Complete inhibition of phosphatase and tensin homolog promotes the normal and oxygen-glucose deprivation/reperfusion-injured PC12 cells to cell death

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Minaei Beyrami Sohrab; KHADEM ANSARI MOHAMMAD HASAN; RASMI YOUSEF; Shakib Nader; KARIMI POURAN

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Journal: Journal of Cardiovascular and Thoracic Research Year:2018 | Volume:10 | Issue:2 Page(s): 83-89

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Title

Complete inhibition of phosphatase and tensin homolog promotes the normal and oxygen-glucose deprivation/reperfusion-injured PC12 cells to cell death

Author(s)

Keywords

OGD

Reperfusion Injury

AKT

p38

MAPK

PC12 Cells

Abstract

Introduction: Lipid phosphatase and tensin homolog deleted from chromosome 10 (PTEN) antagonizes phosphoinositide 3-kinase (PI3K)/AKT cell survival pathway. The effect of PTEN inhibitors has been rarely examined on cell survival following Reperfusion Injury. In this study, we investigated the neuroprotective effect of SF1670, as a new PTEN inhibitor, on an in vitro stroke-like model. Methods: PC12 Cells were exposed to oxygen-glucose deprivation/reperfusion (OGD/R). The cells were treated in five conditions as follows: normoxic normoglycemic (NO/NG); 60 minutes OGD; 60 minutes OGD and 6 h reperfusion (OGD/R); OGD/R treated with 10 μ M SF1670 (OGD/RSF), and NO/NG treated with 10 μ M SF1670 (NO/NG-SF). Then, phosphorylation levels of AKT, p38 in PC12 Cells were measured by immunoblotting. The cell viability was also determined by colorimetric assay. Results: The results of immunoblotting revealed that following OGD/R the levels of phospho-AKT (p-AKT) significantly decreased, compared to NO/NG cells (P < 0. 05). However, the ratio of p-AKT/total AKT significantly increased in the presence of SF1670 in the OGD/R-SF group, compared to the OGD/R condition. On the other hand, SF1670 significantly reduced the p-p38 MAPK and p-JNK levels, compared to OGD/R cells. Moreover, cell viability significantly decreased in the OGD and OGD/R condition compared to NO/NG cells. Surprisingly, SF-treated cells (OGD/R-SF and NO/NG-SF group) showed low cell viability compared to NO/NG condition. Conclusion: Overall, our results demonstrated that complete inhibition of phosphatase activity of PTEN not only did not exhibit neuroprotective effect but also promoted PC12-deprived cells to death.

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APA: Copy

Minaei Beyrami, Sohrab, KHADEM ANSARI, MOHAMMAD HASAN, RASMI, YOUSEF, Shakib, Nader, & KARIMI, POURAN. (2018). Complete inhibition of phosphatase and tensin homolog promotes the normal and oxygen-glucose deprivation/reperfusion-injured PC12 cells to cell death. JOURNAL OF CARDIOVASCULAR AND THORACIC RESEARCH, 10(2), 83-89. SID. https://sid.ir/paper/314965/en

Vancouver: Copy

Minaei Beyrami Sohrab, KHADEM ANSARI MOHAMMAD HASAN, RASMI YOUSEF, Shakib Nader, KARIMI POURAN. Complete inhibition of phosphatase and tensin homolog promotes the normal and oxygen-glucose deprivation/reperfusion-injured PC12 cells to cell death. JOURNAL OF CARDIOVASCULAR AND THORACIC RESEARCH[Internet]. 2018;10(2):83-89. Available from: https://sid.ir/paper/314965/en

IEEE: Copy

Sohrab Minaei Beyrami, MOHAMMAD HASAN KHADEM ANSARI, YOUSEF RASMI, Nader Shakib, and POURAN KARIMI, “Complete inhibition of phosphatase and tensin homolog promotes the normal and oxygen-glucose deprivation/reperfusion-injured PC12 cells to cell death,” JOURNAL OF CARDIOVASCULAR AND THORACIC RESEARCH, vol. 10, no. 2, pp. 83–89, 2018, [Online]. Available: https://sid.ir/paper/314965/en

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