Polycystin 2 is required for glucose deprivation induced Autophagy in human embryonic stem cell derived cardiomyocytes
【摘要】：Autophagy is a ubiquitous process for protein and organelle recycling, critical to numerous forms of stress responsiveness. The activities of m TOR and AMPK, two major regulators of autophagy, are dysregulated in autosomal dominant polycystic kidney disease(ADPKD) which caused by Polycytin 2(PKD2) mutation. Therefore we hypothesized that PKD2 is possible candidate for autophagy regulation in human embryonic stem cell derived cardiomyocytes(h ESC-CMs). The PKD2 was silenced in h ESC-CMs by sh RNA lentivirus-mediated transduction. Short-term glucose deprivation, which mimicked myocardial ischemia, induced robust accumulation LC3 lipidation in scramble h ESC-CMs. However, this phenomenon was attenuated in cardiomyoytes lacking PKD2. These results demonstrate that PKD2 is a novel regulator of autophagy in h ESC-CMs during glucose deprivation.