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. 2018 Mar 14;9(3):405. doi: 10.1038/s41419-018-0439-7

Fig. 5. miR199a-5p regulates autophagy in vitro.

Fig. 5

a-c HepG2 cells and primary hepatocytes that originated from male HFD-fed C57BL/6J WT mice were infected with adenovirus-inhibiting miR199a-5p (Ad-anti-miR199a-5p) or the negative control (Ad-anti-miR NC) for 48 h. d-f HepG2 cells and primary hepatocytes that originated from male C57BL/6J WT mice were infected with adenovirus-expressing miR199a-5p (Ad-miR199a-5p) or the negative control (Ad-miR NC) for 48 h. The expression level of miR199a-5p and the protein levels of ATG14, BECLIN1 and LC3 in HepG2 cells and primary hepatocytes are shown in a, b and d, e, respectively. Primary hepatocytes were co-infected with adenoviruses to express mCherry and GFP double-tagged LC3, and the formation of autophagosomes (yellow) and autolysosomes (red) during the autophagy process were analyzed by fluorescence microscopy (c, f, scale bar: 20 µm, the orange arrows indicate the yellow dots). The two-tailed Student's t-test was applied to determine the difference between the Ad-anti-miR199a-5p group or the Ad-miR199a-5p group and the corresponding control group (**P < 0.01, ***P < 0.001)