Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin–angiotensin system

2008 ◽  
Vol 26 (2) ◽  
pp. 269-275 ◽  
Author(s):  
Dalila B Corry ◽  
Pirooz Eslami ◽  
Kei Yamamoto ◽  
Michael D Nyby ◽  
Hirofumi Makino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Uric Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
And Oxidative Stress

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

2021 ◽  
Author(s):  
Nana Zhang ◽  
Xiaosu Song ◽  
Yunfei Bian ◽  
Rui Bai ◽  
Huiyu Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Neointimal Hyperplasia ◽  
Akt Pathway

Abstract Background Numerous studies have shown that the proliferation and migration of vascular smooth muscle cells (VSMCs) were the pathological basis of restenosis occurrence. And Renin and prorenin could promote the proliferation of VSMCs through (pro)renin receptor ((P)RR). Therefore, this study aimed to observe the role of (P)RR in the proliferation of VSMCs in vitro and neointimal hyperplasia in the arterial injury model. Methods 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; pathological change was observed by HE staining. Results In this study, we demonstrated that renin could promote the proliferation of rat VSMCs by enhanced cell viability and cell cycle proteins, but silencing (P)RR restrained this. Then, we found that renin could enhance the levels of NOX1-mediated oxidative stress and inflammation by activating ERK1/2-AKT pathway in vitro. Similarly, inhibition of (P)RR resulted in opposite phenomenon. Importantly, inhibition of (P)RR could inhibit the neointimal hyperplasia in vivo after common carotid artery injury through restraining NOX1-mediated oxidative stress by down-regulating ERK1/2-AKT pathway. Conclusion We concluded that 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.

Uric Acid Causes Vascular Smooth Muscle Cell Proliferation by Entering Cells via a Functional Urate Transporter

2005 ◽  
Vol 25 (5) ◽  
pp. 425-433 ◽  
Author(s):  
Duk-Hee Kang ◽  
Lin Han ◽  
Xiaosen Ouyang ◽  
Andrew M. Kahn ◽  
John Kanellis ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Uric Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Smooth Muscle Cell Proliferation ◽  
Urate Transporter

Involvement of Cyclooxygenase- and Lipoxygenase-Mediated Conversion of Arachidonic Acid in Controlling Human Vascular Smooth Muscle Cell Proliferation

1990 ◽  
Vol 63 (02) ◽  
pp. 291-297 ◽  
Author(s):  
Herm-Jan M Brinkman ◽  
Marijke F van Buul-Worteiboer ◽  
Jan A van Mourik
Keyword(s):  
Cell Proliferation ◽  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Muscle Cells ◽  
Smooth Muscle Cell Proliferation

SummaryWe observed that the growth of human umbilical arterysmooth muscle cells was inhibited by the phospholipase A2 inhibitors p-bromophenacylbromide and mepacrine. Thesefindings suggest that fatty acid metabolism might be integrated in the control mechanism of vascular smooth muscle cell proliferation. To identify eicosanoids possibly involved in this process, we studied both the metabolism of arachidonic acid of these cells in more detail and the effect of certain arachidonic acid metabolites on smooth muscle cells growth. We found no evidence for the conversion of arachidonic acid via the lipoxygenase pathway. In contrast, arachidonic acid was rapidly converted via the cyclooxy-genase pathway. The following metabolites were identified: prostaglandin E2 (PGE2), 6-keto-prostaglandin F1α (6-k-PGF1α), prostaglandin F2α (PGF2α), 12-hydroxyheptadecatrienoic acid (12-HHT) and 11-hydroxyeicosatetetraenoic acid (11-HETE). PGE2 was the major metabolite detected. Arachidonic acid metabolites were only found in the culture medium, not in the cell. After synthesis, 11-HETE was cleared from the culture medium. We have previously reported that PGE2 inhibits the serum-induced [3H]-thymidine incorporation of growth-arrested human umbilical artery smooth muscle cells. Here we show that also 11-HETEexerts this inhibitory property. Thus, our data suggeststhat human umbilical artery smooth muscle cells convert arachidonic acid only via the cyclooxygenase pathway. Certain metabolites produced by this pathway, including PGE2 and 11-HETE, may inhibit vascular smooth muscle cell proliferation.

Influence of Endothelium on Cultured Vascular Smooth Muscle Cell Proliferation

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 748-751 ◽  
Author(s):  
Concepción Peiró ◽  
Juliana Redondo ◽  
M. Angeles Rodríguez-Martínez ◽  
Javier Angulo ◽  
Jesús Marín ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Smooth Muscle Cell Proliferation
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