vascular Re endothelial permeability is t regulated by different mechanisms. The effects of Vinorelbine ANG II were in different vascular Ren segments both in vivo (24, 42) and in vitro (12, 44, 46) were examined. This study examined the effect of ANG II on the permeability t of HUVEC and its relation to p38 MAPK-way street e The results show that angiotensin II, the permeability t erh HUVEC ht after 48 h of treatment with the model slightly different from that of VEGF. The effects of ANG II and VEGF on the permeability t parallel to the morphological changes were changes, N Namely the Erh Increase of caveolar vesicles. These two factors increased Ht the expression of PV-1, a protein-associated caveolae and fenestrae, a p38-dependent Ngigen way. ANG II (10 7 M) increased Ht the Durchl Permeability of HUVEC monolayers (Fig. 1A).
Higher doses not Increase to an increase of the per-Durchl flow permeability. Similar Naringenin patterns in response to ANG II was also in the stimulation of sodium transport in the proximal tubule (15) and the mikrovaskul Ren Durchl Permeability of the mesenteric venules (42) is observed. This beneficial effect of Durchl Permeability is relatively ANG II This observation was con med by fluorescent Micros-copy, one erh Increase the PV-1 immunostaining Staining after treatment of VEGF and Ang II showed. PV-1 and caveolin-1 showed some colocalization in the treated cells. In previous studies has shown that caveolae and clustered vesikul Ren organelles in increased Hten Durchl Transendothelial permeability are involved (9, 11). We assume therefore that the fused caveolar vesicles, a system of Kan len For transzellul Other transport by providing of particles and may partly contribute to an increased Hten endothelial permeability t. The movement of and k can Also be parazellul Much better way. HUVEC monolayers purchase PS-341 immunostaining Staining for VE-cadherin after ANG II treatment showed no significant Ver Change cell.
This L Sst suspect that the increase in the permeability t in response to ANG II Haupts Chlich transzellul occur R. Several cytokines exert their effects on the permeability t on p38 MAPK. p38 plays a role important in the VEGF, a increased hte Durchl permeability transforming growth factor-1 or thrombin-induced, but their involvement in mediating ANG II-dependent ngigen effects has not been addressed (5, 13, 16, 21). Previous studies have attributed the effect of Ang II on the permeability t to the activation of cAMP PKA order Bortezomib signaling pathway and the increase in PKC activity t or erh Increase of intracellular Ren Ca 2 levels (44, 46). Guo . (14) showed that Ang II-induced phosphorylation of p38 tion in HUVEC, but his participation in the Durchl Permeability has not been investigated. Here we have shown that inhibition of p38 abolished with SB-203580, the effects of ANG II and VEGF in AJP-Cell Physiol 10.2 . 138.2011 physiology of 6 M Downloaded March, 2012 Page 8 – ANG II, C274, PV-1, Fig caveolae. 8th Effects of ANG II or VEGF treatment of PV-1 localization. The image repr Presents HUVEC stained for caveolin-1 and PV-1 (separately and combined) in the contr On, ANG II or VEGF-treated group is shown. PV-1: green, caveolin-1: red. Erh Increase in endothelial permeability t. This suggests that the Durchl is To increased permeability Hen by ANG II, also to VEGF, modulated by intracellular Re p38 MAP kinase-dependent Independent signaling pathways using gene-SIG.
It is known that p38 MAP kinase, au Plays beyond the control of permeability t, a role extracellular matrix Appears in the modulation of gene expression. 9th Effect of p38 mitogen-activated protein kinase-Pro (MAP) kinase blockade with SB-203 580 on VEGF and Ang II-induced increase in the density of caveolae (left) and permeability t and the actin cytoskeleton organization.