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p42/44MAPK regulates baseline permeability and cGMP-induced hyperpermeability in endothelial cells.

Abstract：

:We tested the hypothesis that p42/44MAPK and p38MAPK (mitogen-activated protein kinases; MAPK) signaling pathways regulate endothelial cell permeability to macromolecules. Passage 2-4 human umbilical vein endothelial cells (HUVEC) were grown to confluence on fibronectin-coated Snapwell membranes. The flux of fluorescein isothiocyanate-labeled dextran-70 across the HUVEC monolayers served to determine permeability. Application of 1 mM 8-bromo 3' 5'-cyclic guanosine monophosphate (8-Br-cGMP) increased permeability from 7.0 +/- 1.6 x 10(-6) to 12.5 +/- 2.8 x 10(-6) cm/s (P < 0.05). Pretreatment of HUVEC for 60 min with a selective p42/44MAPK inhibitor (AG126 at 2.7 and 27 microM) blocked 8-Br-cGMP-induced hyperpermeability. However, inhibition of p38MAPK (SB203580 at 0.6 microM) did not influence the cGMP-induced hyperpermeability response. AG126, administered at 27 microM, decreased baseline permeability from 7.9 +/- 0.5 x 10(-6) to 5.9 +/- 0.5 x 10(-6) cm/s (P < 0.05). Our results indicate that the p42/44MAPK signaling pathway is important in the regulation of baseline permeability and cGMP-induced hyperpermeability.

journal_name

Microvasc Res

journal_title

Microvascular research

authors

Varma S,Breslin JW,Lal BK,Pappas PJ,Hobson RW 2nd,Durán WN

doi

10.1006/mvre.2001.2381

keywords:

subject

Has Abstract

pub_date

2002-03-01 00:00:00

pages

172-8

issue

2

eissn

0026-2862

issn

1095-9319

pii

S0026286201923817

journal_volume

63

pub_type

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