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.
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.
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
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.