The aim of this study was to determine the role of smooth muscle 22 (SM22) in aortic dissection (AD) vascular remodeling and its regulatory mechanism on vascular smooth muscle cell function.Methods:
Seven patients who underwent surgery for AD with no genetic predisposition and seven organ donors who died from nonvascular diseases were selected. In each aorta sample, the levels of SM22 were detected using immunohistochemistry and Western blot analysis. We inhibited the expression of SM22 with the application of RNA interference in human aortic smooth muscle cells (HASMCs). Cell-counting Kit-8 (Dojindo, Kumamoto, Japan) analyses were used to detect HASMC proliferation. Furthermore, the intracellular calcium concentration was detected using Rhod-2/AM (Dojindo) staining.Results:
SM22 was significantly downregulated in the media of AD samples compared with controls (P< .05). In an in vitro study, downregulation of SM22 can significantly promote HASMC proliferation. Our research further revealed that cells treated with nifedipine can inhibit the promoter activity of SM22 downregulation on HASMC proliferation. Intracellular calcium concentration was a significantly varied during the process.Conclusions:
SM22 regulates HASMC function activity through intracellular calcium. It presents a downregulation in AD, which might play a potential role in vascular remodeling of AD.Clinical Relevance:
In the population of China, the prevalence of aortic dissection (AD) is predicted to increase. Vascular smooth muscle cell pathological proliferation has been proven to play a role in AD development and vascular remodeling. This study addresses the role of smooth muscle 22 in mediating vascular smooth muscle cell proliferation, which is regulated by cellular calcium concentration. This study will help illuminate the pathological mechanism of aortic diseases and provide a new insight in research of smooth muscle 22 biological behavior and as a potential therapeutic agent for treatment of AD.