Role of mitochondrial ribosomal protein L7/L12 (MRPL12) in diabetic ischemic heart disease.

Autor: Rai AK; Aging + Cardiovascular Discovery Center, Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Temple University, Philadelphia, USA., Sanghvi S; Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Department of Molecular Cellular and Developmental Biology, The Ohio State University, Columbus, OH, USA., Muthukumaran NS; Aging + Cardiovascular Discovery Center, Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Temple University, Philadelphia, USA., Chandrasekera D; Department of Physiology, HeartOtago, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand., Kadam A; Section of Cardiovascular Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, 27157, USA., Kishore J; Aging + Cardiovascular Discovery Center, Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Temple University, Philadelphia, USA., Kyriazis ID; Department of Biology, Faculty of Medicine, University of Thessaly, Larissa, Greece., Tomar D; Section of Cardiovascular Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, 27157, USA., Ponnalagu D; Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Department of Pharmacology, University of Washington, Seattle, WA, USA., Shettigar V; Aging + Cardiovascular Discovery Center, Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Temple University, Philadelphia, USA., Khan M; Dorothy M. Davis Heart Lung and Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Department of Emergency Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA., Singh H; Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Dorothy M. Davis Heart Lung and Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, USA., Goukassian D; Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, USA., Katare R; Department of Physiology, HeartOtago, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand., Garikipati VNS; Aging + Cardiovascular Discovery Center, Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Temple University, Philadelphia, USA; Department of Emergency Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Electronic address: venkata.naga.srikanth.garikipati@temple.edu.
Jazyk: angličtina
Zdroj: Free radical biology & medicine [Free Radic Biol Med] 2024 Sep; Vol. 222, pp. 531-538. Date of Electronic Publication: 2024 Jul 06.
DOI: 10.1016/j.freeradbiomed.2024.07.003
Abstrakt: Background: Myocardial infarction (MI) is a significant cause of death in diabetic patients. Growing evidence suggests that mitochondrial dysfunction contributes to heart failure in diabetes. However, the molecular mechanisms of mitochondrial dysfunction mediating heart failure in diabetes are still poorly understood.
Methods: We examined MRPL12 levels in right atrial appendage tissues from diabetic patients undergoing coronary artery bypass graft (CABG) surgery. Using AC-16 cells overexpressing MRPL12 under normal and hyperglycemic conditions we performed mitochondrial functional assays OXPHOS, bioenergetics, mitochondrial membrane potential, ATP production and cell death.
Results: We observed elevated MRPL12 levels in heart tissue samples from diabetic patients with ischemic heart disease compared to non-diabetic patients. Overexpression of MRPL12 under hyperglycemic conditions did not affect oxidative phosphorylation (OXPHOS) levels, cellular ATP levels, or cardiomyocyte cell death. However, notable impairment in mitochondrial membrane potential (MMP) was observed under hyperglycemic conditions, along with alterations in both basal respiration oxygen consumption rate (OCR) and maximal respiratory capacity OCR.
Conclusions: Overall, our results suggest that MRPL12 may have a compensatory role in the diabetic myocardium with ischemic heart disease, suggesting that MRPL12 may implicate in the pathophysiology of MI in diabetes.
Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest.
(Copyright © 2024. Published by Elsevier Inc.)
Databáze: MEDLINE
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