Phosphatase and Tensin Homologue (PTEN)-Induced Putative Kinase 1 Reduces Pancreatic β-cells Apoptosis in Glucotoxicity Through Activation of Autophagy
Document Type
Article
Publication Title
Biochemical and Biophysical Research Communications
Abstract
Chronic elevated glucose is harmful to pancreatic β-cells, resulting in pancreatic β-cells dysfunction and apoptosis. Understanding the molecular mechanisms associated with β-cells survival is pivotal for the prevention of β-cells injury caused by glucotoxicity. The role of Phosphatase and tensin homologue (PTEN)-induced putative kinase 1 (PINK1) in the fate of pancreatic β-cells constantly exposed to high glucose was studied. Sustained high glucose increased PINK1 protein expression both in rat pancreatic β-cells and INS-1 β-cells, and that this increase can be inhibited by PINK1 knockdown and further enhanced by PINK1 over-expression. PINK1 deficiency aggravated glucotoxicity-induced pancreatic β-cells apoptosis and inhibition of autophagy whereas PINK1 could reverse these adverse effects. This study provides fundamental data supporting the potential protective role of PINK1 as a new therapeutic target necessary to preserve β-cells survival under non-physiological hyperglycemia conditions.
DOI
10.1016/j.bbrc.2016.05.116
Publication Date
8-5-2016
Keywords
Apoptosis, Autophagy, High glucose, Phosphatase and tensin homologue (PTEN)-induced putative kinase 1, β-cells
ISSN
1090-2104
Recommended Citation
Zhang J, Chen K, Wang L, Wan X, Shrestha C, Zhou J, Mo Z. Phosphatase and Tensin Homologue (PTEN)-Induced Putative Kinase 1 Reduces Pancreatic β-cells Apoptosis in Glucotoxicity Through Activation of Autophagy. Biochemical and Biophysical Research Communications. 2016; 476(4). doi: 10.1016/j.bbrc.2016.05.116.
