Effects of acute exercise over heart proteome from monogenic obese (ob/ob) mice

Abstract

Exercise is recognized to prevent and attenuate several metabolic and cardiovascular disorders. Obesity is commonly related to cardiovascular diseases, frequently resulting in heart failure and death. To elucidate the effects of acute exercise in heart tissue from obese animals, 12-week-old C57BL6/J obese (ob/ob) and non-obese (ob/OB) mice were submitted to a single bout of swimming and had their hearts analyzed by proteomic techniques. Mice were divided into three groups: control (ob/ob, n = 3; ob/OB, n = 3); a moderate intensity consisting of 20 min of swimming around 90% of Maximal Lactate Steady State (ob/ob, n = 3; ob/OB, n = 3), and a high intensity exercise performed as an incremental overload test (ob/ob, n = 3; ob/OB, n = 3). Obesity modulations were analyzed by comparing ob/ob and ob/OB control groups. Differential 2-DE analysis revealed that single session of exercise was able to up-regulate: myoglobin (ob/ob), aspartate aminotransferase (ob/OB) and zinc finger protein (ob/OB) and down-regulate: nucleoside diphosphate kinase B (ob/OB), mitochondrial aconitase (ob/ob and ob/OB) and fatty acid binding protein (ob/ob). Zinc finger protein and α-actin were up-regulated by the effect of obesity on heart proteome. These data demonstrate the immediate response of metabolic and stress-related proteins after exercise so as contractile protein by obesity modulation on heart proteome.

NanoUPLC/MSE proteomic analysis reveals modulation on left ventricle proteome from hypertensive rats after exercise training

“…Myocyte fibrosis and impairment contractility affects the Ca 2+ -dependent cross-bridge interaction with actin, influencing the progression of hypertensive LVH to HF. Differentially, hypertrophy induced by exercise improves force and contraction regulators, leading to positive cardiac adaptations [13,28,30]. In contrast to the down-regulation of myosin light chain 1 observed in LV in SHR [67], the abundance of proteins related to force regulation (myosin light chain 4) and thin filament structure (tropomyosin beta and alpha chains 1,2, 3, and troponin T) was enhanced by both training intensities (Fig.…”

“…Despite the large body of heart proteome research in response to a number of diseases, little research has been conducted in response to exercise stimulus on the nonpathologic heart [28][29][30][31][32] and even less on pathologic conditions such as ischemic insult [33], infarction [34], and obesity [13]. Although the majority of these data are gathered by gel-based techniques, LC-MS methods are the most up-to-date, being used as qualitative and quantitative analytical approaches to complement gel-based methods and considerably enhance proteomic data [35][36][37].…”

“…The literature describes myocardium hypertrophy as a rapid response to hemodynamic stress due to heart plasticity. The heart proteome is also acutely regulated in a few hours followed by afterload insult, leading to rapid heart phenotype remodelling [12], as well as to other stimuli such as exercise [13], which can restore maladaptive remodelling and delay heart failure [14,15].…”

Methyl donor deficiency in H9c2 cardiomyoblasts induces ER stress as an important part of the proteome response

“…First, absence of folate (i) increased abundance of Ppa1 that contributes to ATPase activity in oxidative phosphorylation and, (ii) decreased abundance of Nme2 that is essential to the synthesis of nucleoside triphosphates other than ATP. The latter change has been associated with cardiac contractile dysfunction (Petriz et al, 2013). Second, MD deficiency decreased the abundances of mitochondrial Etfa, an electron acceptor for transfer to the respiratory chain, and Glud1 that catalyzes oxidative deamination of glutamine into ˛-ketoglutarate (Zhang et al, 2006).…”

Effects of Hypertension and Exercise on Cardiac Proteome Remodelling

“…Further research in LV proteome showed that moderate treadmill running led to diverse alteration in the contractile, stress-related, and metabolic function of cardiac proteins, where heart fatty acid binding proteins (HFABP), thioesterase-1, and short-chain acyl-CoA dehydrogenase were upregulated [98]. Moreover, one single bout of high intensity swimming at moderate and high intensity was also shown to modulate LV proteins from obese (ob/ob) and control nonobese mice (ob/OB) [100]. However, in this study, HFABP was downregulated after high intensity exercise in nonobese mice but not in obese mice.…”