title: Vascular Adventitia Calcification and Its Underlying Mechanism.
abstract: Previous research on vascular calcification has mainly focused on the vascular intima and media. However, we show here that vascular calcification may also occur in the adventitia. The purpose of this work is to help elucidate the pathogenic mechanisms underlying vascular calcification. The calcified lesions were examined by Von Kossa staining in ApoE-/- mice which were fed high fat diets (HFD) for 48 weeks and human subjects aged 60 years and older that had died of coronary heart disease, heart failure or acute renal failure. Explant cultured fibroblasts and smooth muscle cells (SMCs)were obtained from rat adventitia and media, respectively. After calcification induction, cells were collected for Alizarin Red S staining. Calcified lesions were observed in the aorta adventitia and coronary artery adventitia of ApoE-/-mice, as well as in the aorta adventitia of human subjects examined. Explant culture of fibroblasts, the primary cell type comprising the adventitia, was successfully induced for calcification after incubation with TGF-β1 (20 ng/ml) + mineralization media for 4 days, and the phenotype conversion vascular adventitia fibroblasts into myofibroblasts was identified. Culture of SMCs, which comprise only a small percentage of all cells in the adventitia, in calcifying medium for 14 days resulted in significant calcification.Vascular calcification can occur in the adventitia. Adventitia calcification may arise from the fibroblasts which were transformed into myofibroblasts or smooth muscle cells.
authors.affiliation: Department of Health Care, China-Japan Friendship Hospital, Ministry of Health, Beijing, China.
authors.forename: Na
authors.initials: N
authors.lastname: Li
authors.affiliation: Center for Cardiovascular Diseases, China-Japan Friendship Hospital, Ministry of Health, Beijing, China.
authors.forename: Wenli
authors.initials: W
authors.lastname: Cheng
authors.affiliation: Department of Health Care, China-Japan Friendship Hospital, Ministry of Health, Beijing, China.
authors.forename: Tiequn
authors.initials: T
authors.lastname: Huang
authors.affiliation: Graduate School, Beijing University of Traditional Chinese Medicine, Beijing, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Yuan
authors.affiliation: Graduate School, Beijing University of Traditional Chinese Medicine, Beijing, China.
authors.forename: Xi
authors.initials: X
authors.lastname: Wang
authors.affiliation: Graduate School, Beijing University of Traditional Chinese Medicine, Beijing, China.
authors.forename: Meiyue
authors.initials: M
authors.lastname: Song
mesh_terms: D063194:Adventitia / Q000378:metabolism / Q000473:pathology; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency; D002478:Cells, Cultured; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D005260:Female; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D061205:Vascular Calcification / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*
chemical_list: D001057:Apolipoproteins E; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1