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Protein tyrosine phosphatase L1 represses endothelialmesenchymal transition by inhibiting IL-1β/NF-κB/Snail signaling

  
@article{APS10186,
	author = {Xiao-min Wei and Gulinuer Wumaier and Ning Zhu and Liang Dong and Cheng-wei Li and Jing-wen Xia and You-zhi Zhang and Peng Zhang and Xiu-juan Zhang and Yuan-yuan Zhang and Sheng-qing Li},
	title = {Protein tyrosine phosphatase L1 represses endothelialmesenchymal transition by inhibiting IL-1β/NF-κB/Snail signaling},
	journal = {Acta Pharmacologica Sinica},
	volume = {41},
	number = {8},
	year = {2020},
	keywords = {},
	abstract = {Endothelial–mesenchymal transition (EnMT) plays a pivotal role in various diseases, including pulmonary hypertension (PH), and transcription factors like Snail are key regulators of EnMT. In this study we investigated how these factors were regulated by PH risk factors (e.g. inflammation and hypoxia) in human umbilical vein endothelial cells (HUVECs). We showed that treatment with interleukin 1β (IL‐1β) induced EnMT of HUVECs via activation of NF-κB/Snail pathway, which was further exacerbated by knockdown of protein tyrosine phosphatase L1 (PTPL1). We demonstrated that PTPL1 inhibited NF-κB/Snail through dephosphorylating and stabilizing IκBα. IL‐1β or hypoxia could downregulate PTPL1 expression in HUVECs. The deregulation of PTPL1/NF-κB signaling was validated in a monocrotaline-induced rat PH (MCT-PH) model and clinical PH specimens. Our findings provide novel insights into the regulatory mechanisms of EnMT, and have implications for identifying new therapeutic targets for clinical PH.},
	url = {http://www.chinaphar.com/article/view/10186}
}