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. 2021 Sep 16;9:744320. doi: 10.3389/fcell.2021.744320

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Copyright © 2021 Liu, Bao, Fan, Li, Yao, Han, Zhang, Jiang and Qi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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PMVs induced Lamtor1 expression and promoted VSMC dedifferentiation both in vivo and in vitro. (A) Representative images of Elastin Van-Gieson staining showed that the intimal hyperplasia was significantly thickened after 1-week wire injury in mouse model. Scale bars: 100 μm. (B) Representative images of immunostaining showed that Lamtor1 (red) was expressed in the injured intima after 1-week surgery. Green fluorescence was SMA, nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. (C) Immunofluorescence staining showed the activated platelet signal labeled with CD62P (red) at the injury site 3 h after intimal injury surgery. Green fluorescence was SMA, nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. (D) Western blot revealed that Lamtor1 expression was significantly increased and differentiated markers of VSMCs, including SMA, Calponin, and SM22 were decreased after incubating with PMVs for 24 h (n = 5). Data represent mean ± SD. P < 0.001. (E) Immunofluorescence staining indicated that PMVs (red) markedly decreased the expression of SMA (green) a differentiation marker. Nuclei were counterstained with DAPI (blue). Scale bars: 50 μm.