Lipopolysaccharide promotes lung fibroblast proliferation through autophagy inhibition via activation of the PI3K-Akt-mTOR pathway.
Identifieur interne : 000687 ( Main/Exploration ); précédent : 000686; suivant : 000688Lipopolysaccharide promotes lung fibroblast proliferation through autophagy inhibition via activation of the PI3K-Akt-mTOR pathway.
Auteurs : Tingting Xie [République populaire de Chine] ; Qiaoyi Xu [République populaire de Chine] ; Hanxi Wan [République populaire de Chine] ; Shunpeng Xing [République populaire de Chine] ; Chen Shang [République populaire de Chine] ; Yuan Gao [République populaire de Chine] ; Zhengyu He [République populaire de Chine]Source :
- Laboratory investigation; a journal of technical methods and pathology [ 1530-0307 ] ; 2019.
Abstract
Pulmonary fibrosis is a major cause of death in patients with acute respiratory distress syndrome (ARDS). Our previous study revealed that lipopolysaccharide (LPS) challenge could lead to mouse lung fibroblast proliferation. Additionally, inhibition of autophagy in lung fibroblasts was also reported to be crucial during the process of pulmonary fibrosis. However, the correlation between proliferation and inhibition of autophagy of lung fibroblasts and the underlying mechanism remain unknown. In this study, we report that autophagy was inhibited in mouse lung fibroblasts after LPS challenge, and was accompanied by activation of the PI3K-Akt-mTOR signaling pathway. Treating mouse lung fibroblasts with LPS resulted in mTOR and Akt phosphorylation, p62 up-regulation, and significant down-regulation of autophagosomes, which could be reversed by PI3K-Akt inhibitors (Ly294002) or mTOR inhibitors (rapamycin, RAPA). Furthermore, either LPS or hydroxychloroquine (HCQ), an autophagy inhibitor, could promote mouse lung fibroblast proliferation, which could be reversed by RAPA application. The present research therefore reveals that LPS promotes lung fibroblast proliferation through autophagy inhibition via activation of the PI3K-Akt-mTOR pathway.
DOI: 10.1038/s41374-018-0160-2
PubMed: 30760865
Affiliations:
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Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Qiaoyi" sort="Xu, Qiaoyi" uniqKey="Xu Q" first="Qiaoyi" last="Xu">Qiaoyi Xu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Wan, Hanxi" sort="Wan, Hanxi" uniqKey="Wan H" first="Hanxi" last="Wan">Hanxi Wan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de 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Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Gao, Yuan" sort="Gao, Yuan" uniqKey="Gao Y" first="Yuan" last="Gao">Yuan Gao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China. rj_gaoyuan@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="He, Zhengyu" sort="He, Zhengyu" uniqKey="He Z" first="Zhengyu" last="He">Zhengyu He</name><affiliation wicri:level="1"><nlm:affiliation>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China. zhengyuheshsmu@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author></analytic><series><title level="j">Laboratory investigation; a journal of technical methods and pathology</title><idno type="eISSN">1530-0307</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pulmonary fibrosis is a major cause of death in patients with acute respiratory distress syndrome (ARDS). Our previous study revealed that lipopolysaccharide (LPS) challenge could lead to mouse lung fibroblast proliferation. Additionally, inhibition of autophagy in lung fibroblasts was also reported to be crucial during the process of pulmonary fibrosis. However, the correlation between proliferation and inhibition of autophagy of lung fibroblasts and the underlying mechanism remain unknown. In this study, we report that autophagy was inhibited in mouse lung fibroblasts after LPS challenge, and was accompanied by activation of the PI3K-Akt-mTOR signaling pathway. Treating mouse lung fibroblasts with LPS resulted in mTOR and Akt phosphorylation, p62 up-regulation, and significant down-regulation of autophagosomes, which could be reversed by PI3K-Akt inhibitors (Ly294002) or mTOR inhibitors (rapamycin, RAPA). Furthermore, either LPS or hydroxychloroquine (HCQ), an autophagy inhibitor, could promote mouse lung fibroblast proliferation, which could be reversed by RAPA application. The present research therefore reveals that LPS promotes lung fibroblast proliferation through autophagy inhibition via activation of the PI3K-Akt-mTOR pathway.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Xie, Tingting" sort="Xie, Tingting" uniqKey="Xie T" first="Tingting" last="Xie">Tingting Xie</name></noRegion><name sortKey="Gao, Yuan" sort="Gao, Yuan" uniqKey="Gao Y" first="Yuan" last="Gao">Yuan Gao</name><name sortKey="He, Zhengyu" sort="He, Zhengyu" uniqKey="He Z" first="Zhengyu" last="He">Zhengyu He</name><name sortKey="Shang, Chen" sort="Shang, Chen" uniqKey="Shang C" first="Chen" last="Shang">Chen Shang</name><name sortKey="Wan, Hanxi" sort="Wan, Hanxi" uniqKey="Wan H" first="Hanxi" last="Wan">Hanxi Wan</name><name sortKey="Xing, Shunpeng" sort="Xing, Shunpeng" uniqKey="Xing S" first="Shunpeng" last="Xing">Shunpeng Xing</name><name sortKey="Xu, Qiaoyi" sort="Xu, Qiaoyi" uniqKey="Xu Q" first="Qiaoyi" last="Xu">Qiaoyi Xu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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