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Involvement of Early Growth Responsive Gene Egr-1 in Hyperglycemia Induced Beta-cells Apoptosis
Li Cong1, Jiang Shan2, Shen Ning2, Gao Jimin1*, Li Chaojun2*
1School of Laboratory and Life Sciences, Wenzhou Medical College, Wenzhou 325035, China; 2Model Animal Research Center of Nanjing University, Nanjing 210093, China
Abstract: Diabetes is a chronic metabolic syndrome caused by the impaired function or reduced amount of pancreas beta cells. Herein， we studied the detailed mechanism by which the early growth responsive gene-1 (Egr-1) was involved in the high glucose induced apoptosis of beta cells. Using NIT-1 cells as a cell model， we measured the effect of consistent high glucose on the cell viability and apoptosis through MTT， DAPI， DNA Ladder and flow cytometry by comparing the control group with the high glucose group. The Egr-1 expression level was determined by Real-time PCR and Western blot. We also detected the cell viability and apoptosis after inhibiting the Egr-1 function. We found that the high glucose treatment decreased the cell viability and increased the cell apoptosis significantly (48 h， P<0.05; 72 h， P<0.01). Egr-1 was highly expressed (P<0.01). Inhibiting the Egr-1 function could improve the cell viability and reduce apoptosis (48 h， P<0.05). These results suggested that Egr-1 was involved in the high glucose induced beta cell apoptosis.
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