDs) administration in accordance with a decrease in DAS28. CM from RA-FLS cultured with TNFa promoted chemotactic migration of human peripheral blood mononuclear cells (PBMCs) and subsequent osteoclast (OC) formation, effects that were attenuated by an anti-IL-34 antibody. CONCLUSIONS: These data provide novel information about the production of IL-34 in RA FLS and indicate that IL-34 is an additional osteoclastogenic factor regulated by TNFa in RA, suggesting a discrete role of IL-34 in inflammatory RA diseases.

Interleukin-34 produced by human fibroblast-like synovial cells in rheumatoid arthritis supports osteoclastogenesis.

R&eacute;sum&eacute; : INTRODUCTION : interleukine-34 (34-IL) est une cytokine d&eacute;finie r&eacute;cemment, montrant un chevauchement fonctionnel avec la colonie de macrophage stimulating factor (M-CSF). Cette &eacute;tude visait &agrave; r&eacute;pondre &agrave; l&#39;expression d&#39;IL-34 chez les patients de la polyarthrite rhumato&iuml;de (PR) et &agrave; scruter son r&egrave;glement et le r&ocirc;le pathog&egrave;ne RA. M&eacute;thodes: IL-34 niveaux ont &eacute;t&eacute; d&eacute;termin&eacute;s dans la membrane synoviale de RA, le liquide synovial (SF) et fibroblastes-comme des cellules synoviales (FLS) par immunohistochimie, en temps r&eacute;el de PCR, enzyme-linked immunosorbent assay et immunoblotting. Activit&eacute; de RA a &eacute;t&eacute; &eacute;valu&eacute;e &agrave; l&#39;aide d&#39;activit&eacute; maladie activit&eacute; Score 28 (DAS28) dans le plasma recueilli au d&eacute;part et 1 an apr&egrave;s le traitement. Milieux conditionn&eacute;s (CM) a &eacute;t&eacute; pr&eacute;par&eacute;e &agrave; partir de culture de FLS RA avec le facteur de n&eacute;crose tumorale alpha (TNFa) pendant 24 h et utilis&eacute; pour l&#39;analyse fonctionnelle. R&Eacute;SULTATS: IL-34 a &eacute;t&eacute; exprim&eacute;e dans la membrane synoviale, SF et FLS de polyarthrite rhumatoide. La production de IL-34 en FLS &eacute;tait r&eacute;gul&eacute;e par TNFa dans des &eacute;chantillons de RA par rapport aux patients souffrant d&#39;arthrose (OA). Ce qui est important, l&#39;induction pr&eacute;f&eacute;rentielle de IL-34 plut&ocirc;t que le M-CSF de TNFa dans RA-FLS est m&eacute;di&eacute;e par la transcription factor kappa B (NF-kappaB) de la facteur nucl&eacute;aire et l&#39;activation de la kinase c-Jun N-terminal (JNK). Altitude IL-34 dans le plasma de polyarthrite rhumatoide a diminu&eacute; apr&egrave;s que les modificateurs anti-rhumatismaux drugs administration (AMEM) conform&eacute;ment &agrave; une diminution de DAS28. CM du RA-FLS cultiv&eacute;es avec TNFa promu chimiotactique migration des cellules mononucl&eacute;aires de sang p&eacute;riph&eacute;rique (PBMC) et la formation des ost&eacute;oclastes ult&eacute;rieures (OC), effets qui ont &eacute;t&eacute; att&eacute;nu&eacute;es par un anticorps anti-IL-34. CONCLUSIONS : Ces donn&eacute;es fournissent des informations nouvelles sur la production d&#39;IL-34 en RA FLS et indiquent qu&#39;IL-34 est un facteur d&#39;osteoclastogenic suppl&eacute;mentaires r&eacute;gi par TNFa dans la polyarthrite rhumato&iuml;de, sugg&eacute;rant un r&ocirc;le discret de IL-34 dans les maladies inflammatoires de RA.

Interleukine-34 produites par les humains comme des fibroblastes cellules synoviales dans la polyarthrite rhumato&iuml;de prend en charge osteoclastogenesis.

Zusammenfassung: Einleitung: Interleukin-34 (IL-34) ist eine vor kurzem definierte Cytokine, zeigt eine funktionale &Uuml;berlappung mit Makrophagen-Kolonie-anregende Faktor (M-CSF). Diese Studie wurde durchgef&uuml;hrt, um den Ausdruck des IL-34 in Patienten mit rheumatoider Arthritis (RA) zu behandeln und um ihre Verordnung und pathogene Rolle in RA zu untersuchen Methoden: IL-34 Levels waren bestimmt in der Synovialis RA Gelenkfl&uuml;ssigkeit (SF) und Fibroblasten-wie synovial Zellen (FLS) von Immunohistochemistry, Real-Time PCR, Enzym-Immunoassay und Immunoblotting. RA-Aktivit&auml;t wurde mithilfe von Disease Activity Score 28 (DAS28)-Aktivit&auml;t im Plasma bei Studienbeginn gesammelt und 1-Jahres-Chart nach der Behandlung bewertet. Konditionierte Medien (CM) wurde von RA FLS Kultur mit Tumor-Nekrose-Faktor-Alpha (TNFa) f&uuml;r 24 h und f&uuml;r funktionelle Assay verwendet. Ergebnisse: IL-34 wurde in der Synovialis, SF und FLS von RA-Patienten ge&auml;u&szlig;ert. Die Produktion von IL-34 in der FLS war oben-geregelt durch TNFa in RA-Proben im Vergleich-Osteoarthritis (OA) Patienten. Wichtig ist, die bevorzugte Induktion von IL-34 M-CSF von TNFa in RA-FLS durch die Transkription vermittelt wurde, anstatt Faktor nuklearer Faktor Kappa B (NF-KappaB) und Aktivierung der c-Jun N-Terminal Kinase (JNK). IL-34 Erhebung im Plasma von Patienten mit rheumatoider Arthritis wurde reduziert, nachdem Krankheitsmodifizierende antirheumatische verabreichen (DMARD) zu einem R&uuml;ckgang der DAS28 Medikamente. CM von RA-FLS kultiviert mit TNFa bef&ouml;rdert chemotaktische Migration der menschlichen peripheren mononukle&auml;ren Blutzellen (PBMCs) und anschlie&szlig;ende Osteoklast (OC) Bildung, Effekte, die durch ein Anti-IL-34-Antik&ouml;rper abgeschw&auml;cht wurden. Schlussfolgerungen: Diese Daten neuartige informieren &uuml;ber die Produktion von IL-34 in RA FLS und anzugeben, dass IL-34 eine zus&auml;tzliche Osteoclastogenic-Faktor von TNFa in RA ist, schl&auml;gt eine diskrete Rolle des IL-34 in RA Entz&uuml;ndungen reguliert.

Interleukin-34 produziert von menschlichen Fibroblasten-wie synovial Zellen bei rheumatoider Arthritis unterst&uuml;tzt Osteoclastogenesis.

ABSTRACT: Introduzione: interleuchina-34 (IL-34) &egrave; una citochina recentemente definita, mostrando una sovrapposizione funzionale con Colonia dei macrofagi (M-CSF) fattore stimolante. Questo studio &egrave; stato intrapreso per affrontare l&#39;espressione di IL-34 nei pazienti di artrite reumatoide (RA) e di indagare il suo regolamento e ruolo patogeno in ra Metodi: Livelli di IL-34 sono stati determinati in RA sinoviale, liquido sinoviale (SF) e cellule sinoviali del fibroblasto-simili (FLS) di immunoistochimica, PCR in tempo reale, analisi enzima-collegata dell&#39;immunosorbente e immunoblotting. Attivit&agrave; RA &egrave; stata valutata utilizzando attivit&agrave; di malattia attivit&agrave; punteggio 28 (DAS28) nel plasma raccolto al basale e 1 anno dopo il trattamento. Condizionata media (CM) &egrave; stato preparato dalla cultura RA FLS con fattore di necrosi tumorale alfa (TNFa) per 24 h e utilizzato per l&#39;analisi funzionale. RISULTATI: IL-34 &egrave; stato espresso nella sinovia, SF e FLS da pazienti con RA. La produzione di IL-34 in FLS &egrave; up-regolata da TNFa in RA campioni rispetto ai pazienti l&#39;osteoartrite (OA). Soprattutto, l&#39;induzione preferenziale di IL-34 anzich&eacute; M-CSF di TNFa in RA-FLS era mediata dalla trascrizione fattore kappa B (NF-kappaB) di fattore nucleare ed attivazione di c-Jun N-terminal chinasi (JNK). IL-34 elevazione nel plasma di pazienti RA era diminuito dopo antireumatici modificanti la malattia (DMARD) amministrazione secondo una diminuzione nel DAS28 di droga. CM da RA-FLS coltivate con TNFa promosso migrazione chemiotattica delle cellule mononucleate del sangue periferico (PBMCs) e formazione successiva degli osteoclasti (OC), effetti che sono stati attenuati da un anticorpo anti-IL-34. CONCLUSIONI: Questi dati forniscono informazioni romanzo sulla produzione di IL-34 in RA FLS e indicano che IL-34 &egrave; un fattore aggiuntivo osteoclastogenic regolato dal TNFa in RA, suggerendo un ruolo discreto IL-34 in malattie infiammatorie RA.

Interleuchina-34 prodotto da umane del fibroblasto-come le cellule sinoviali nell&#39;artrite reumatoide supporta osteoclastogenesis.

&#x8981;&#x7D04;&#xFF1A; &#x5C0E;&#x5165;: &#x30A4;&#x30F3;&#x30BF;&#x30FC;&#x30ED;&#x30A4;&#x30AD;&#x30F3;-34 (IL-34&#xFF09; &#x306F;&#x3001;&#x6700;&#x8FD1;&#x5B9A;&#x7FA9;&#x3055;&#x308C;&#x305F;&#x30B5;&#x30A4;&#x30C8;&#x30AB;&#x30A4;&#x30F3; &#x30DE;&#x30AF;&#x30ED;&#x30D5;&#x30A1;&#x30FC;&#x30B8;&#x30B3;&#x30ED;&#x30CB;&#x30FC;&#x523A;&#x6FC0;&#x56E0;&#x5B50; (M-CSF) &#x3068;&#x6A5F;&#x80FD;&#x7684;&#x306A;&#x91CD;&#x8907;&#x3092;&#x793A;&#x3057;&#x307E;&#x3059;&#x3002;&#x672C;&#x7814;&#x7A76;&#x306F;&#x3001;&#x6162;&#x6027;&#x95A2;&#x7BC0;&#x30EA;&#x30A6;&#x30DE;&#x30C1; (RA) &#x60A3;&#x8005;&#x306B;&#x304A;&#x3051;&#x308B; IL 34 &#x306E;&#x767A;&#x73FE;&#x306B;&#x5BFE;&#x51E6;&#x3057;&#x3066;&#x305D;&#x306E;&#x898F;&#x5236;&#x3068;&#x30E9;&#x30FC;&#x306B;&#x304A;&#x3051;&#x308B;&#x75C5;&#x539F;&#x6027;&#x306E;&#x5F79;&#x5272;&#x3092;&#x8ABF;&#x67FB;&#x3059;&#x308B;&#x305F;&#x3081;&#x306B;&#x884C;&#x308F;&#x308C;&#x307E;&#x3057;&#x305F;&#x3002;&#x65B9;&#x6CD5;: IL 34 &#x30EC;&#x30D9;&#x30EB; RA &#x6ED1;&#x3067;&#x6C7A;&#x5B9A;&#x3055;&#x308C;&#x305F;&#x6ED1;&#x6DB2; (SF) &#x3068;&#x514D;&#x75AB;&#x7D44;&#x7E54;&#x5316;&#x5B66;&#x3001;&#x30EA;&#x30A2;&#x30EB;&#x30BF;&#x30A4;&#x30E0; PCR&#x3001;elisa &#x30A2;&#x30C3;&#x30BB;&#x30A4;&#x304A;&#x3088;&#x3073;&#x30A4;&#x30E0;&#x30CE;&#x30D6;&#x30ED;&#x30C3;&#x30C8;&#x6CD5;&#x306B;&#x3088;&#x308B;&#x7DDA;&#x7DAD;&#x82BD;&#x7D30;&#x80DE;&#x306E;&#x3088;&#x3046;&#x306A;&#x6ED1;&#x819C;&#x7D30;&#x80DE; &#xFF08;FLS&#xFF09;&#x3002;RA &#x6D3B;&#x52D5;&#x306F;&#x3001;&#x6CBB;&#x7642;&#x5F8C;&#x30D9;&#x30FC;&#x30B9;&#x30E9;&#x30A4;&#x30F3;&#x3067;&#x3001;&#x53CE;&#x96C6;&#x30FB; 1 yr &#x306B;&#x304A;&#x3051;&#x308B;&#x30D7;&#x30E9;&#x30BA;&#x30DE;&#x75C5;&#x30A2;&#x30AF;&#x30C6;&#x30A3;&#x30D3;&#x30C6;&#x30A3; &#x30B9;&#x30B3;&#x30A2; 28 &#xFF08;DAS28&#xFF09; &#x6D3B;&#x52D5;&#x3092;&#x7528;&#x3044;&#x3066;&#x8A55;&#x4FA1;&#x3057;&#x307E;&#x3057;&#x305F;&#x3002;&#x30A8;&#x30A2;&#x30B3;&#x30F3; &#x30E1;&#x30C7;&#x30A3;&#x30A2; &#xFF08;CM&#xFF09; 24 h &#x306E; RA FLS &#x6587;&#x5316;&#x3068;&#x816B;&#x760D;&#x58CA;&#x6B7B;&#x56E0;&#x5B50; &alpha; (TNFa) &#x304B;&#x3089;&#x6E96;&#x5099;&#x3055;&#x308C;&#x6A5F;&#x80FD;&#x7684;&#x306A;&#x8A66;&#x91D1;&#x306E;&#x305F;&#x3081;&#x306B;&#x4F7F;&#x7528;&#x3057;&#x307E;&#x3059;&#x3002;&#x7D50;&#x679C;: RA &#x60A3;&#x8005;&#x304B;&#x3089;&#x6ED1;&#x3001;SF&#x3001;&#x305D;&#x3057;&#x3066; FLS &#x3067; IL 34 &#x3092;&#x8868;&#x73FE;&#x3057;&#x307E;&#x3057;&#x305F;&#x3002;IL-34 FLS &#x3067;&#x306E;&#x751F;&#x7523;&#x306B;&#x3088;&#x3063;&#x3066; TNFa &#x306E;&#x30A2;&#x30C3;&#x30D7;&#x898F;&#x5236; RA &#x8A66;&#x6599;&#x306E;&#x5909;&#x5F62;&#x6027;&#x95A2;&#x7BC0;&#x75C7; (OA) &#x60A3;&#x8005;&#x3068;&#x6BD4;&#x8F03;&#x3055;&#x308C;&#x307E;&#x3057;&#x305F;&#x3002;&#x91CD;&#x8981;&#x306A;&#x306F;&#x3001;IL-34 &#x306E;&#x512A;&#x9047;&#x8A98;&#x5C0E; M-CSF RA FLS &#x3067; TNFa &#x306B;&#x3088;&#x3063;&#x3066;&#x306B;&#x3088;&#x308B;&#x8EE2;&#x5199;&#x3092;&#x4ECB;&#x3059;&#x308B;&#x3060;&#x3063;&#x305F;&#x306E;&#x3067;&#x306F;&#x306A;&#x304F;&#x56E0;&#x5B50; &kappa; B &#xFF08;NF-&#x30AB;&#x30C3;&#x30D1; b&#xFF09; &#x3068; c C-jun N &#x672B;&#x7AEF;&#x30AD;&#x30CA;&#x30FC;&#x30BC; (JNK) &#x306E;&#x6D3B;&#x6027;&#x5316;&#x3002;&#x75BE;&#x60A3;&#x4FEE;&#x98FE;&#x6297;&#x30EA;&#x30A6;&#x30DE;&#x30C1;&#x85AC; &#xFF08;DMARDs&#xFF09; &#x7BA1;&#x7406; DAS28 &#x306E;&#x6E1B;&#x5C11;&#x306B;&#x5F93;&#x3063;&#x3066;&#x5F8C; IL 34 &#x6A19;&#x9AD8;&#x30D7;&#x30E9;&#x30BA;&#x30DE; RA &#x60A3;&#x8005;&#x304B;&#x3089;&#x3067;&#x6E1B;&#x5C11;&#x3057;&#x3066;&#x3044;&#x305F;.CM &#x304B;&#x3089; RA FLS TNFa &#x3067;&#x57F9;&#x990A;&#x3057;&#x305F;&#x3072;&#x3068;&#x672B;&#x68A2;&#x8840;&#x5358;&#x6838;&#x7403; (Pbmc) &#x3068;&#x5F8C;&#x7D9A;&#x7834; (OC) &#x5F62;&#x6210;&#x6297; IL 34 &#x6297;&#x4F53;&#x306B;&#x3088;&#x3063;&#x3066;&#x6E1B;&#x8870;&#x3055;&#x308C;&#x305F;&#x52B9;&#x679C;&#x306E;&#x8D70;&#x5316;&#x6027;&#x79FB;&#x884C;&#x6607;&#x683C;&#x3002;&#x7D50;&#x8AD6;: &#x3053;&#x308C;&#x3089;&#x306E;&#x30C7;&#x30FC;&#x30BF;&#x306F; IL-34 RA FLS &#x3067;&#x306E;&#x751F;&#x7523;&#x306B;&#x95A2;&#x3059;&#x308B;&#x65B0;&#x898F;&#x60C5;&#x5831;&#x3057;&#x3001;IL-34 TNFa RA &#x306E;&#x708E;&#x75C7;&#x6027;&#x75C5;&#x6C17;&#x3067; IL 34 &#x306E;&#x96E2;&#x6563;&#x5F79;&#x5272;&#x3092;&#x793A;&#x5506; RA &#x306B;&#x304A;&#x3051;&#x308B;&#x306B;&#x3088;&#x3063;&#x3066;&#x898F;&#x5236;&#x3055;&#x308C;&#x3066;&#x8FFD;&#x52A0; osteoclastogenic &#x8981;&#x56E0;&#x3067;&#x3042;&#x308B;&#x3053;&#x3068;&#x3092;&#x793A;&#x3057;&#x307E;&#x3059;&#x3002;

&#x30A4;&#x30F3;&#x30BF;&#x30FC;&#x30ED;&#x30A4;&#x30AD;&#x30F3;-34 &#x95A2;&#x7BC0;&#x30EA;&#x30A6;&#x30DE;&#x30C1;&#x306B;&#x304A;&#x3051;&#x308B;&#x3072;&#x3068;&#x7DDA;&#x7DAD;&#x82BD;&#x7D30;&#x80DE;&#x306E;&#x3088;&#x3046;&#x306A;&#x6ED1;&#x819C;&#x7D30;&#x80DE;&#x306B;&#x3088;&#x3063;&#x3066;&#x751F;&#x6210;&#x3055;&#x308C;&#x308B;&#x7834;&#x9AA8;&#x7D30;&#x80DE;&#x5F62;&#x6210;&#x3092;&#x30B5;&#x30DD;&#x30FC;&#x30C8;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;

&#xAC1C;&#xC694;: &#xC18C;&#xAC1C;: &#xC778;&#xD130; &#xB8E8; &#xD0A8;-34 (IL-34)&#xC740; &#xCD5C;&#xADFC; &#xC815;&#xC758; cytokine &#xB300; &#xC2DD; &#xC138;&#xD3EC; &#xCF5C;&#xB85C; &#xB2C8; &#xC790;&#xADF9; &#xC778;&#xC790; (M-CSF)&#xC640; &#xAE30;&#xB2A5; &#xC911;&#xBCF5; &#xAC8C;&#xC7AC;. &#xC774; &#xC5F0;&#xAD6C;&#xB294; &#xB958; &#xB9C8;&#xD2F0;&#xC2A4; &#xAD00;&#xC808;&#xC5FC; (RA) &#xD658;&#xC790;&#xC5D0;&#xC11C; IL-34&#xC758; &#xC2DD;&#xC744; &#xD574;&#xACB0; &#xD558; &#xACE0; &#xADDC;&#xC81C;&#xC640; &#xB77C;&#xC2A4;&#xC5D0;&#xC11C; &#xBCD1;&#xC6D0; &#xC131; &#xC5ED;&#xD560; &#xC870;&#xC0AC;&#xC5D0; &#xCC29;&#xC218; &#xD588;&#xB2E4; &#xBC29;&#xBC95;: IL-34 &#xB808;&#xBCA8; &#xB77C; &#xB9C9;&#xC5D0;&#xC11C; &#xC815;&#xD574; &#xC9C0;&#xB294; synovial &#xC720;&#xCCB4; (SF)&#xACFC; &#xC12C;&#xC720; &#xC544; &#xC138;&#xD3EC;&#xC640; &#xAC19;&#xC740; &#xD65C; &#xC561; &#xC140; (FLS) &#xAE30;&#xC220;, &#xC2E4;&#xC2DC;&#xAC04; PCR &#xD6A8;&#xC18C; &#xC5F0;&#xACB0; &#xB41C; immunosorbent &#xBD84;&#xC11D; &#xACB0;&#xACFC; &#xBC0F; immunoblotting&#xC5D0; &#xC758;&#xD574;. RA &#xD65C;&#xB3D9; &#xCD08;&#xAE30;&#xC5D0; &#xC218;&#xC9D1; &#xD558; &#xACE0; 1 &#xC608;&#xBA58; &#xC544;&#xB78D; &#xACF5;&#xD654;&#xAD6D; &#xD50C;&#xB77C;&#xC988;&#xB9C8;&#xC5D0; &#xC9C8;&#xBCD1; &#xD65C;&#xB3D9; &#xC810;&#xC218; 28 (DAS28) &#xD65C;&#xB3D9;&#xC744; &#xC0AC;&#xC6A9; &#xD558; &#xC5EC; &#xCE58;&#xB8CC; &#xD6C4; &#xD3C9;&#xAC00; &#xB418;&#xC5C8;&#xB2E4;. &#xBC14;&#xB978;&#xB41C; &#xBBF8;&#xB514;&#xC5B4; (CM) &#xC885;&#xC591; &#xAD34; &#xC0AC; &#xC694;&#xC778; &#xC54C;&#xD30C; (TNFa) RA FLS &#xBB38;&#xD654;&#xC5D0;&#xC11C; 24 &#xC2DC;&#xAC04; &#xC900;&#xBE44; &#xB418;&#xC5C8;&#xACE0; &#xAE30;&#xB2A5; &#xBD84;&#xC11D; &#xACB0;&#xACFC; &#xB300; &#xD55C; &#xC0AC;&#xC6A9;. &#xACB0;&#xACFC;: IL-34 &#xB9C9;, SF, FLS&#xC5D0;&#xC11C; RA &#xD658;&#xC790;&#xC5D0;&#xC11C; &#xD45C;&#xD604; &#xD588;&#xB2E4;. FLS&#xC5D0;&#xC11C; IL-34&#xC758; &#xC0DD;&#xC0B0; &#xCD5C;&#xB300;-&#xC758;&#xD574; &#xADDC;&#xC81C; TNFa RA &#xC0D8;&#xD50C; &#xACE8; &#xAD00;&#xC808;&#xC5FC; (OA) &#xD658;&#xC790;&#xC640; &#xBE44;&#xAD50; &#xD588;&#xB2E4;. &#xC911;&#xC694; &#xD55C; &#xAC83;&#xC740;, IL-34&#xC758; &#xC6B0;&#xB300; &#xC720;&#xB3C4; &#xBCF4;&#xB2E4;&#xB294; RA FLS&#xC5D0;&#xC11C; TNFa &#xC5EC; M-CSF&#xB294; &#xC804;&#xC0AC;&#xC5D0; &#xC758;&#xD574; &#xC911;&#xC7AC; &#xC694;&#xC778; &#xD575; &#xC778;&#xC790; &#xCE74;&#xD30C; B (NF kappaB) &#xBC0F; c 6 &#xC6D4; N &#xB9E8;&#xB05D; &#xD0A4; (JNK)&#xC758; &#xD65C;&#xC131;&#xD654;. RA &#xD658;&#xC790;&#xC5D0;&#xC11C; &#xD50C;&#xB77C;&#xC988;&#xB9C8;&#xC5D0;&#xC11C; IL-34 &#xC0C1;&#xC2B9; &#xD6C4; &#xC9C8;&#xBCD1; &#xC218;&#xC815; anti-rheumatic &#xC57D; DAS28 &#xAC10;&#xC18C;&#xC5D0; &#xB530;&#xB77C; &#xAD00;&#xB9AC; (DMARDs) &#xAC10;&#xC18C; &#xD588;&#xB2E4;. RA FLS Tnfa&#xC640; &#xAD50;&#xC591;&#xC5D0;&#xC11C; CM &#xC778;&#xAC04;&#xC758; &#xB9D0; &#xCD08; &#xD608;&#xC561; &#xB2E8; &#xC140; (PBMCs) &#xBC0F; &#xD6C4;&#xC18D; osteoclast (OC) &#xD615;&#xC131;, &#xC548;&#xD2F0;-&#xC77C;&#xB9AC;&#xB178;&#xC774;-34 &#xD56D; &#xCCB4;&#xC5D0; &#xC758;&#xD574; &#xAC10;&#xC1E0; &#xB41C; &#xD6A8;&#xACFC;&#xC758; &#xD608; &#xB9C8;&#xC774;&#xADF8;&#xB808;&#xC774;&#xC158; &#xCD94;&#xC9C4;. &#xACB0;&#xB860;: &#xC774;&#xB7EC;&#xD55C; &#xB370;&#xC774;&#xD130; RA FLS&#xC5D0;&#xC11C; IL-34&#xC758; &#xC0DD;&#xC0B0;&#xC5D0; &#xB300; &#xD55C; &#xC0C8;&#xB85C;&#xC6B4; &#xC815;&#xBCF4;&#xB97C; &#xC81C;&#xACF5; &#xD558; &#xACE0; IL 34 TNFa RA, &#xC790;&#xADF9;&#xC801;&#xC778; RA &#xBCD1;&#xC5D0;&#xC11C; IL-34&#xC758; &#xAC1C;&#xBCC4; &#xC5ED;&#xD560; &#xC81C;&#xC548;&#xC5D0; &#xC758;&#xD574; &#xADDC;&#xC81C; &#xD558;&#xB294; &#xCD94;&#xAC00; osteoclastogenic &#xC694;&#xC18C; &#xC784;&#xC744; &#xB098;&#xD0C0;&#xB0C5;&#xB2C8;&#xB2E4;.

&#xC778;&#xD130; &#xB8E8; &#xD0A8;-34 &#xB958; &#xB9C8;&#xCE58; &#xC2A4; &#xC131; &#xAD00;&#xC808;&#xC5FC;&#xC5D0;&#xC11C; &#xC778;&#xAC04;&#xC758; &#xC12C;&#xC720; &#xC544; &#xC138;&#xD3EC;&#xC640; &#xAC19;&#xC740; &#xD65C; &#xC561; &#xC138;&#xD3EC;&#xC5D0; &#xC758;&#xD574; &#xC0DD;&#xC0B0; &#xB418;&#xB294; osteoclastogenesis&#xB97C; &#xC9C0;&#xC6D0; &#xD569;&#xB2C8;&#xB2E4;.

Resumen: Introducci&oacute;n: Interleukin-34 (IL-34) es una citoquina recientemente definida, mostrando una superposici&oacute;n funcional con factor (M-CSF) estimulante de colonias de macr&oacute;fagos. Este estudio fue emprendido para hacer frente a la expresi&oacute;n de IL-34 en pacientes con artritis reumatoide (RA) y para investigar su Reglamento y el papel pat&oacute;geno en RA M&Eacute;TODOS: Se determinaron los niveles de IL-34 en la membrana sinovial de la RA, l&iacute;quido sinovial (SF) y fibroblasto-como las de c&eacute;lulas sinoviales (FLS) por inmunohistoqu&iacute;mica, PCR en tiempo real, enzyme-linked immunosorbent assay e immunoblotting. Actividad de RA se evalu&oacute; mediante actividad 28 de puntuaci&oacute;n de actividad de la enfermedad (DAS28) en el plasma recogido en condiciones basales y 1 a&ntilde;o despu&eacute;s del tratamiento. Acondicionado media (CM) fue preparado a partir de la cultura de FLS RA con el factor de necrosis tumoral alfa (TNFa) durante 24 h y utilizado para el an&aacute;lisis funcional. Resultados: IL-34 se expres&oacute; en la membrana sinovial, SF y FLS de pacientes con ar. La producci&oacute;n de IL-34 en FLS era para arriba-regulado por TNFa en muestras de RA en comparaci&oacute;n con pacientes de osteoartritis (OA). Lo importante es la inducci&oacute;n preferencial del IL-34 en lugar de M-CSF por TNFa en RA-FLS fue mediado por la transcripci&oacute;n factor factor nuclear kappa B (NF-kappaB) y activaci&oacute;n de la quinasa c-Jun N-terminal (JNK). IL-34 elevaci&oacute;n en plasma de pacientes con AR disminuy&oacute; despu&eacute;s de administraci&oacute;n (FARME) seg&uacute;n una disminuci&oacute;n DAS28 los f&aacute;rmacos antirreum&aacute;ticos modificadores de la enfermedad. CM de RA-FLS cultivadas con TNFa promovido migraci&oacute;n quimiot&aacute;ctica de c&eacute;lulas mononucleares de sangre perif&eacute;rica (PBMCs) y la formaci&oacute;n de osteoclastos posterior (OC), efectos que fueron atenuadas por un anticuerpo anti-IL-34. CONCLUSIONES: Estos datos proporcionan informaci&oacute;n novedosa sobre la producci&oacute;n de IL-34 en RA FLS e indican que la IL-34 es un factor de osteoclastogenic adicional reglamentado por TNFa en RA, sugiriendo un papel discreto del IL-34 en enfermedades inflamatorias de la RA.

Interleucina-34 producida por las c&eacute;lulas sinoviales humanas fibroblasto-como en la artritis reumatoide apoya osteoclastog&eacute;nesis.

To analyze the effects of supplemental epidermal growth factor (EGF) and the roles of inflammatory cytokines (interleukin [IL]-6) in an ex vivo dry-eye model under hyperosmotic stress using a multilayered culture of human conjunctival epithelial cells (HCECs).

Osmoprotective effects of supplemental epidermal growth factor in an ex vivo multilayered human conjunctival model under hyperosmotic stress.

We reported the expression of phosphorylated HSP27 during epithelial wound healing in murine corneas (Jain et al., 2012) in July of 2012. This in vivo investigation demonstrated that the expression levels of phosphorylated HSP27 were greater in wounded corneal epithelial cells than in unwounded controls and that the localization of phosphorylated HSP27 was in the basal and superficial epithelia three days following corneal epithelial wounding. We suggested that phosphorylated HSP27 had a role in the early phase of corneal epithelial wound healing. The purpose of this study was to investigate the exact role of heat shock protein 27 (HSP27) phosphorylation for the wound healing of cultured human corneal epithelial cells (HCECs). HSP27-specific siRNAs and control-siRNAs, with no known homologous targets in HCECs, were created. The cultured HCECs were divided into two groups: Scrambled control-siRNA-transfected group vs. HSP27-specific siRNA-transfected group. The scratch-induced directional wounding assay, Western blotting, using antibodies against non-phosphorylated and phosphorylated HSP27, non-phosphorylated and phosphorylated Akt, and Bcl-2-associated X protein (Bax), immunofluorescence staining to determine the filament actin, flow cytometry to measure apoptosis, and proliferation assay were performed to determine the role of HSP27. Western blot assay showed that the expression of phosphorylated HSP27 significantly increased at 5, 10, and 30 min after scratch wounding, compared with those in unwounded HCECs (all p < 0.05). Western blot assay also showed HSP27-specific siRNAs effectively blocked the expression of non-phosphorylated HSP27. The HSP27-specific siRNA-transfected group had more Bax expression, less phosphorylated Akt expression, and less non-phosphorylated and phosphorylated HSP27 expression (all p < 0.05). The scratch-induced directional wounding assay showed the HSP27-specific siRNA-transfected group with a less migrating cell number than the control-siRNA-transfected group (p < 0.05). Immunofluorescence staining showed that reorganization of actin cytoskeleton prominently decreased in the HSP27-specific siRNA-transfected group, compared with the control siRNA-tranfected group. Flow cytometry revealed that the HSP27-specific siRNA-transfected group had more HCEC apoptosis. Proliferation assay showed no difference between the two groups. In conclusion, the role of HSP27 in corneal epithelial wound healing can be epithelial cell apoptosis, as well as epithelial migration. HSP27 is involved in HCEC migration by the reorganization of actin cytoskeleton.

Heat shock protein 27 phosphorylation is involved in epithelial cell apoptosis as well as epithelial migration during corneal epithelial wound healing.

To evaluate the effects of nerve growth factor (NGF), which is activated during inflammatory episodes of ocular diseases, on the apoptotic response in cultured human primary conjunctival epithelial cells (pHCECs).

Effect of nerve growth factor on the in vitro induction of apoptosis of human conjunctival epithelial cells by hyperosmolar stress.

Secretory clusterin (sCLU)/apolipoprotein J is a multifunctional glycoprotein that is ubiquitously expressed in various tissues. Reduced sCLU in the joints of patients with bone erosive disease is associated with disease activity; however, its exact role has yet to be elucidated. Here, we report that CLU is expressed and secreted during osteoclastogenesis in mouse bone marrow-derived macrophages (BMMs) that are treated with receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). CLU-deficient BMMs obtained from CLU(-/-) mice exhibited no significant alterations in OC differentiation in comparison with BMMs obtained from wild-type mice. In contrast, exogenous sCLU treatment significantly inhibited OC formation in both BMMs and OC precursor cultures. The inhibitory effect of sCLU was more prominent in BMMs than OC precursor cultures. Interestingly, treating BMMs with sCLU decreased the proliferative effects elicited by M-CSF and suppressed M-CSF-induced ERK activation of OC precursor cells without causing apoptotic cell death. This study provides the first evidence that sCLU reduces OC formation by inhibiting the actions of M-CSF, thereby suggesting its protective role in bone erosion.

Secretory clusterin inhibits osteoclastogenesis by attenuating M-CSF-dependent osteoclast precursor cell proliferation.

To evaluate the effects of prostaglandin analogs (PGAs) on cell viability and apoptosis in cultured astrocytes obtained from the lamina cribrosa (LC) of the human optic nerve head (ONH).

In vitro Effects of Prostaglandin Analogs on Cultured Astrocytes Obtained from the Lamina Cribrosa.

We evaluated the effects of N-acetylcysteine (NAC), which is known to inhibit reactive oxygen species (ROS)-dependent apoptosis, on high glucose-induced ROS, apoptosis, inflammation, and delayed-wounding closure in primary cultured human conjunctival epithelial cells (pHCECs), and the regulatory effects of cleaved caspase-3, BAX, nuclear factor κB (NF-κB), IL-6, and TNF-α on these processes.

Soon-Suk Kang

Department of Ophthalmology,
University of Ulsan College of Medicine,
Department of Ophthalmology, University of Ulsan College of Medicine

Asan Medical Center

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing

Soon-Suk Kang

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Ophthalmology,University of Ulsan College of Medicine,Department of Ophthalmology, University of Ulsan College of Medicine

Asan Medical Center

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing

Department of Ophthalmology,
University of Ulsan College of Medicine,
Department of Ophthalmology, University of Ulsan College of Medicine