Apela improves cardiac and renal function in mice with acute myocardial infarction.

Journal of Cellular and Molecular Medicine
Yang PanZhi Wang

Abstract

Apela was recently identified as a new ligand of the apelin peptide jejunum (APJ) receptor. The purpose of this study was to investigate the role of apela in post-myocardial infarction (post-MI) recovery from cardiorenal damage. A murine MI model was established, and apela was then infused subcutaneously for two weeks. Echocardiographs were performed before and after infarction at the indicated times. Renal function was evaluated by serum and urine biochemistry. Immunohistochemistry of heart and kidney tissue was performed by in situ terminal deoxynucleotidyl transferase-mediated dUPT nick end-labelling reaction. Compared to the control group (MI/vehicle), the average value of the left ventricular ejection fraction in apela-treated mice increased by 32% and 39% at 2- and 4-week post-MI, respectively. The mean levels of serum blood urea nitrogen,creatinine, N-terminal pro-brain natriuretic peptide and 24-hour urine protein were significantly decreased at 4-week post-MI in apela-treated mice relative to that of control animals. At the cellular level, we found that apela treatment significantly reduced myocardial fibrosis and cellular apoptosis in heart and kidney tissue. These data suggest that apela improves cardiac and renal fu...Continue Reading

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Citations

Mar 22, 2021·Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association·Peter JanssensDjalila Mekahli
Jul 23, 2021·Journal of Cellular and Molecular Medicine·Liangli JinZhi Wang
Sep 14, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Liangli JinZhi Wang

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Methods Mentioned

BETA
ELISA

Software Mentioned

GraphPad Prism5

Related Concepts

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis