BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration
Identifieur interne : 000A14 ( Main/Exploration ); précédent : 000A13; suivant : 000A15BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration
Auteurs : Min Liu [République populaire de Chine] ; Tongyu Sun [République populaire de Chine] ; Ni Li [République populaire de Chine] ; Junjie Peng [République populaire de Chine] ; Da Fu [République populaire de Chine] ; Wei Li [République populaire de Chine] ; Li Li [République populaire de Chine] ; Wei-Qiang Gao [République populaire de Chine]Source :
- Nature Communications [ 2041-1723 ] ; 2019.
Abstract
Autophagy is a central component of integrated stress responses that influences many inflammatory diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). While the core machinery is known, the molecular basis of the epigenetic regulation of autophagy and its role in colon inflammation remain largely undefined. Here, we report that BRG1, an ATPase subunit of the SWI/SNF chromatin remodeling complex, is required for the homeostatic maintenance of intestinal epithelial cells (IECs) to prevent the inflammation and tumorigenesis. BRG1 emerges as a key regulator that directly governs the transcription of
Url:
DOI: 10.1038/s41467-019-12573-z
PubMed: 31601814
PubMed Central: 6787222
Affiliations:
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institution-id-type="ISNI">0000 0004 0368 8293</institution-id><institution-id institution-id-type="GRID">grid.16821.3c</institution-id><institution>Med-X Research Institute,</institution><institution>Shanghai Jiao Tong University,</institution></institution-wrap>Shanghai, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai</wicri:regionArea></affiliation></author></analytic><series><title level="j">Nature Communications</title><idno type="eISSN">2041-1723</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Autophagy is a central component of integrated stress responses that influences many inflammatory diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). While the core machinery is known, the molecular basis of the epigenetic regulation of autophagy and its role in colon inflammation remain largely undefined. Here, we report that BRG1, an ATPase subunit of the SWI/SNF chromatin remodeling complex, is required for the homeostatic maintenance of intestinal epithelial cells (IECs) to prevent the inflammation and tumorigenesis. BRG1 emerges as a key regulator that directly governs the transcription of <italic>Atg16l1</italic>, <italic>Ambra1</italic>, <italic>Atg7</italic> and <italic>Wipi2</italic>, which are important for autophagosome biogenesis. Defective autophagy in BRG1-deficient IECs results in excess reactive oxygen species (ROS), which leads to the defects in barrier integrity. Together, our results establish that BRG1 may represent an autophagy checkpoint that is pathogenetically linked to colitis and is therefore likely a potential therapeutic target for disease intervention.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ekbom, A" uniqKey="Ekbom A">A Ekbom</name></author><author><name sortKey="Helmick, C" uniqKey="Helmick C">C Helmick</name></author><author><name sortKey="Zack, M" uniqKey="Zack M">M Zack</name></author><author><name sortKey="Adami, Ho" uniqKey="Adami H">HO Adami</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Grivennikov, Si" uniqKey="Grivennikov S">SI Grivennikov</name></author><author><name sortKey="Greten, Fr" uniqKey="Greten F">FR Greten</name></author><author><name sortKey="Karin, M" uniqKey="Karin M">M Karin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Turner, Jr" uniqKey="Turner J">JR 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de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Liu, Min" sort="Liu, Min" uniqKey="Liu M" first="Min" last="Liu">Min Liu</name></noRegion><name sortKey="Fu, Da" sort="Fu, Da" uniqKey="Fu D" first="Da" last="Fu">Da Fu</name><name sortKey="Gao, Wei Qiang" sort="Gao, Wei Qiang" uniqKey="Gao W" first="Wei-Qiang" last="Gao">Wei-Qiang Gao</name><name sortKey="Gao, Wei Qiang" sort="Gao, Wei Qiang" uniqKey="Gao W" first="Wei-Qiang" last="Gao">Wei-Qiang Gao</name><name sortKey="Li, Li" sort="Li, Li" uniqKey="Li L" first="Li" last="Li">Li Li</name><name sortKey="Li, Li" sort="Li, Li" uniqKey="Li L" first="Li" last="Li">Li Li</name><name sortKey="Li, Ni" sort="Li, Ni" uniqKey="Li N" first="Ni" last="Li">Ni Li</name><name sortKey="Li, Wei" sort="Li, Wei" uniqKey="Li W" first="Wei" last="Li">Wei Li</name><name sortKey="Liu, Min" sort="Liu, Min" uniqKey="Liu M" first="Min" last="Liu">Min Liu</name><name sortKey="Peng, Junjie" sort="Peng, Junjie" uniqKey="Peng J" first="Junjie" last="Peng">Junjie Peng</name><name sortKey="Sun, Tongyu" sort="Sun, Tongyu" uniqKey="Sun T" first="Tongyu" last="Sun">Tongyu Sun</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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