The peripheral Epac1/p-Cav-1 pathway underlies the disruption of the vascular endothelial barrier following skin/muscle incision and retraction-induced chronic postsurgical pain.

ABSTRACT:

Background

Vascular endothelial barrier disruption is pivotal in the development of acute and chronic pain. Here, we demonstrate a previously unidentified molecular mechanism in which activation of the peripheral Epac1/p-Cav-1 pathway accelerated the disruption of the vascular endothelial barrier, thereby promoting chronic postsurgical pain (CPSP).

Methods

We established a rat model of CPSP induced by skin/muscle incision and retraction (SMIR). Pain behaviors were assessed by the mechanical withdrawal threshold (MWT) at different times. Local muscle tissues around the incision were isolated to detect the vascular permeability and the expression of Epac1 and Cav-1. They were assessed by western blot and immunofluorescence staining.

Results

SMIR increased vascular endot

SUBMITTER: Chen H 

PROVIDER: S-EPMC9843368 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature