Work

Renin and (pro)renin receptors induce vascular smooth muscle cell proliferation and neointimal hyperplasia by activating oxidative stress and inflammation

Year: 2024

Type: article

Abstract: This study aimed to observe the role of (pro)renin receptor ((P)RR) in the proliferation of vascular smooth muscle cells (VSMCs) in vitro and neointimal hyperplasia in the arterial injury model. Cell proliferation was measured by CCK-8 and flow cytometry; RT-PCR and WB assays were used to detect the expressions of cyclin D1, PCNA, (P)RR, NOX1, and PI3K/AKT signal proteins; immunofluorescent staining was conducted to measure the expression of (P)RR; the levels of renin, PDGF-BB, inflammatory factors, and oxidative stress were determined by ELISA; the pathological change was observed by HE staining. Renin could promote the proliferation of rat VSMCs by enhancing cell viability and cell cycle proteins, but silencing (P)RR restrained this. Furthermore, renin could enhance the levels of NOX1-mediated oxidative stress and inflammation by activating the ERK1/2-AKT pathway in vitro. Similarly, inhibition of (P)RR resulted in an opposite phenomenon. Importantly, inhibition of (P)RR could inhibit neointimal hyperplasia in vivo after common carotid artery injury through restraining NOX1-mediated oxidative stress by downregulating the ERK1/2-AKT pathway. Renin and (P)RR induced vascular smooth muscle cell proliferation and neointimal hyperplasia by activating oxidative stress, inflammation, and ERK1/2-AKT pathway in an angiotensin Ⅱ (Ang Ⅱ)-independent manner.

Source: Vascular Medicine

DOI: 10.1177/1358863x241261368