Peroxisome Proliferator-Activated Receptor γ Ligands Retard Cultured Vascular Smooth Muscle Cells Calcification Induced by High Glucose

被引：19

作者：

Zhou, Ye-Bo ^{[1
,2
]}

Zhang, Jing ^{[3
]}

Peng, Ding-Qiong ^{[4
]}

Chang, Jin-Rui ^{[5
]}

Cai, Yan ^{[5
]}

Yu, Yan-Rong ^{[5
]}

Jia, Mo-Zhi ^{[5
]}

Wu, Wei ^{[5
]}

Guan, You-Fei ^{[5
]}

Tang, Chao-Shu ^{[1
,5
]}

Qi, Yong-Fen ^{[1
,5
]}

机构：

[1] Capital Med Univ, Beijing An Zhen Hosp, Minist Educ, Key Lab Remodeling Related Cardiovasc Dis, Beijing 100029, Peoples R China

[2] Nanjing Med Univ, Dept Physiol, Nanjing 210029, Jiangsu, Peoples R China

[3] Beijing Normal Univ, Sch Phys Educ & Sports, Beijing 100875, Peoples R China

[4] Gen Hosp Civil Aviat Adm China, Dept Endocrinol, Beijing 100123, Peoples R China

[5] Peking Univ, Hlth Sci Ctr, Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China

来源：

CELL BIOCHEMISTRY AND BIOPHYSICS | 2013年 / 66卷 / 03期

基金：

中国国家自然科学基金;

关键词：

High glucose; PPAR gamma; Vascular smooth muscle cells; Calcification; BONE-MINERAL DENSITY; PPAR-GAMMA; GENE-EXPRESSION; FATTY-ACIDS; THIAZOLIDINEDIONE; PROTEIN; DIFFERENTIATION; MECHANISMS; INCREASES; DISEASE;

D O I：

10.1007/s12013-012-9490-7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Peroxisome proliferator-activated receptor gamma (PPAR gamma) and its ligands have profound effects on glucose homeostasis, cardiovascular diseases, and bone metabolism. To explore the pathophysiological roles of PPAR gamma in diabetes with concomitant vascular calcification, we investigated changes in PPAR gamma expression and the effect of the PPAR gamma ligands troglitazone and rosiglitazone on vascular smooth muscle cell (VSMC) calcification induced by high glucose (HG, 25 mmol/L). Compared with low glucose, HG-induced VSMC calcification, and PPAR gamma mRNA, protein level was decreased. Troglitazone and rosiglitazone treatment markedly attenuated the VSMC calcification, whereas PPAR gamma antagonist GW9662 abolished the effect of rosiglitazone on calcification. Pretreatment of VSMCs with rosiglitazone, but not troglitazone, restored the loss of lineage marker expression: the protein levels of alpha-actin and SM-22 alpha were increased 52 % (P < 0.05) and 53.1 % (P < 0.01), respectively, as compared with HG alone. Troglitazone and rosiglitazone reversed the change in bone-related protein expression induced by HG: decreased the mRNA levels of osteocalcin, bone morphogenetic protein 2 (BMP2), and core binding factor alpha 1 (Cbf alpha-1) by 26.9 % (P > 0.05), 50.0 % (P < 0.01), and 24.4 % (P < 0.05), and 48.4 % (P < 0.05), 41.4 % (P < 0.01) and 56.2 % (P < 0.05), respectively, and increased that of matrix Gla protein (MGP) 84.2 % (P < 0.01) and 70.0 %, respectively (P < 0.05), as compared with HG alone. GW9662 abolished the effect of rosiglitazone on Cbf alpha-1 and MGP expression. PPAR gamma ligands can inhibit VSMCs calcification induced by high glucose.

引用

页码：421 / 429

页数：9