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. 2020 Oct 2;5(19):e137969. doi: 10.1172/jci.insight.137969

Figure 3. Regulation of glucose metabolism by miR-34a in fLfs.

Figure 3

(A) hfLfs were transduced with lentivirus-expressing empty vector (Lv-Ev) or –precursor–miR-34a (Lv–Pre–miR-34a) to overexpress miR-34a. Naive hnLfs and hfLfs were used as controls. After 48 hours of infection, total cell extracts were analyzed for HK2, PFKP, PKM, PFKFB3, and HIF-1α by immunoblotting. Images are representative of 2 independent experiments. (B) Total RNA isolated from n = 4 naive hnLf and hfLfs, or hfLfs transduced with Lv-Ev or Lv–Pre–miR-34a as in A, was analyzed for HK2, PFKP, PKM, PFKFB3, and HIF1A by qPCR (n = 4). (C) hnLfs were transduced with Lv-Ev or Lv-expressing miR-34a antisense (Lv–miR-34a–As). Naive hnLfs and hfLfs were used as controls. After 48 hours of infection, the cell lysates were analyzed for the expression of HK2, PFKP, PKM, PFKFB3, and HIF-1α by Western blotting. The representative images of 2 independent experiments are shown. (D) Total RNA isolated from n = 4 naive hnLfs or hfLfs, or hnLfs transduced with Lv-Ev or Lv–miR-34a–As as in C, was tested for HK2, PFKP, PKM, PFKFB3, and HIF1A mRNA by qPCR (n = 4). Data represented as mean ± SD were analyzed by 1-way ANOVA followed by Tukey’s post hoc test. **P < 0.01, ***P < 0.001, ****P < 0.0001.