Suppression of cideb under endoplasmic reticulum stress exacerbated hepatic inflammation by inducing hepatic steatosis and oxidative stress
Previous studies have shown that endoplasmic reticulum (ER) stress contributes to inflammation in several manners. However, whether cell death inducing DFF45-like effector b (Cideb), a lipid droplet (LD) associated protein that plays an important role in hepatic lipid metabolism, participates in thi...
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| Veröffentlicht in: | Free radical biology & medicine 2022-05, Vol.185, p.67-75 |
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| creator | Chen, Qiuchi Fang, Wei Shen, Yanan Xu, Dan Chen, Qiang Cui, Kun Mai, Kangsen Ai, Qinghui |
| description | Previous studies have shown that endoplasmic reticulum (ER) stress contributes to inflammation in several manners. However, whether cell death inducing DFF45-like effector b (Cideb), a lipid droplet (LD) associated protein that plays an important role in hepatic lipid metabolism, participates in this process has not been reported. In the present study, we demonstrated that deficiency of cideb alone did not trigger violent inflammation in the liver. However, the expression of cideb was suppressed by Chop (C/EBP homologous protein) under ER stress, which inhibited the transport of lipoproteins in the liver and led to the exacerbation of hepatic steatosis and oxidative stress, and ultimately exacerbated inflammation. Our results might provide a novel mechanism explaining inflammation triggered by ER stress.
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•ER stress inhibited the expression of cideb through Perk-Chop pathway.•The deficiency of cideb aggravated the inflammation triggered by ER stress.•Suppression of cideb by ER stress inhibited the transport of lipoproteins in the liver, which led to hepatic steatosis and oxidative stress. |
| doi_str_mv | 10.1016/j.freeradbiomed.2022.04.009 |
| format | Article |
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[Display omitted]
•ER stress inhibited the expression of cideb through Perk-Chop pathway.•The deficiency of cideb aggravated the inflammation triggered by ER stress.•Suppression of cideb by ER stress inhibited the transport of lipoproteins in the liver, which led to hepatic steatosis and oxidative stress.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/j.freeradbiomed.2022.04.009</identifier><identifier>PMID: 35489563</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Apoptosis Regulatory Proteins - metabolism ; Cideb ; Endoplasmic Reticulum Stress ; ER stress ; Fatty Liver - genetics ; Fatty Liver - metabolism ; Hepatic steatosis ; Humans ; Inflammation ; Inflammation - metabolism ; Liver - metabolism ; Oxidative Stress</subject><ispartof>Free radical biology & medicine, 2022-05, Vol.185, p.67-75</ispartof><rights>2022 Elsevier Inc.</rights><rights>Copyright © 2022 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c313t-d51dad09d06f8f3c05b53598be1aa7f711f227c909064c40e0e1b5e998a033bd3</citedby><cites>FETCH-LOGICAL-c313t-d51dad09d06f8f3c05b53598be1aa7f711f227c909064c40e0e1b5e998a033bd3</cites><orcidid>0000-0002-3958-474X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0891584922001551$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35489563$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Qiuchi</creatorcontrib><creatorcontrib>Fang, Wei</creatorcontrib><creatorcontrib>Shen, Yanan</creatorcontrib><creatorcontrib>Xu, Dan</creatorcontrib><creatorcontrib>Chen, Qiang</creatorcontrib><creatorcontrib>Cui, Kun</creatorcontrib><creatorcontrib>Mai, Kangsen</creatorcontrib><creatorcontrib>Ai, Qinghui</creatorcontrib><title>Suppression of cideb under endoplasmic reticulum stress exacerbated hepatic inflammation by inducing hepatic steatosis and oxidative stress</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>Previous studies have shown that endoplasmic reticulum (ER) stress contributes to inflammation in several manners. However, whether cell death inducing DFF45-like effector b (Cideb), a lipid droplet (LD) associated protein that plays an important role in hepatic lipid metabolism, participates in this process has not been reported. In the present study, we demonstrated that deficiency of cideb alone did not trigger violent inflammation in the liver. However, the expression of cideb was suppressed by Chop (C/EBP homologous protein) under ER stress, which inhibited the transport of lipoproteins in the liver and led to the exacerbation of hepatic steatosis and oxidative stress, and ultimately exacerbated inflammation. Our results might provide a novel mechanism explaining inflammation triggered by ER stress.
[Display omitted]
•ER stress inhibited the expression of cideb through Perk-Chop pathway.•The deficiency of cideb aggravated the inflammation triggered by ER stress.•Suppression of cideb by ER stress inhibited the transport of lipoproteins in the liver, which led to hepatic steatosis and oxidative stress.</description><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Cideb</subject><subject>Endoplasmic Reticulum Stress</subject><subject>ER stress</subject><subject>Fatty Liver - genetics</subject><subject>Fatty Liver - metabolism</subject><subject>Hepatic steatosis</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Liver - metabolism</subject><subject>Oxidative Stress</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc-OFCEQxonRuOPqKxgSL166LRrogXgym_VPsokH9UxoKJRJd9NC92b3GXzpZTKzJt48AVW_-r4UHyFvGLQMWP_u0IaMmK0fYprQtx10XQuiBdBPyI6pPW-E1P1TsgOlWSOV0BfkRSkHABCSq-fkgkuhtOz5jvz5ti1LxlJimmkK1EWPA91mj5ni7NMy2jJFRzOu0W3jNtGyHnGKd9ZhHuyKnv7CxdY2jXMY7TTVexUb7uvbby7OP_8CZUW7phILtbOn6S76Wr7Fs-ZL8izYseCr83lJfny8_n71ubn5-unL1YebxnHG18ZL5q0H7aEPKnAHcpBcajUgs3Yf9oyFrts7DRp64QQgIBskaq0scD54fknennSXnH5vWFYzxeJwHO2MaSum66XqOiWkqOj7E-pyKiVjMEuOk833hoE5pmEO5p80zDENA8LUNOr067PRNhx7j7OP31-B6xOAdd3biNkUF3F26GNGtxqf4n8ZPQD3zaeI</recordid><startdate>20220520</startdate><enddate>20220520</enddate><creator>Chen, Qiuchi</creator><creator>Fang, Wei</creator><creator>Shen, Yanan</creator><creator>Xu, Dan</creator><creator>Chen, Qiang</creator><creator>Cui, Kun</creator><creator>Mai, Kangsen</creator><creator>Ai, Qinghui</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3958-474X</orcidid></search><sort><creationdate>20220520</creationdate><title>Suppression of cideb under endoplasmic reticulum stress exacerbated hepatic inflammation by inducing hepatic steatosis and oxidative stress</title><author>Chen, Qiuchi ; Fang, Wei ; Shen, Yanan ; Xu, Dan ; Chen, Qiang ; Cui, Kun ; Mai, Kangsen ; Ai, Qinghui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c313t-d51dad09d06f8f3c05b53598be1aa7f711f227c909064c40e0e1b5e998a033bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Cideb</topic><topic>Endoplasmic Reticulum Stress</topic><topic>ER stress</topic><topic>Fatty Liver - genetics</topic><topic>Fatty Liver - metabolism</topic><topic>Hepatic steatosis</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Liver - metabolism</topic><topic>Oxidative Stress</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Qiuchi</creatorcontrib><creatorcontrib>Fang, Wei</creatorcontrib><creatorcontrib>Shen, Yanan</creatorcontrib><creatorcontrib>Xu, Dan</creatorcontrib><creatorcontrib>Chen, Qiang</creatorcontrib><creatorcontrib>Cui, Kun</creatorcontrib><creatorcontrib>Mai, Kangsen</creatorcontrib><creatorcontrib>Ai, Qinghui</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Qiuchi</au><au>Fang, Wei</au><au>Shen, Yanan</au><au>Xu, Dan</au><au>Chen, Qiang</au><au>Cui, Kun</au><au>Mai, Kangsen</au><au>Ai, Qinghui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of cideb under endoplasmic reticulum stress exacerbated hepatic inflammation by inducing hepatic steatosis and oxidative stress</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2022-05-20</date><risdate>2022</risdate><volume>185</volume><spage>67</spage><epage>75</epage><pages>67-75</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>Previous studies have shown that endoplasmic reticulum (ER) stress contributes to inflammation in several manners. However, whether cell death inducing DFF45-like effector b (Cideb), a lipid droplet (LD) associated protein that plays an important role in hepatic lipid metabolism, participates in this process has not been reported. In the present study, we demonstrated that deficiency of cideb alone did not trigger violent inflammation in the liver. However, the expression of cideb was suppressed by Chop (C/EBP homologous protein) under ER stress, which inhibited the transport of lipoproteins in the liver and led to the exacerbation of hepatic steatosis and oxidative stress, and ultimately exacerbated inflammation. Our results might provide a novel mechanism explaining inflammation triggered by ER stress.
[Display omitted]
•ER stress inhibited the expression of cideb through Perk-Chop pathway.•The deficiency of cideb aggravated the inflammation triggered by ER stress.•Suppression of cideb by ER stress inhibited the transport of lipoproteins in the liver, which led to hepatic steatosis and oxidative stress.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>35489563</pmid><doi>10.1016/j.freeradbiomed.2022.04.009</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-3958-474X</orcidid></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Apoptosis Regulatory Proteins - metabolism Cideb Endoplasmic Reticulum Stress ER stress Fatty Liver - genetics Fatty Liver - metabolism Hepatic steatosis Humans Inflammation Inflammation - metabolism Liver - metabolism Oxidative Stress |
| title | Suppression of cideb under endoplasmic reticulum stress exacerbated hepatic inflammation by inducing hepatic steatosis and oxidative stress |
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