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Inhibition of YAP1 activity ameliorates acute lung injury through promotion of M2 macrophage polarization

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资源类型：
Pubmed体系：
作者：
Liang Lu[1] * ; Xu Wenyan[1] * ; Shen Ao[1] * ; Fu Xiaomei[1] ; Cen Huiyu[1] ; Wang Siran[2] ; Lin Zhongxiao[1,3] ; Zhang Lingmin[1] ; Lin Fangyu[4] ; Zhang Xin[3] ; Zhou Na[3] ; Chang Jishuo[1] ; Chen Zhe-Sheng[5,*2] ; Li Chuwen[1,*1] ; Yu Xiyong[1,*1] ;
机构： [1]Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The State & NMPA Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China [2]Department of Preventive Dentistry, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangdong Engineering Research Center of Oral Restoration and Reconstruction, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou, China [3]State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, AvenidaWailong, Taipa, Macau, China [4]Department of Ophthalmology, B5500 Clinic B, 1365B Clifton Road NE, Emory University, Atlanta, Georgia, USA [5]Department of Pharmaceutical Sciences, Institute for Biotechnology, College of Pharmacy and Health Sciences, St. John’s University, Queens, New York, USA
出处：
DOI： 10.1002/mco2.293

关键词： Yes-associated protein 1 macrophage polarization acute lung injury pulmonary inflammation

摘要：
The balance of M1/M2 macrophage polarization plays an important role in regulating inflammation during acute lung injury (ALI). Yes-associated protein (YAP1) is a key protein in the Hippo-YAP1 signaling pathway and is involved in macrophage polarization. We aimed to determine the role of YAP1 in pulmonary inflammation following ALI and regulation of M1/M2 polarization. Pulmonary inflammation and injury with upregulation of YAP1 were observed in lipopolysaccharide (LPS)-induced ALI. The YAP1 inhibitor, verteporfin, attenuated pulmonary inflammation and improved lung function in ALI mice. Moreover, verteporfin promoted M2 polarization and inhibited M1 polarization in the lung tissues of ALI mice and LPS-treated bone marrow-derived macrophages (BMMs). Additionally, siRNA knockdown confirmed that silencing Yap1 decreased chemokine ligand 2 (CCL2) expression and promoted M2 polarization, whereas silencing large tumor suppressor 1 (Lats1) increased CCL2 expression and induced M1 polarization in LPS-treated BMMs. To investigate the role of inflammatory macrophages in ALI mice, we performed single-cell RNA sequencing of macrophages isolated from the lungs. Thus, verteporfin could activate the immune-inflammatory response, promote the potential of M2 macrophages, and alleviate LPS-induced ALI. Our results reveal a novel mechanism where YAP1-mediated M2 polarization alleviates ALI. Therefore, inhibition of YAP1 may be a target for the treatment of ALI.© 2023 The Authors. MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.

基金：
National Natural Science Foundation of China, Grant/Award Numbers: 82000080, 82070406, 82104374; Guangzhou Science and Technology Plan Project, Grant/Award Number: 202102020073; Guangzhou Higher Education Teaching Quality and Teaching Reform Project-Excellent Talent Training Program, Grant/Award Number: 2022ZXRCPR008; Guangdong Medical Research Foundation, Grant/Award Number: A2023261; Outstanding Youth Development Program of Guangzhou Medical University, Grant/Award Number: 02-410-2302377XM; Peak Discipline construction project of Guangzhou Medical University-Epigenetic Drug Development Project, Grant/Award Numbers: 02-445-2301220XM, 02-445-2301164XM; First-class professional construction project of Guangzhou Medical University, Grant/Award Number: 02-408-2304-13029XM
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2022]版：
无
最新[2025]版：
大类 | 1 区 医学
小类 | 1 区 医学：研究与实验
第一作者：
第一作者机构： [1]Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The State & NMPA Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China
共同第一作者：
通讯作者：
通讯机构： [1]Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The State & NMPA Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China [5]Department of Pharmaceutical Sciences, Institute for Biotechnology, College of Pharmacy and Health Sciences, St. John’s University, Queens, New York, USA [*1]Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the State & NMPA Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou 511436, China. [*2]Department of Pharmaceutical Sciences, Institute for Biotechnology, College of Pharmacy and Health Sciences, St. John’s University, Queens, NY 11439, USA.
推荐引用方式(GB/T 7714)：
Liang Lu,Xu Wenyan,Shen Ao,et al.Inhibition of YAP1 activity ameliorates acute lung injury through promotion of M2 macrophage polarization[J].MedComm.2023,4(3):e293.doi:10.1002/mco2.293.
APA：
Liang Lu,Xu Wenyan,Shen Ao,Fu Xiaomei,Cen Huiyu...&Yu Xiyong.(2023).Inhibition of YAP1 activity ameliorates acute lung injury through promotion of M2 macrophage polarization.MedComm,4,(3)
MLA：
Liang Lu,et al."Inhibition of YAP1 activity ameliorates acute lung injury through promotion of M2 macrophage polarization".MedComm 4..3(2023):e293

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