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. 2019 Feb 14;19(4):3105–3113. doi: 10.3892/mmr.2019.9955

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Copyright: © He et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — HASMC autophagy is regulated by Rab7 in vitro. (A) Immunofluorescence assays revealed that LC3 expression was decreased in Rab7 knockdown cells compared with the control (Case 4; ***P<0.001 vs. Ctrl) and upregulated in Rab7 overexpressing HASMCs compared with the control (Case 8; **P<0.01 vs. Ctrl). Scale bar=200 µm. (B) Rab7, Beclin1 and LC3-II protein levels decreased in siRab#1 and siRab#2 groups, and P62 protein levels were increased compared with the siCtrl group (Case 4) as determined by western blotting. Overexpression of Rab7 notably increased the expression of Rab7, Beclin1 and LC3-II, and downregulated that of P62 levels compared with the control (Case 8). Scale bar=200 µm. Ctrl, control; HASMCs, human aortic smooth muscle cells; LC3, microtubule-associated protein light chain 3; siCtrl, small interfering RNA control; siRab7, siRNA Rab7.