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Cardiorenal Med. 2019 Nov 6:1-9. doi: 10.1159/000503224. [Epub ahead of print]

Mitochondrial-Derived Peptide MOTS-c Attenuates Vascular Calcification and Secondary Myocardial Remodeling via Adenosine Monophosphate-Activated Protein Kinase Signaling Pathway.

Author information

1
Department of Pharmacology, Xi'an Medical University, Xi'an, China.
2
Shaanxi Key Laboratory of Ischemic Cardiovascular Disease, Xi'an Medical University, Xi'an, China.
3
Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, China.
4
Department of Gynecology, Shaanxi Provincial People's Hospital, The Third Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
5
College of Medical Laboratory Science, Guilin Medical University, Guilin, China.
6
Ultrasound Diagnostics Department, Shaanxi Provincial People's Hospital, Xi'an, China.
7
Department of Pharmacology, Xi'an Medical University, Xi'an, China, suxingli@xiyi.edu.cn.
8
Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, China, suxingli@xiyi.edu.cn.
9
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Abstract

INTRODUCTION:

Vascular calcification (VC) is a complex, regulated process involved in many disease entities. So far, there are no treatments to reverse it. Exploring novel strategies to prevent VC is important and necessary for VC-related disease intervention.

OBJECTIVE:

In this study, we evaluated whether MOTS-c, a novel mitochondria-related 16-aa peptide, can reduce vitamin D3 and nicotine-induced VC in rats.

METHODS:

Vitamin D3 plus nicotine-treated rats were injected with MOTS-c at a dose of 5 mg/kg once a day for 4 weeks. Blood pressure, heart rate, and body weight were measured, and echocardiography was performed. The expression of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and the angiotensin II type 1 (AT-1) and endothelin B (ET-B) receptors was determined by Western blot analysis.

RESULTS:

Our results showed that MOTS-c treatment significantly attenuated VC. Furthermore, we found that the level of phosphorylated AMPK was increased and the expression levels of the AT-1 and ET-B receptors were decreased after MOTS-c treatment.

CONCLUSIONS:

Our findings provide evidence that MOTS-c may act as an inhibitor of VC by activating the AMPK signaling pathway and suppressing the expression of the AT-1 and ET-B receptors.

KEYWORDS:

Adenosine monophosphate-activated protein kinase; Angiotensin II type 1; Endothelin B; MOTS-c; Rat model of vascular calcification

PMID:
31694019
DOI:
10.1159/000503224
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