Article citationsMore>>

Sawada, F., Inoguchi, T., Tsubouchi, H., Sasaki, S., Fujii, M., Maeda, Y., Morinaga, H., Nomura, M., Kobayashi, K. and Takayanagi, R. (2008) Differential effect of sulfonylureas on production of reactive oxygen species and apoptosis in cultured pancreatic beta-cell line, MIN6. Metabolism, 57, 1038-1045. doi:10.1016/j.metabol.2008.01.038

has been cited by the following article:

• TITLE: Autophagy induced by glibenclamide serves as a defense against apoptosis in INS-1 rat insulinoma cells

  AUTHORS: Hua Su, Xingyan Liu, Ling Su, Li Zhang, Xiangguo Liu, Hong Ji, Haiqin Rong

  KEYWORDS: Glibenclamide; Pancreatic Beta-Cell; Autophagy; Apoptosis; p70 S6K

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.3 No.3, July 22, 2013

  ABSTRACT: Glibenclamide, a blocker of ATP-sensitive potassium channels, has been found to induce apoptosis in some cell types, including pancreatic beta-cells. Since autophagy plays doubleedged roles in pancreatic beta-cell survival, frequently through cross-talking with apoptosis, we investigated if glibenclamide induced autophagy in INS-1 rat insulinoma cells and the influence of autophagy on apoptosis. Mammalian target of rapamycin (mTOR) is a negative regulator of autophagy. As one of the substrates of mTOR, p70 S6 kinase (p70 S6K) is phosphorylated upon mTOR activation. Our results showed that glibenclamide induced an elevated protein level of the autophagy marker LC3-II, while decreasing phosphorylated p70 S6K, indicative of inhibition on mTOR signaling in INS-1 cells. Furthermore, inhibiting glibenclamide-induced autophagy via knocking down the autophagy essential gene Atg7 decreased cell viability and increased apoptosis in INS-1 cells. Our results indicate that glibenclamide induces autophagy in INS-1 cells, and that autophagy activation is exerting a protective activity against apoptosis.