Microscopy-Cells were grown on gelatin  nectin-coated Millicell culture one Tze in v Lliger M199 medium for 4 days to reach connce. In the measurements was complete medium with medium containing 5% FBS replaced and the cells were treated with 1 ANG 7 II or 1 ng  ml VEGF or vehicle. After 48 h of treatment of endothelial cells ed with Zamboni tive DNA-PK Inhibitors (4% paraformaldehyde in 0.1 M phosphate buffer, pH 7.4) for 1 h at room temperature. Fixative was blood address for reprint requests and other correspondence: L. Rosivall, Hun-Hungarian Academy of Sciences and Semmelweis University.

Research Group for Pediatrics and Nephrology, Department of Pathophysiology, Medical Faculty t, Semmelweis University t, Budapest, Nagyvárad tér 4, H-1089, Hungary (: Rosivallnet.sote ). and interstitium (7). Caveolae are small invaginations of the cell surface SK Surface with a diameter of 5565 nm. Caveolin, a protein of 21 kDa, is the essential component of caveolae (27, 33). Functionally caveolae in endocytosis, and transcytosis potocytosis (26) are associated. Often open Ings caveolar membranes and contain fenestrae, with the exception of glomerular Ren capillaries, afferent arterioles, and sinus The liver (31, 43, 45). The membranes are anchored by radial  ls to the edge and center button in a mix together. The component thereof  ls bile plasma-1 (PV-1) protein, a 60 kDa -, clamping, cationic, type II transmembrane glycoprotein that forms homodimers (38, 39). It was suggested that the membranes in the Openings of the caveolae and fenestrae function as a screen is such that ae Durchl Permeability of these structures (11) matches. Recently, new important features to PV-1 was transzellul as relief Reindeer migration of immune cells across the endothelial cell layer (19) attributed.

In vivo studies have shown that PV-1 expression with a St Tion of the blood-brain barrier into the brain isch-emic and diabetic mikrovaskul Correlated leakage re-retinop Athy (36, 37). Angiotensin II (Ang II), a vasoactive molecule, hypertension and kidney failure, involved, among other things. ANG II can stimulate the release of vasoactive and other proinmma Tory cytokines (35). ANG II increased Ht leukocyte rolling, adhesion Sion and migration in mesenteric postkapill Ren venules of rats (1, 29). Involvement of nuclear VX-950 factor-B, p38 mitogen-activated protein kinase (MAP) kinase, and the production of reactive oxygen species was assigned to the R Proinmmatory of ANG II (8). The vascular Re endothelial growth factor (VEGF) go Rt to a family of dimeric glycoproteins which VEGF-A growth factor-E and placenta (PIGF). Includes VEGF-A. EA isoforms, VEGF 165 being the h Most frequent and biologically active, the fenestrated adjacent to here as VEGF (23) constitutive expression of VEGF in endothelial plexus epithelial cells showed Choro-called Of renal glomeruli and uli (2, 3). VEGF acts by binding to the receptor tyrosine kinase (VEGFR-1 and -2), to the activation of various molecules, including normal p38 signal transduction (2 28), which in turn part of the stress-activated serine  threonine protein kinases. This kinase is activated by phosphorylation by kinases MKK3 and MKK6 upstream Rts (25). The activation of p38 is involved in endothelial responses to migration, Durchl Liquid and the survival of the cell (21, 34) and the stability of t of the different heart mRNAs by activating MAPKAP2 (MK2) (22) controls. VEGF, as m Chtiger Agent Durchl To increased permeability Hen,  0363-614312 Copyright 2012 the American Physiological Society C267 .physiology from 6 M Downloaded March.