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. 2017 May 19;6(7):651–663. doi: 10.1016/j.molmet.2017.05.005

Figure 8.

Figure 8

Silencing of TFB2M in insulin-producing cells results in increased production of reactive oxygen species (ROS). Quantification of ROS using the fluorogenic dye 2′,7′ –dichlorofluorescin diacetate (DCFDA) in control and TFB2M-deficient INS-1 832/13 clonal cells in the presence and absence of 10 μM of N-acetyl-l-cysteine (NAC) at 2.8 mM (A) and 16.7 mM (B) glucose. (C) Insulin secretion from control and TFB2M-deficient INS-1 832/13 clonal cells in the presence and absence of 10 μM NAC that were incubated for 1 h in 2.8 mM and 16.7 mM glucose. (D–H) qRT-PCR analysis of PDX1, TFAM, INS1, INS2, and SLC2A2 mRNA in control and TFB2M-deficient INS-1 832/13 clonal cells in the presence and absence of 10 μM NAC. (I) qRT-PCR analysis of CAT, SOD2, and GLRX2 mRNA in control and TFB2M-deficient INS-1 832/13 clonal cells; n = 5 different cell passages/group. Statistical differences were examined by a one-way ANOVA followed by Tukey's post-hoc test (A–H) or by unpaired Student's t-test (I). *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 versus the corresponding value for controls.