Effects of high glucose on expression of OPG and RANKL in rat aortic vascular smooth muscle cells
10.1016/S1995-7645(14)60317-5
- Author:
Hong-Juan CHANG
1
;
Xin MENG
1
;
Tian-Fa LI
2
;
Jun-Li GUO
2
;
You-Ling LAN
2
;
Yue-Qiong KONG
2
;
Xian-Ji MA
2
;
Xiao-Ling LU
3
;
Wei-Ying LU
4
;
Shao-Jiang ZHENG
5
Author Information
1. Department of Neurology, The Second People's Hospital of Xinxiang
2. Department of Cardiovascular Institute, Affiliated Hospital of Hainan Medical College
3. National Center for International Research of Biological Targeting Diagnosis and Therapy, Guangxi Key Laboratory of Biological Targeting Diagnosis and Therapy Research, Guangxi Medical University
4. Reproductive Medicine Center, Affiliated Hospital of Hainan Medical College
5. Department of Pathology, Affiliated Hospital of Hainan Medical College
- Publication Type:Journal Article
- Keywords:
High glucose;
Osteoprotegerin;
Receptor activator of NF- κ B ligand;
Vascular smooth muscle cells
- From:
Asian Pacific Journal of Tropical Medicine
2015;8(3):209-213
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore effect of high glucose on expression of osteoprotegerin (OPG) and receptor activator of NF- κ B ligand (RANKE) in rat aortic vascular smooth muscle cells. Methods: SD rats were intraperitoneally injected with streptozotocin, OPG and RANKL expression in rat thoracic aortas were detected by immunohistochemical staining. In cultured vascular smooth muscle cells (VSMCs) (A7r5), qRT-PCR and Western blot analysis were used to examine the mRNA and protein levels of OPG and RANKL. Results: Our results demonstrated that OPG expression was increased in hyperglycemic rat aortic VSMCs, while RANKL expression was decreased. Besides, in vitro experiments high glucose induced OPG expression, but depressed RANKL expression by dose- and time-dependent manner in cultured A7r5. Conclusions: Our findings suggested that high glucose could promote the expression of OPG, and inhibit the expression of RANKL in VSMCs, which may be partly be the molecular mechanism of diabetic vascular calcification.
