Increased Clearance of Reactive Aldehydes and Damaged Proteins in Hypertension-Induced Compensated Cardiac Hypertrophy: Impact of Exercise Training

Author(s)

Campos, Juliane Cruz ^[1] ; Fernandes, Tiago ^[2] ; Grassmann Bechara, Luiz Roberto ^[1] ; da Paixao, Nathalie Alves ^[2] ; Brum, Patricia Chakur ^[2] ; de Oliveira, Edilamar Menezes ^[2] ; Batista Ferreira, Julio Cesar ^[1]

Affiliation

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, BR-05508000 Sao Paulo, SP - Brazil

^[2] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508030 Sao Paulo, SP - Brazil

• Document type: Journal article
• Source: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY; 2015.
• Web of Science Citations: 16

Abstract

Background. We previously reported that exercise training (ET) facilitates the clearance of damaged proteins in heart failure. Here, we characterized the impact of ET on cardiac protein quality control during compensated ventricular hypertrophy in spontaneously hypertensive rats (SHR). Methods and Results. SHR were randomly assigned into sedentary and swimming-trained groups. Sedentary SHR displayed cardiac hypertrophy with preserved ventricular function compared to normotensive rats, characterizing a compensated cardiac hypertrophy. Hypertensive rats presented signs of cardiac oxidative stress, depicted by increased lipid peroxidation. However, these changes were not followed by accumulation of lipid peroxidation-generated reactive aldehydes and damaged proteins. This scenario was explained, at least in part, by the increased catalytic activity of both aldehyde dehydrogenase 2 (ALDH2) and proteasome. Of interest, ET exacerbated cardiac hypertrophy, improved ventricular function, induced resting bradycardia, and decreased blood pressure in SHR. These changes were accompanied by reduced cardiac oxidative stress and a consequent decrease in ALDH2 and proteasome activities, without affecting small chaperones levels and apoptosis in SHR. Conclusion. Increased cardiac ALDH2 and proteasomal activities counteract the deleterious effect of excessive oxidative stress in hypertension-induced compensated cardiac hypertrophy in rats. ET has a positive effect in reducing cardiac oxidative stress without affecting protein quality control. (AU)

• FAPESP's process: 12/05765-2 - Contribution of aldehyde dehydrogenase 2 to heart failure development
• Grantee: Julio Cesar Batista Ferreira
• Support type: Research Grants - Young Investigators Grants
• FAPESP's process: 06/56321-6 - Involvement of protein kinase C βII and ε isoforms in heart failure induced by myocardial infarction
• Grantee: Julio Cesar Batista Ferreira
• Support type: Scholarships in Brazil - Doctorate