Regulation of Cardiac-Specific Proteins Expression by Moderate-Intensity Aerobic Exercise Training in Mice With Myocardial Infarction Induced Heart Failure Using MS-Based Proteomics

Abstract

This study aims to systematically reveal the changes in protein levels induced by regular exercise in mice with ischemic-induced heart failure (HF). Aerobic exercise training for the ischemic-induced HF mice lasted for 4 weeks and then we used the liquid chromatography-mass spectrometry method to identify and quantify the protein profile in the myocardium of mice. As a whole, 1,304 proteins (597 proteins up-regulated; 707 proteins down-regulated) were differentially expressed between the exercise group and the sedentary group, including numerous proteins related to energy metabolism. The significant alteration of the component (E1 component subunit alpha and subunit beta) and the activity-regulating enzyme (pyruvate dehydrogenase kinase 2 and pyruvate dehydrogenase kinase 4) of pyruvate dehydrogenase complex and poly [ADP-ribose] polymerase 3, a nicotinamide adenine dinucleotide(+)-consuming enzymes, was further verified in targeted analysis. Generally, this proteomics profiling furnishes a systematic insight of the influence of aerobic exercise on HF.

Antimicrobial and Antiviral Nanofibers Halt Co‐Infection Spread via Nuclease‐Mimicry and Photocatalysis

“…Samples were prepared as described previously. [ 46 ] Briefly, tissues were lysed with protease inhibitors (Roche), sonicated, and centrifuged. Supernatants' protein content was measured using a BCA protein assay.…”

LncRNAs and CircRNAs in Endoplasmic Reticulum Stress: A Promising Target for Cardiovascular Disease?

“…Several molecular and biophysical mechanisms are triggered to reverse and restore ER homeostasis such as (1) ER-associated degradation (ERAD), which triggers the misfolded protein degradation from ER lumen; (2) Unfolded protein response (UPR) involving the restoration of ER proteostasis by activation of three transduction signalling –IRE1, ATF6 and PERK branch-; and (3) Reticulophagy, the process of ER remodelling by autophagy of membranes and associated proteins (see reviews [ 9 , 10 , 11 , 12 , 13 , 14 ]). Pathophysiological factors occurring in cardiovascular diseases (CVDs) such as metabolic derangement, hypoxia, hypertrophy or inflammation require an increased protein expression, thus enhancing the disruption of the cellular proteostasis [ 15 , 16 , 17 , 18 , 19 , 20 , 21 ]. As a consequence of the increased requirement of protein synthesis, ER homeostasis is ruptured and different subpopulations of cardiac cells suffer an unfolded and misfolded protein accumulation, which in turn, induces ER stress [ 22 , 23 , 24 , 25 ].…”