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Role of various imbalances centered on alveolar epithelial cell/fibroblast apoptosis imbalance in the pathogenesis of idiopathic pulmonary fibrosis

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Chinese Medical Journal 2021年第3期134卷 261-274页

作者： Qing Wang Zhao-Liang Xie Qi Wu Zhi-Xian Jin Chao Yang Jing Feng Department of Respiratory and Critical Care Medicine of Kunming Municipal First People’s Hospital KunmingYunnan 650000China Graduate School Tianjin Medical UniversityTianjin 300070China Respiratory Department of Sanming Yongan General Hospital SanmingFujian 366000China Medical School Tianjin University SchoolTianjin 300072China Department of Respiratory and Critical Care Medicine Tianjin Medical University General HospitalTianjin 300052China

There have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis(IPF),and intricate pathogenesis of IPF has been suggested.The purpose of this study was to clarify the logical relationship between these mechanisms.An extensive search was undertaken of the PubMed using the following keywords:"etiology,""pathogenesis,""alveolar epithelial cell(AEC),""fibroblast,""lymphocyte,""macrophage,""epigenomics,""histone,"acetylation,""methylation,""endoplasmic reticulum stress,""mitochondrial dysfunction,""telomerase,""proteases,""plasminogen,""epithelial-mesenchymal transition,""oxidative stress,""inflammation,""apoptosis,"and"idiopathic pulmonary fibrosis."This search covered relevant research articles published up to April 30,2020.Original articles,reviews,and other articles were searched and reviewed for content;240 highly relevant studies were obtained after screening.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors:environmental exposures affect epigenetic marks;epigenetic processes translate environmental exposures into the regulation of chromatin;epigenetic processes shape gene expression profiles;in turn,an individual’s genetic background determines epigenetic marks;finally,these genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung tissue.The pathogenesis of IPF involves various imbalances including endoplasmic reticulum,telomere length homeostasis,mitochondrial dysfunction,oxidant/antioxidant imbalance,Th1/Th2 imbalance,M1-M2 polarization of macrophages,protease/antiprotease imbalance,and plasminogen activation/inhibition imbalance.These affect each other,promote each other,and ultimately promote AEC/fibroblast apoptosis imbalance directly or indirectly.Excessive AEC apoptosis and impaired apoptosis of fibroblasts contribute to fibrosis.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors.The pathogenesis of IPF involves

关键词： alveolar epithelial cell Apoptosis Idiopathic pulmonary fibrosis Fibroblast Pathogenesis

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Cigarette Smoke Extract Inhibits the Proliferation of alveolar epithelial cells and Augments the Expression of P21^(WAF1)

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2008年第1期28卷 6-10页

作者：焦宗宪敖启林葛晓娜熊密 Institute of Pathology Tongji Hospital Department of Pathology Tongji Medical College Huazhong University of Science and Technology Key laboratory of Respiratory Diseases Ministry of Health

Cigarette smoking is intimately related with the development of chronic obstructive pulmonary diseases, and alveolar epithelium is a major target for the exposure of cigarette smoke extract. In order to investigate the effect of cigarette smoke extract on the proliferation of alveolar epithelial cell type Ⅱ and its relationship with P21^WAF1, the alveolar epithelial type Ⅱ cell line （A549） cells were chosen as surrogate cells to represent alveolar epithelial type Ⅱ cells. MTT assay was used to detect cell viability after interfered with different concentrations of cigarette smoke extract. It was observed cigarette smoke extract inhibited the growth of A549 cells in a dose- and time-dependent manner. The morphological changes, involving the condensation and margination of nuclear chromatin, even karyorrhexis, were observed by both Hoechst staining and electronic microscopy. Flow cytometry analysis demonstrated the increased cell percentages in G1 and subG1 phases after the cells were incubated with cigarette smoke extract. The expression of p21^WAF1 protein and mRNA was also significantly increased as detected by the methods of Western blot or reverse transcription-polymerase chain reaction respectively. In conclusion, cigarette smoke extract inhibits the proliferation of alveolar epithelial cell type Ⅱ and blocks them in G1/S phase. The intracelhilar accumulation of P21^WAF1 may be one of the mechanisms which contribute to cigarette smoke extract-induced inhibition of cell proliferation.

关键词： cigarette smoke extract alveolar epithelial cell cell proliferation P21^WAF1

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