Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.

Vascular hyperplasia after vascular trauma is one of the difficult problems in clinical treatment. Nowadays, there is no effective treatment for vascular hyperplasia. Previous studies have shown that integrinβ1 andβ3 activity play an important role in vascular hyperplasia. Kindlin-2 has been shown t...

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Main Authors: Xiaolin Wu, Fang Bian, He Hu, Tongjian Zhu, Chenyu Li, Qing Zhou
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2020-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0225173
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spelling doaj-63af9a62cc5c48059d516464c33b1fd92021-03-03T22:05:04ZengPublic Library of Science (PLoS)PLoS ONE1932-62032020-01-01156e022517310.1371/journal.pone.0225173Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.Xiaolin WuFang BianHe HuTongjian ZhuChenyu LiQing ZhouVascular hyperplasia after vascular trauma is one of the difficult problems in clinical treatment. Nowadays, there is no effective treatment for vascular hyperplasia. Previous studies have shown that integrinβ1 andβ3 activity play an important role in vascular hyperplasia. Kindlin-2 has been shown to modulate integrinβ1 andβ3 activity in cancer. Therefore, in this study, we hope to explore the relationship between Kindlin-2 and vascular hyperplasia. We overexpressed or knocked down Kindlin-2 by adenovirus. The results showed that Kindlin-2 overexpression could regulate integrinβ1 andβ3 activity through FAK-PIK3 signaling pathways ex vivo and in vivo, thereby affecting the proliferation and migration of VSMC, and then it causes the consequences of vascular hyperplasia. Therefore, Our results show that Kindlin-2 may be a potential target for the treatment of vascular hyperplasia.https://doi.org/10.1371/journal.pone.0225173
collection DOAJ
language English
format Article
sources DOAJ
author Xiaolin Wu
Fang Bian
He Hu
Tongjian Zhu
Chenyu Li
Qing Zhou
spellingShingle Xiaolin Wu
Fang Bian
He Hu
Tongjian Zhu
Chenyu Li
Qing Zhou
Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.
PLoS ONE
author_facet Xiaolin Wu
Fang Bian
He Hu
Tongjian Zhu
Chenyu Li
Qing Zhou
author_sort Xiaolin Wu
title Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.
title_short Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.
title_full Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.
title_fullStr Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.
title_full_unstemmed Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.
title_sort effects of kindlin-2 on proliferation and migration of vsmc and integrinβ1 andβ3 activity via fak-pi3k signaling pathway.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2020-01-01
description Vascular hyperplasia after vascular trauma is one of the difficult problems in clinical treatment. Nowadays, there is no effective treatment for vascular hyperplasia. Previous studies have shown that integrinβ1 andβ3 activity play an important role in vascular hyperplasia. Kindlin-2 has been shown to modulate integrinβ1 andβ3 activity in cancer. Therefore, in this study, we hope to explore the relationship between Kindlin-2 and vascular hyperplasia. We overexpressed or knocked down Kindlin-2 by adenovirus. The results showed that Kindlin-2 overexpression could regulate integrinβ1 andβ3 activity through FAK-PIK3 signaling pathways ex vivo and in vivo, thereby affecting the proliferation and migration of VSMC, and then it causes the consequences of vascular hyperplasia. Therefore, Our results show that Kindlin-2 may be a potential target for the treatment of vascular hyperplasia.
url https://doi.org/10.1371/journal.pone.0225173
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