Open AccessTRIM72 mediates lung epithelial cell death upon hyperoxia exposure
Author(s) -
Liang Huang,
Hsiu Chu Chou,
Chung-Ming Chen
Publication year - 2020
Publication title -
journal of the chinese medical association
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.535
H-Index - 42
eISSN - 1728-7731
pISSN - 1726-4901
DOI - 10.1097/jcma.0000000000000413
Subject(s) - hyperoxia , bronchopulmonary dysplasia , medicine , lung , andrology , in vivo , respiratory distress , downregulation and upregulation , pathology , a549 cell , in vitro , viability assay , room air distribution , programmed cell death , immunology , biology , apoptosis , anesthesia , biochemistry , physics , microbiology and biotechnology , gene , genetics , gestational age , pregnancy , thermodynamics
Premature infants often require oxygen (O2) therapy for respiratory distress syndrome; however, excessive use of O2 can cause clinical conditions such as bronchopulmonary dysplasia. Although many treatment methods are currently available, they are not effective in preventing bronchopulmonary dysplasia. Herein, we explored the role of tripartite motif protein 72 (TRIM72), a factor involved in repairing alveolar epithelial wounds, in regulating alveolar cells upon hyperoxia exposure.