Dan Predescu

Transport of nitrated albumin across continuous vascular endothelium.

E. coli pneumonia induces CD18-independent airway neutrophil migration in the absence of increased lung vascular permeability.

Intersectin regulates fission and internalization of caveolae in endothelial cells.

Functional and morphological studies of protein transcytosis in continuous endothelia.

Inactivation of CD11b in a mouse transgenic model protects against sepsis-induced lung PMN infiltration and vascular injury.

Constitutive eNOS-derived nitric oxide is a determinant of endothelial junctional integrity.

Cholesterol-dependent syntaxin-4 and SNAP-23 clustering regulates caveolar fusion with the endothelial plasma membrane.

siRNA-induced caveolin-1 knockdown in mice increases lung vascular permeability via the junctional pathway.

Role of phosphatidylinositol 3-kinase-gamma in mediating lung neutrophil sequestration and vascular injury induced by E. coli sepsis.

Intersectin-1s regulates the mitochondrial apoptotic pathway in endothelial cells.

RhoGDI-1 modulation of the activity of monomeric RhoGTPase RhoA regulates endothelial barrier function in mouse lungs.

Molecular determinants of endothelial transcytosis and their role in endothelial permeability.

Role of NF-kappaB-dependent caveolin-1 expression in the mechanism of increased endothelial permeability induced by lipopolysaccharide.

Tiam1 and Rac1 are required for platelet-activating factor-induced endothelial junctional disassembly and increase in vascular permeability.

Intersectin-2L regulates caveola endocytosis secondary to Cdc42-mediated actin polymerization.

LIM kinase 1 promotes endothelial barrier disruption and neutrophil infiltration in mouse lungs.

Regulation of dynamin-2 assembly-disassembly and function through the SH3A domain of intersectin-1s.

Pro-inflammatory endothelial cell dysfunction is associated with intersectin-1s down-regulation.

Impaired caveolae function and upregulation of alternative endocytic pathways induced by experimental modulation of intersectin-1s expression in mouse lung endothelium.

In vivo knockdown of intersectin-1s alters endothelial cell phenotype and causes microvascular remodeling in the mouse lungs.