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. 2008 May 1;149(8):3832–3841. doi: 10.1210/en.2008-0015

Figure 4.

Figure 4

ER stress-induced suppression of insulin gene transcription is mediated by ATF6. A, Upper panel, Effect of ATF6 on insulin promoter activity. INS-1 cells were cotransfected with the insulin promoter (200 ng/well) and the indicated amounts of an expression vector for active form of ATF6 for 24 h. Middle panel, Effect of XBP-1 on insulin promoter activity. INS-1 cells were cotransfected with the insulin promoter (200 ng/well) and the indicated amounts of an expression vector for the spliced form of XBP-1 for 24 h. Lower panel, Effect of ATF4 on insulin promoter activity. INS-1 cells were cotransfected with the insulin promoter (200 ng/well) and the indicated amounts of an expression vector for ATF4 for 24 h. Data represent the means ± se of three independent measurements. *, P < 0.05; **, P < 0.01; #, P < 0.001, compared with untreated cells. B, INS-1 cells were transfected with 100 nmol/liter of siRNA-ATF6 or control siRNA (Con) and then incubated with the indicated concentrations of glucose for 48 h. The RNA levels at the various time points were normalized by using the β-actin levels. C, Representative Northern blot analysis of the effect of siRNA-ATF6 on the high glucose concentration-induced decrease in insulin gene expression. INS-1 cells were transfected with 100 nmol/liter of siRNA-ATF6 or control siRNA and then incubated with the indicated concentrations of glucose for 48 h. 18S rRNA levels were analyzed as an internal control. Data in the bar graph are the means ± se of three independent measurements (bottom panel). *, P < 0.01, compared with 30 mmol/liter glucose with or without control siRNA (Con).