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. 2021 Oct 27;12:185–197. doi: 10.1016/j.bioactmat.2021.10.021

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© 2021 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 4 — EV-NID1 regulates the formation and assembly of FAs by targeting myosin-10. (A)Adenovirus was used to overexpress NID1 in RAECs, and the overexpression efficiency was detected by WB. (B) The effect of endogenous overexpression of NID1 (adenovirus infection for 48h) on the wound healing ability of RAECs. (C) The effect of NID1 overexpression on the migration of RAECs. (D) Overexpression of NID1 affected the tubule formation of RAECs. (E) The effects of NID1 overexpression on the expression of Rac1/cdc42 and vinculin. (F)The binding of NID1 and myosin-10 was verified in Co-RAECs. Co-immunoprecipitation of myosin-10 by NID1 antibody. (G) Reverse Co-immunoprecipitation of NID1 by myosin-10 antibody. (H) The intracellular location and distribution of NID1 and myosin-10. (I) The expression of Rac1/cdc42, focal adhesion complex (vinculin/paxillin/FAK) and myosin-10 were measured by WB. Co-RAECs were used as positive control. (J) Relative mRNA expression of vinculin, paxillin, BCL6, MMP10 and MMP13 in RAECs. Data were represented as the mean ± SD. *p < 0.05; **p < 0.01; ns, not significant from Student's t-test.