MiR-23b controls TGF-β1 induced airway smooth muscle cell proliferation via TGFβR2/p-Smad3 signals
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- 作者：Ming Chena ; Linjie Huanga ; 1 ; Wei Zhangb ; Jianting Shia ; Xiaoling Lina ; Zhiqiang Lva ; Wei Zhanga ; Ruiyun Lianga ; Shanping Jianga ; shanpingjiang@126.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：ASMCs ; airway smooth muscle cells ; BSA ; bovine serum albumin ; DMEM ; Dulbecco&rsquo ; s modified Eagle&rsquo ; s medium ; Smad ; drosophila mothers against decapentaplegic protein ; FBS ; fetal bovine serum ; HBSS ; Hanks&rsquo ; balanced salt solution ; NC ; negative control ; PBS ; phosphate-buffered saline ; PVDF ; polyvinylidene difluoride ; TGF-β1 ; transforming growth factor-β1 ; TGFβR2 ; transforming growth factor-β1 receptor II
- 刊名：Molecular Immunology
- 出版年：2016
- 出版时间：February 2016
- 年：2016
- 卷：70
- 期：Complete
- 页码：84-93
- 全文大小：3665 K
文摘
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Overexpression of miR-23b significantly inhibited TGF-β1-induced
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ASMCs proliferation and promoted apoptosis.
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MiR-23b negatively regulates the expression of TGFβR2 and p-Smad3 in ASMCs.
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MiR-23b may function as an inhibitor of asthma airway remodeling by suppressing ASMCs proliferation through inactivation of TGFβR2/p-Smad3 pathway.