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作 者:Gibran Ali Mo Zhang Runzhen Zhao Krishan GJain Jianjun Chang Satoshi Komatsu Beiyun Zhou Jiurong Liang Michael AMatthay Hong-Long Ji
机构地区:[1]Department of Cellular and Molecular Biology,University of Texas Health Science Center at Tyler,Tyler,TX,USA [2]Institute of Lung and Molecular Therapy,Xinxiang Medical University,Xinxiang,Henan,China [3]Institute of Health Sciences,China Medical University,Shenyang,Liaoning,China [4]Division of Pulmonary,Critical Care and Sleep Medicine,University of Southern California,Los Angeles,CA,USA [5]Hastings Center for Pulmonary Research,University of Southern California,Los Angeles,CA,USA [6]Norris Comprehensive Cancer Center,University of Southern California,Los Angeles,CA,USA [7]Department of Medicine,Keck School of Medicine,University of Southern California,Los Angeles,CA,USA [8]Department of Medicine,Cedars-Sinai Medical Center,Los Angeles,CA,USA [9]Department of Medicine and Anesthesia,University of California San Francisco,San Francisco,CA,USA [10]Cardiovascular Research Institute,University of California San Francisco,San Francisco,CA,USA [11]Texas Lung Injury Institute,University of Texas Health Science Center at Tyler,Tyler,TX,USA
出 处:《Signal Transduction and Targeted Therapy》2021年第3期618-620,共3页信号转导与靶向治疗(英文)
基 金:supported by NIH grant R01 HL134828.
摘 要:Dear Editor,COVID-19,SARS,and MERS are featured by suppressed lungfibrinolysis.The primary objective of this study was to decipherthe role of the fibrinolytic niche in the progenitor alveolar type 2(AT2)cell-mediated re-alveolarization.The expression of Piau inAT2 cells has been confirmed at the mRNA,protein,and functionallevel across species.We employed influenza-infected&Plau^(-/-)mice,3D organoids,and polarized monolayers to track AT2 fate.We found a marked reduction in total AT2 cells and CD44^(+)subpopulation when the fibrinolytic niche was disrupted.
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