NanoUPLC/MS(E) proteomic analysis reveals modulation on left ventricle proteome from hypertensive rats after exercise training.

UNLABELLED

NanoUPLC/MS(E) was used to verify the effects of 8weeks of low (SHR-LIT=4) and high (SHR-HIT=4) intensity training over the left ventricle proteome of hypertensive rats (SHR-C=4). Training enhanced the aerobic capacity and reduced the systolic blood pressure in all exercised rats. NanoUPLC/MS(E) identified 250 proteins, with 233 in common to all groups and 16 exclusive to SHR-C, 2 to SHR-LIT, and 2 to the SHR-HIT. Cardiac hypertrophy related proteins appeared only in SHR-C. The SHR-LIT enhanced the abundance of 30 proteins and diminished 6, while SHR-HIT enhanced the abundance of 39 proteins and reduced other 7. The levels of metabolic (β and γ-enolase, adenine phosphoribosultransferase, and cytochrome b-c1), myofibril (myosin light chain 4, tropomyosin α and β-chain), and transporter proteins (hemoglobin, serum albumin, and hemopexin) were increased by both intensities. Transcription regulator and histone variants were enhanced by SHR-LIT and SHR-HIT respectively. SHR-LIT reduced the concentration of myosin binding protein C, while desmin and membrane voltage dependent anion selective channel protein-3 were reduced only by SHR-HIT. In addition, polyubiquitin B and C, and transcription regulators decreased in both intensities. Exercise also increased the concentration of anti-oxidant proteins, peroxiredozin-6 and glutathione peroxidase-1.

BIOLOGICAL SIGNIFICANCE

Pathologic left ventricle hypertrophy if one of the major outcomes of hypertension being a strong predictor of heart failure. Among the various risk factors for cardiovascular disorders, arterial hypertension is responsible for the highest rates of mortality worldwide. In this way, this present study contribute to the understanding of the molecular mechanisms involved in the attenuation of hypertension and the regression of pathological cardiac hypertrophy induced by exercise training.