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Low intensity exercise training alters pathological cardiac hypertrophy molecular phenotypes and apoptosis regulatory proteins in Spontaneously hypertensive rat

김명기|조인호|오윤선|김철현|이규성|황대연|조준용|엄현섭|남기태|김윤만|양춘호|이영익
한국운동생리학회|2005.11|운동과학 (Exercise Science)|제14권 제4호|pp. 555-568

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키워드

apoptosis세포사멸트레드밀 운동treadmill exercisespontaneously hypertensive rat본태성 고혈압 쥐병리학적 심근비대pathological cardiac hypertrophy

초록

이영익, 김철현, 조인호, 엄현섭, 김윤만, 김명기, 오윤선, 양춘호, 황대연, 남기태, 이규성, 조준용. 저 강도 운동에 따른 본태성고혈압 쥐의 병리학적 심근 비대 관련 분자적 표현형과 세포사멸 조절 단백질의 변화. 운동과학, 제14권 제4호, 555-568, 2005. 고혈압은 병리학적 심근비대를 유발하는 반면 지구성 운동은 생리학적 심근비대를 유발시킨다. 이 연구는 본태성고혈압 쥐를 대상으로 지구성 운동이 병리학적생리학적 심근비대 관련 유전자들의 표현형과 세포사멸 관련 유전자의 발현에 미치는 영향을 규명하였다. SHR-운동집단은 혈압, 좌심실 두께, 혈중 지질 수준과 호모시스테인 수준이 감소하는 생리적 적응 현상을 보였다. 심장의 caveolin-3와 eNOS mRNA는 SHR-비교집단이 WKY-비교집단과 SHR-운동집단보다 낮은 수준으로 발현된 반면, ACE, ET-1와 BNP mRNA 발현은 SHR-비교집단이 WKY-비교집단과 SHR-운동집단에 비해 높게 발현되었다. 또한 세포사멸과 관련 단백질인 Bcl-2의 경우 SHR-운동집단이 WKY-비교집단, SHR-비교집단에 비해 높게 발현된 반면 Bax는 SHR-운동집단이 WKY-비교집단과 SHR-비교집단보다 낮게 발현되었다. 특히 caspase-3 (20-kDa) 단백질 활성형의 발현은 WKY-비교집단과 SHR-운동집단이 SHR-비교집단에 비해 낮은 수준으로 발현되었다. 결론적으로 운동이 심근비대 관련 표현형 유전자들 변화를 통해 병리학적 심근비대를 예방할 수 있음을 의미하며 병리학적 심근비대로 인한 세포사멸을 억제할 수 있음을 보여주고 있다.

Abstract

Lee, Y.I., Kim, C.H., Cho, I.H., Um, H.S., Kim, Y.M., Kim, M.K., Oh, Y.S., Yang, C.H., Hwang, D.Y., Nam, K.T., Lee, K.S., Cho, J.Y. Low intensity exercise training alters pathological cardiac hyper trophy molecular phenotypes and apoptosis regulatory prote ins in spontaneously hypertensive rat(SHR). Exercise Science, 14(4): 555-568, 2005. This study was designed to dete rmine the effects of exercise training on cardiac function, myocardial gene expression, and apoptosis. Exercise-trained SHR showed clear adaptive changes such as reduced body weight, heart rate, blood pressures, left ventricle wall thic kness, lipid profiles, and homocysteine level. The mRNA expression of angiotensin convert ting enzyme, endothelin -1, and brain natriuretic peptides in the heart was significa ntly higher in the non-exercise SHR, whereas mRNA expres sion of caveolin-3 and eNOS in the heart was significantly lower in the non-exercise SHR. Bcl-2 protein levels were significantly higher in the exercise-trained SHR. In contra st, Bax protein levels were significantly higher in the non- exercise SHR. Further more, the levels of the active forms of caspase-3 were significantly lower in the WKY. These findings suggested that endurance exercise training interfered with a signal transduction pathway of apoptosis seconday to the pathological cardiac hypertrophy.

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