The regulatory role of smooth muscle 22 on the proliferation of aortic smooth muscle cells participates in the development of aortic dissection.
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.



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.



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.



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.
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
Yudong
Y
Sun
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
Zhiqing
Z
Zhao
Department of General Surgery, No. 454 Hospital of PLA, Nanjing, China.
Lewei
L
Hou
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
Yu
Y
Xiao
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
Feng
F
Qin
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
Junyi
J
Yan
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China. Electronic address: zhoujian1-2@163.com.
Jian
J
Zhou
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China. Electronic address: xueguanky@163.com.
Zaiping
Z
Jing
D000328:Adult; D000784:Aortic Dissection / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001013:Aorta, Thoracic / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D017545:Aortic Aneurysm, Thoracic / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling; D049109:Cell Proliferation; D002478:Cells, Cultured; D015536:Down-Regulation; D005260:Female; D006801:Humans; D008297:Male; D008840:Microfilament Proteins / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism* / Q000473:pathology; D011401:Promoter Regions, Genetic; D034622:RNA Interference; D014158:Transcription, Genetic; D014162:Transfection; D066253:Vascular Remodeling
D008840:Microfilament Proteins; D009124:Muscle Proteins; C051615:transgelin; D002118:Calcium