Mitochondrial-Derived Peptide MOTS-c Attenuates Vascular Calcification and Secondary Myocardial Remodeling via Adenosine Monophosphate-Activated Protein Kinase Signaling Pathway
| Autor: | Jin Rui Chang, Zheng Liu, Ming Wei, Da Chuan Yin, Lu Gan, Hui Ling Cao, Li Liu, Wanli W. Smith, Xing Li Su |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
Adenosine monophosphate Nicotine Urology 030232 urology & nephrology AMP-Activated Protein Kinases 030204 cardiovascular system & hematology Pharmacology Receptor Angiotensin Type 1 Mitochondrial Proteins Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Vascular Calcification Receptor Protein kinase A Cholecalciferol Ventricular Remodeling business.industry AMPK Receptor Endothelin B Adenosine Angiotensin II Rats chemistry Models Animal Signal transduction Cardiology and Cardiovascular Medicine Endothelin receptor business Signal Transduction medicine.drug |
| Zdroj: | Cardiorenal Medicine. 10:42-50 |
| ISSN: | 1664-5502 1664-3828 |
| DOI: | 10.1159/000503224 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|