title: [Establishing an organic model of SMC proliferation with cultured aorta of rats and exploring the underlying mechanism].
abstract: To study the mechanism of proliferous vascular disease as well as its prevention and treatment, an organic model was established with cultured aortas of rats, and the mechanism there-in invloved was probed. Immunostaining histology showed that smooth muscle cell (SMC) proliferation was observed in the aorta segments of rats, after their endothelia being injured and cultured in vitro with 20% fetal bovine serum. After being cultured for 5 days, various degrees of proliferation of SMC on cultured artery segments were observed by HE staining, and conspicuous plaques were developed after being cultured for 13 days. The proliferous SMC was also observed by Brdu labeling. RT-PCR examination showed that the mRNA expression of hypertension-related gene-1 (Hrg-1) and smooth muscle 22 alpha (SM22a) in the aortas decreased with the prolongation of culture time, and completely disappeared after being cultured for 13 days . But when cultured in vitro for ten days, the ET-1 content of supernatant and the proliferous SMC labeled by Brdu increased obviously and the expressions of Hrg-1 and SM22a decreased after the endothelium was destroyed. Compared with the injured endothelium groups, the proliferous SMC of injured endothelium plus BQ123 groups decreased visibly. The same significant differences between serum groups and serum-free groups were also observed. These results suggest that the culturing of rat aorta segments in vitro can induce the proliferation of SMC and the transform of phenotype from contractile type to synthetic type. The ET-1 and serum are the main factors in the proliferation of SMC and in the transform of phenotype. This organic model could serve as a good experimental platform for the researches into the mechanism of proliferous vascular disease as well as its prevention and treatment.
authors.affiliation: Medical School of Suzhou University, Suzhou 215123, China.
authors.forename: Yanlin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Caiying
authors.initials: C
authors.lastname: Wang
authors.forename: Qin
authors.initials: Q
authors.lastname: Yang
authors.forename: Yaan
authors.initials: Y
authors.lastname: Yang
authors.forename: Yongping
authors.initials: Y
authors.lastname: Gu
authors.forename: Mincheng
authors.initials: M
authors.lastname: Wang
authors.forename: Kaiyun
authors.initials: K
authors.lastname: Wu
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000166:cytology*; D049109:Cell Proliferation; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000235:genetics / Q000378:metabolism*; D005260:Female; D008297:Male; D008840:Microfilament Proteins / Q000235:genetics / Q000378:metabolism; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D009924:Organ Culture Techniques; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D019332:Endothelin-1; D008840:Microfilament Proteins; D009124:Muscle Proteins; D012333:RNA, Messenger; C051615:transgelin