Dipeptidyl peptidase-4 promotes calcification of human vascular smooth muscle cells through ERK1/2 signaling pathway
10.3760/cma.j.issn.1000-6699.2017.04.013
- VernacularTitle:二肽基肽酶4通过ERK1/2信号通路促进人血管平滑肌细胞钙化
- Author:
Weidan LUO
;
Xueqin WANG
;
Huqiang HE
;
Lei ZHANG
;
Hong ZENG
;
Xin LIU
;
Yong LIU
- Keywords:
Dipeptidyl peptidase 4;
Vascular smooth muscle cells;
Calcification;
ERK1/2 signaling pathway
- From:
Chinese Journal of Endocrinology and Metabolism
2017;33(4):335-340
- CountryChina
- Language:Chinese
-
Abstract:
Objective To further investigate direct effects of dipeptidyl peptidase-4(DPP4) on calcification and to identify responsible signaling pathways in human vascular smooth muscle cells (HVSMC). Methods The effect of DPP-4 on calcification of HVSMC was observed by alizarin red, and Western blot was used to detect whether DPP4 induced calcification-related protein expressions through extracellular signal-regulated kinases 1/2 (ERK1/2) pathway. Results The Alizarin red staining results showed that calcified nodules in DPP4 group were significantly increased as compared with control group, similar to calcification group.The protein expressions of osteoprotegerin (OPG), osteopontin (OPN), Runt-related transcription factor 2 (RUNX2), and bone morphogenetic protein 2 (BMP2) were stimulated by DPP4 in a concentration- and time-dependent manner. The phosphorylation level of ERK1/2 was significantly increased after DPP4 incubation for 15 min (P<0.05). PD98059, an ERK1/2 inhibitor, significantly lowered DPP4-stimulated expressions of calcification-related proteins (P<0.05). Conclusion DPP4 may promote the calcification of HVSMC through ERK1/2 signaling pathways.
