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Published on: November 20, 2017
Cortistatin attenuates vascular calcification in rats
Yue Liu1, Ye Bo Zhou, Gai Gai Zhang
1Department of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Regulatory Peptides
|September 22, 2009
Summary
Cortistatin (CST) effectively inhibits vascular calcification in rats and cultured cells by reducing calcium deposition and improving hemodynamics. These beneficial effects are mediated through the growth hormone secretagogue receptor 1a (GHSR1a).
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Pharmacology
Background:
- Cortistatin (CST) is a polypeptide with diverse biological roles.
- Its specific involvement in cardiovascular disease pathogenesis, particularly vascular calcification, is not well understood.
- Vascular calcification is a significant risk factor for cardiovascular events.
Purpose of the Study:
- To investigate the inhibitory effects of Cortistatin (CST) on vascular calcification in vivo and in vitro.
- To elucidate the underlying molecular mechanisms of CST's action.
- To explore the potential role of specific receptors in mediating CST's effects on vascular calcification.
Main Methods:
- Vascular calcification was induced in rats using vitamin D3 and nicotine, and in cultured rat vascular smooth muscle cells (VSMCs) using beta-glycerophosphate.
- Hemodynamic variables, alkaline phosphatase (ALP) activity, calcium deposition, and pathological changes were assessed.
- Messenger RNA (mRNA) expression of type III sodium-dependent phosphate co-transporter-1 (Pit-1) was analyzed.
- The effects of ghrelin, somatostatin-14, proadrenomedullin N-terminal 20 peptide, and growth hormone-releasing peptide-6[D-lys] were evaluated.
Main Results:
- CST treatment significantly improved hemodynamic parameters and arterial compliance in rats with vascular calcification.
- CST markedly reduced alkaline phosphatase (ALP) activity and calcium deposition in both in vivo and in vitro models.
- CST down-regulated the mRNA expression of Pit-1 and alleviated pathological injury.
- The observed effects of CST were mimicked by ghrelin and reversed by a growth hormone secretagogue receptor 1a (GHSR1a) antagonist, suggesting GHSR1a mediation.
Conclusions:
- Cortistatin (CST) demonstrates significant inhibitory effects against vascular calcification.
- CST improves cardiovascular function by reducing arterial calcification and associated pathological changes.
- The therapeutic effects of CST in vascular calcification are primarily mediated via the GHSR1a pathway.
