Pingnian He

Tumor necrosis factor-alpha-induced leukocyte adhesion and microvessel permeability.

Internalization of caveolin-1 scaffolding domain facilitated by Antennapedia homeodomain attenuates PAF-induced increase in microvessel permeability.

fMLP-stimulated neutrophils increase endothelial [Ca2+]i and microvessel permeability in the absence of adhesion: role of reactive oxygen species.

Dissecting the molecular control of endothelial NO synthase by caveolin-1 using cell-permeable peptides.

Platelet-activating factor increases endothelial [Ca2+]i and NO production in individually perfused intact microvessels.

Sphingosine 1-phosphate prevents platelet-activating factor-induced increase in hydraulic conductivity in rat mesenteric venules: pertussis toxin sensitive.

fMLP-stimulated release of reactive oxygen species from adherent leukocytes increases microvessel permeability.

Leukocyte-platelet aggregate adhesion and vascular permeability in intact microvessels: role of activated endothelial cells.

Three-dimensional localization and quantification of PAF-induced gap formation in intact venular microvessels.

Spent culture medium from virulent Borrelia burgdorferi increases permeability of individually perfused microvessels of rat mesentery.

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability.

Beyond tie-ing up endothelial adhesion: new insights into the action of angiopoietin-1 in regulation of microvessel permeability.

Endothelial [Ca2+]i and caveolin-1 antagonistically regulate eNOS activity and microvessel permeability in rat venules.

Leucocyte/endothelium interactions and microvessel permeability: coupled or uncoupled?

Sphingosine-1-phosphate prevents permeability increases via activation of endothelial sphingosine-1-phosphate receptor 1 in rat venules.

Improved measurements of intracellular nitric oxide in intact microvessels using 4,5-diaminofluorescein diacetate.

Temporal and spatial correlation of platelet-activating factor-induced increases in endothelial [Ca²⁺]i, nitric oxide, and gap formation in intact venules.

Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules.

H2O2-induced endothelial NO production contributes to vascular cell apoptosis and increased permeability in rat venules.

Caveolin-1 scaffolding domain promotes leukocyte adhesion by reduced basal endothelial nitric oxide-mediated ICAM-1 phosphorylation in rat mesenteric venules.

Enhanced permeability responses to inflammation in streptozotocin-induced diabetic rat venules: Rho-mediated alterations of actin cytoskeleton and VE-cadherin.

In vitro recapitulation of functional microvessels for the study of endothelial shear response, nitric oxide and [Ca2+]i.