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PDGF-mediated PI3K/AKT/β-catenin signaling regulates gap junctions in corpus cavernosum smooth muscle cells.

Abstract：

:Erectile dysfunction (ED) is the most common sexual disorder that men report to healthcare providers. Gap junctions (GJs) are thought to be responsible for synchronous shrinkage of corpus cavernosum smooth muscle cells (CCSMCs), and play thus an important role in the maintenance of an erection. Hypoxia has been suggested as a pathological mechanism underlying ED. Here we demonstrate that hypoxia increased the expression of platelet-derived growth factor (PDGF) and the main GJ component connexin (Cx)43 in CCSMCs. Inhibiting PDGF receptor (PDGFR) activity decreased Cx43 expression. Treatment with different concentrations of PDGF increased the levels of phosphorylated protein kinase B (AKT), β-catenin, and Cx43, whereas inhibition of PDGFR or activation of phosphatidylinositol 3 kinase (PI3K)/AKT signaling altered β-catenin and Cx43 expression. Meanwhile, silencing β-catenin resulted in the downregulation of Cx43. These results demonstrate that PDGF secretion by CCSMCs and vascular endothelial cells is enhanced under hypoxic conditions, leading to increased Cx43 expression through PI3K/AKT/β-catenin signaling and ultimately affecting GJ function in ED. Thus, targeting this pathway is a potential therapeutic strategy for the treatment of ED.

journal_name

Exp Cell Res

journal_title

Experimental cell research

authors

Zhang X,Zhao F,Zhao JF,Fu HY,Huang XJ,Lv BD

doi

10.1016/j.yexcr.2017.11.025

subject

Has Abstract

pub_date

2018-01-15 00:00:00

pages

252-259

issue

2

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(17)30627-4

journal_volume

362

pub_type

杂志文章

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