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[PTEN negatively regulates isoproterenol-induced cardiac hypertrophy and effects of captopril on PTEN expression].

Yizhong Zhou, Shan-jun Zhu, Lin-jun Yu, Ying Tian, Jiang Wang

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Abstract

OBJECTIVE: To examine the negative regulation role of PTEN in isoproterenol-induced cardiac hypertrophy by testing the expression of PTEN mRNA and protein and to explore the effects of captopril (Cap) on PTEN expression. METHODS: Twenty four rats were randomly divided into three groups: control group, ISO group, and ISO+Cap group. The following parameters were examined:body weight (BW), heart weight (HW), left ventricular weight (LVW), left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP) and +/- dp/dt(max). The ratio of HW/BW and LVW/BW was calculated. PTEN mRNA and protein were tested by RT-PCR and Western blot, respectively. RESULTS: (1) Compared with the control group, the ratio of HW/BW and LVW/BW, LVEDP and LVESP were all increased in ISO group and ISO+Cap group (P < 0.05), but +/- dp/dt(max) was decreased (P < 0.05); (2) compared with the ISO group, the ratio of HW/BW and LVW/BW, LVEDP, LVESP were all decreased in ISO+Cap group (P < 0.05), but +/- dp/dt(max) was increased (P < 0.05); (3) compared with the control group, PTEN mRNA and protein were up-regulated in ISO group and ISO+Cap group; (4) compared with the ISO group, PTEN mRNA and protein were up-regulated in ISO+Cap group. CONCLUSIONS: PTEN mRNA and protein are up-regulated in isoproterenol-induced cardiac hypertrophy. Captopril can up-regulate PTEN expression in cardiac hypertrophy. There is a negative regulative mechanism in cardiac hypertrophy process, in which PTEN is probably an endogenous negative regulator of cardiac hypertrophy.

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OBJECTIVE: To examine the negative regulation role of PTEN in isoproterenol-induced cardiac hypertrophy by testing the expression of PTEN mRNA and protein and to explore the effects of captopril (Cap) on PTEN expression. METHODS: Twenty four rats were randomly divided into three groups: control group, ISO group, and ISO+Cap group. The following parameters were examined:body weight (BW), heart weight (HW), left ventricular weight (LVW), left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP) and +/- dp/dt(max). The ratio of HW/BW and LVW/BW was calculated. PTEN mRNA and protein were tested by RT-PCR and Western blot, respectively. RESULTS: (1) Compared with the control group, the ratio of HW/BW and LVW/BW, LVEDP and LVESP were all increased in ISO group and ISO+Cap group (P < 0.05), but +/- dp/dt(max) was decreased (P < 0.05); (2) compared with the ISO group, the ratio of HW/BW and LVW/BW, LVEDP, LVESP were all decreased in ISO+Cap group (P < 0.05), but +/- dp/dt(max) was increased (P < 0.05); (3) compared with the control group, PTEN mRNA and protein were up-regulated in ISO group and ISO+Cap group; (4) compared with the ISO group, PTEN mRNA and protein were up-regulated in ISO+Cap group. CONCLUSIONS: PTEN mRNA and protein are up-regulated in isoproterenol-induced cardiac hypertrophy. Captopril can up-regulate PTEN expression in cardiac hypertrophy. There is a negative regulative mechanism in cardiac hypertrophy process, in which PTEN is probably an endogenous negative regulator of cardiac hypertrophy.

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Available abstract

OBJECTIVE: To examine the negative regulation role of PTEN in isoproterenol-induced cardiac hypertrophy by testing the expression of PTEN mRNA and protein and to explore the effects of captopril (Cap) on PTEN expression. METHODS: Twenty four rats were randomly divided into three groups: control group, ISO group, and ISO+Cap group. The following parameters were examined:body weight (BW), heart weight (HW), left ventricular weight (LVW), left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP) and +/- dp/dt(max). The ratio of HW/BW and LVW/BW was calculated. PTEN mRNA and protein were tested by RT-PCR and Western blot, respectively. RESULTS: (1) Compared with the control group, the ratio of HW/BW and LVW/BW, LVEDP and LVESP were all increased in ISO group and ISO+Cap group (P < 0.05), but +/- dp/dt(max) was decreased (P < 0.05); (2) compared with the ISO group, the ratio of HW/BW and LVW/BW, LVEDP, LVESP were all decreased in ISO+Cap group (P < 0.05), but +/- dp/dt(max) was increased (P < 0.05); (3) compared with the control group, PTEN mRNA and protein were up-regulated in ISO group and ISO+Cap group; (4) compared with the ISO group, PTEN mRNA and protein were up-regulated in ISO+Cap group. CONCLUSIONS: PTEN mRNA and protein are up-regulated in isoproterenol-induced cardiac hypertrophy. Captopril can up-regulate PTEN expression in cardiac hypertrophy. There is a negative regulative mechanism in cardiac hypertrophy process, in which PTEN is probably an endogenous negative regulator of cardiac hypertrophy.

Key concepts: PTEN, Preload, Internal medicine, Endocrinology, Captopril, Muscle hypertrophy, Medicine, Messenger RNA

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[PTEN negatively regulates isoproterenol-induced cardiac hypertrophy and effects of captopril on PTEN expression]. — Research Paper | ScholarLens