Title of article :
Role of Endurance Training in Preventing Pathological Hypertrophy via Large Tumor Suppressor (LATS) Changes
Author/Authors :
Tabrizi, Arezoo Department of Physical Education - Sharif University of Technology, Tehran, IR Iran , Soori, Rahman Department of Exercise Physiology - Faculty of Physical Education and Sports Sciences - University of Tehran, Tehran, IR Iran , Choobineh, Siroos Department of Exercise Physiology - Faculty of Physical Education and Sports Sciences - University of Tehran, Tehran, IR Iran , Gholipour, Majid Department of Physical Education - Sharif University of Technology, Tehran, IR Iran
Abstract :
Background: One of the negative effects of cardiac sympathetic hyperactivity is pathologic
hypertrophy. Recent studies have indicated that large tumor suppressor (LATS) is one of the
molecules which play a critical role in cardiomyocyte apoptosis. Considering the preventive
role of exercise training, we evaluated the effects of endurance training on LATS gene
expression and its upstream pathway in the present study.
Methods: Eighteen male Wistar rats were randomly divided into 2 groups: endurance and control.
Endurance training was performed for 8 weeks, 1 hour per day, and 6 days per week on the
treadmill at a 15° inclination. Pathologic hypertrophy was induced with the injection of
3 mg/kg-1 of isoproterenol for 7 days; and after 24 hours, the left ventricle was separated and
the gene expressions of LATS, MST, and MAP4K were measured. The apoptosis cells of the
left ventricle were counted via TUNEL assay. The data were analyzed using the t-test and the
Mann–Whitney test.
Results: The gene expressions of LATS and MAP4K in the training group decreased significantly
(P ≤ 0.001). In addition, the apoptosis levels of cardiomyocytes in the training group decreased
and the left ventricular weight increased significantly. There were no differences in MST gene
expression between the groups (P = 0.061).
Conclusions: Our results showed that endurance exercise training diminished LATS suppression by
reducing the expression of MAP4K, preventing the propagation of apoptosis induced by
hypertrophy in the cardiomyocytes of the Wistar rats.
Keywords :
Induced pathologic hypertrophy , MAP4K , MST , LATS , Endurance training
Journal title :
Astroparticle Physics