Involvement of the H1 Histamine Receptor, p38 MAP Kinase, Myosin Light Chains Kinase, and Rho/ROCK in Histamine-Induced Endothelial Barrier Dysfunction.

ABSTRACT:

Objective

The mechanisms by which histamine increases microvascular permeability remain poorly understood. We tested the hypothesis that H1 receptor activation disrupts the endothelial barrier and investigated potential downstream signals.

Methods

We used confluent EC monolayers, assessing TER as an index of barrier function. HUVEC, HCMEC, and HDMEC were compared. Receptor expression was investigated using Western blotting, IF confocal microscopy and RT-PCR. Receptor function and downstream signaling pathways were tested using pharmacologic antagonists and inhibitors, respectively.

Results

We identified H1-H4 receptors on all three EC types. H1 antagonists did not affect basal TER but prevented the histamine-induced decrease in TER. Blockade of H2 or H3 attenuated the

SUBMITTER: Adderley SP 

PROVIDER: S-EPMC4412777 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature