Negative Feedback of the cAMP/PKA Pathway Regulates the Effects of Endoplasmic Reticulum Stress-Induced NLRP3 Inflammasome Activation on Type II Alveolar Epithelial Cell Pyroptosis as a Novel Mechanism of BLM-Induced Pulmonary Fibrosis.
Negative Feedback of the cAMP/PKA Pathway Regulates the Effects of Endoplasmic Reticulum Stress-Induced NLRP3 Inflammasome Activation on Type II Alveolar Epithelial Cell Pyroptosis as a Novel Mechanism of BLM-Induced Pulmonary Fibrosis.
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cAMP/PKA 通路的负反馈调节内质网应激诱导的 NLRP3 炎症小体激活对 II 型肺泡上皮细胞焦亡的影响，作为 BLM 诱导的肺纤维化的新机制
DOI：
10.1155/2022/2291877
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发表时间：
2022
影响因子：
4.1
通讯作者：
Meng, Ying
中科院分区：
文献类型：
--
作者：
Hong, Qiaohui;Zhang, Yue;Lin, Weixian;Wang, Wei;Yuan, Yafei;Lin, Jiajia;Xie, Zhanzhan;Li, Xu;Meng, Ying
Endoplasmic reticulum stress (ER stress) contributes to the development of pulmonary fibrosis, especially in type II alveolar epithelial cells (AECs) apoptosis. ER stress also promotes NLRP3 inflammasome activation which is inhibited by upregulation of cAMP/PKA pathway. However, it is confused whether ER stress-induced NLRP3 inflammasome activation and pyroptosis in type II alveolar epithelial cells which exacerbates pulmonary fibrosis via a mechanism that is suppressed by cAMP/PKA pathway. In our research, we explored that potential links among NLRP3 inflammasome, ER stress, and cAMP/PKA pathway in type II AECs to explain the new mechanisms of pulmonary fibrosis. We found that in vivo, ER stress, NLRP3 inflammasome, and PKA upregulated in the alveolar epithelial area in animal models of pulmonary fibrosis. In addition, immunofluorescence staining further confirmed that ER stress, NLRP3 inflammasome, and cAMP/PKA had potential links on type II AECs in BLM group. In vitro, ER stress stimulated NLRP3 inflammasome activation, promoted pyroptosis, and also upregulated cAMP/PKA pathway. Upregulation of cAMP/PKA pathway inhibited ER stress-induced pyroptosis of A549 cells and vice versa. These results initially supported conclusion that ER stress may stimulate NLRP3 inflammasome activation and pyroptosis in type II AECs, which exacerbated pulmonary fibrosis, and cAMP/PKA pathway may act as a feedback regulator.
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影响因子：
29
作者：
Lerner AG;Upton JP;Praveen PV;Ghosh R;Nakagawa Y;Igbaria A;Shen S;Nguyen V;Backes BJ;Heiman M;Heintz N;Greengard P;Hui S;Tang Q;Trusina A;Oakes SA;Papa FR
通讯作者：
Papa FR
DOI：
10.4049/jimmunol.1401343
发表时间：
2015-06-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Sokolowska M;Chen LY;Liu Y;Martinez-Anton A;Qi HY;Logun C;Alsaaty S;Park YH;Kastner DL;Chae JJ;Shelhamer JH
通讯作者：
Shelhamer JH
针对特发性肺纤维化疗法的GPCR信号传导。
影响因子：
13.8
作者：
Haak AJ;Ducharme MT;Diaz Espinosa AM;Tschumperlin DJ
通讯作者：
Tschumperlin DJ
影响因子：
13.5
作者：
Lebeaupin, Cynthia;Vallee, Deborah;Bailly-Maitre, Beatrice
通讯作者：
Bailly-Maitre, Beatrice
DOI：
10.1083/jcb.201602089
发表时间：
2016-06-20
期刊：
The Journal of cell biology
影响因子：
--
作者：
Sharma D;Kanneganti TD
通讯作者：
Kanneganti TD