The expression of overexpressed PTEN enhanced IR-induced apoptosis of myocardial cells

Y.-B. Zhu, N. Ding, H.-L. Yi, Z.-Q. Li

Department of Cardiovascular Surgery II, Beijing Children’s ospital, Capital Medical University, National Center for Children’s Health, Beijing, China. chongdejia8865na@126.com

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• Cardiology

OBJECTIVE: Myocardial cell apoptosis is an important pathologic basis of ischemia-reperfusion injury (I/R). PI3K/Akt signaling pathway involves in cell growth, survival, and apoptosis regulation, thus playing an important role in the protection of I/R injury. PTEN is a negative regulatory factor of PI3K/Akt signaling pathway. This study established rat I/R injury model after AMI and myocardial cell I/R injury model to explore the regulatory role of PTEN-PI3K/Akt signaling pathway in myocardial I/R injury in vivo and in vitro.
MATERIALS AND METHODS: Rat myocardial I/R injury model was established. PTEN and p-Akt expressions in myocardial tissue were compared. H9C2 cells were incubated in I/R condition for 12 h, followed by reoxygenation for 12 h. H9C2 cells were divided into three groups, including I/R+pSicoR-Blank, I/R+pSicoR-PTEN, and I/R+pSicoR-PTEN+VO-Ohpic. PTEN, p-Akt, Bcl-2, and Bax expressions were detected. Cell apoptosis was measured by flow cytometry.
RESULTS: PTEN expression significantly increased, while p-Akt level markedly declined in myocardial tissue in I/R group compared with Sham group. Temporary PTEN downregulation and p-Akt elevation appeared at 2 h after I/R. I/R treatment markedly enhanced PTEN and Bax expressions, increased cell apoptosis, and reduced p-Akt and Bcl-2 levels. PTEN overexpression significantly enhanced Bax expression and cell apoptosis, while declined p-Akt and Bcl-2 in H9C2 after I/R. PTEN inhibited by VO-Ohpic markedly downregulated p-Akt and Bcl-2 expressions, whereas reduced Bax level and cell apoptosis.
CONCLUSIONS: The overexpression of PTEN aggravated myocardial cell apoptosis after I/R. The blockage of PTEN enhanced PI3K/Akt signaling pathway and attenuated cell apoptosis induced by I/R.

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