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. 2020 Jul 16;883:173374. doi: 10.1016/j.ejphar.2020.173374

Fig. 6.

Fig. 6

Inhibition of miR-122-5p exerted the protective effects on ATII-mediated pro-apoptosis, pro-oxidant, pro-inflammation, and anti-autophagy viaactivatingthe ELA-ACE2 signaling in rat AFs. (A) The relative mRNA level of ELA was downregulated in AFs after the knockdown of ELA. (B-D) Decreased mRNA and protein levels of ACE2 were performed to ensure the effective transfection of ACE2 siRNA. (E-F) Percentage of apoptotic cells of AFs by flow cytometry analysis. (G-H) The production of oxidative stress in rat AFs by dihydroethidium staining. (I) Relative mRNA levels of IL-10, IL-18, and IL-33 in rat AFs. (J) Immunofluorescence images of p62 (red) and LC3 (green) to examine autophagic flux of rat AFs. (K-L) The expression of ACE2 in rat AFs in the absence and presence of ATII, ELA, and ACE2 siRNA, respectively. GAPDH was used as an endogenous control. n = 3–4 for each group except for I where n = 5–6. *, P < 0.05, **, P < 0.01 compared with control or NC siRNA group; ##, P < 0.01 compared with ATII or ATII + NC group; &&, P < 0.01 compared with ATII + ELA + NC siRNA group; $, P < 0.05, $$, P < 0.01 compared with ATII + miR-122 inhibitor + NC siRNA group. A.U., arbitrary units; R.E., relative expression; ATII, angiotensin II; AFs, adventitial fibroblasts; NC, negative control; ELA, elabela; ACE2, angiotensin-converting enzyme 2; IL-10, interleukin-10; IL-18, interleukin-18; IL-33, interleukin-33.