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FAM172A Deletion May Enhance Hepatic Steatosis by Promoting ER Stress
Background Endoplasmic reticulum (ER) stress is one of the major causes to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study showed that maintains the homeostasis of ER could effectively alleviate NAFLD. In this study, we found that the loss of FAM172A increased ER str...
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Published in: | Digestive diseases and sciences 2021-09, Vol.66 (9), p.3054-3061 |
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creator | Xiao, Fan Gao, Meixin Yang, Junru He, Lingling Wei, Hongshan |
description | Background
Endoplasmic reticulum (ER) stress is one of the major causes to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study showed that maintains the homeostasis of ER could effectively alleviate NAFLD. In this study, we found that the loss of FAM172A increased ER stress.
Aims
The aims of this study were to explore whether FAM172A could improve NAFLD by inhibiting ER stress.
Methods
The expression levels of FAM172A and ER stress were detected by western blot. The method of immunofluorescence was used to determine FAM172A location. The interacted proteins of FAM172A were identified by immunocoprecipitation. The methods of MTS and caspase-3/7 activity were taken to confirm the effect of FAM172A on cell viability and proliferation. The expression levels of inflammation were detected by qPCR.
Results
We confirmed that FAM172A might alleviate NAFLD through inhibiting ER stress. Loss of FAM172A increased the expressions of ATF6, peIF2α, but decreased the expression of IRE1α. Then, it was shown that FAM172A located in ER and FAM172A directly interacted with ATF6 and peIF2α and IRE1α. More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group. However, the binding of FAM172A and ATF6 or IRE1α did not change. Next, we found that the lack of FAM172A could produce more apoptosis and inflammation.
Conclusions
Our results suggest that FAM172A improve steatosis by alleviating ER stress. |
doi_str_mv | 10.1007/s10620-020-06601-y |
format | article |
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Endoplasmic reticulum (ER) stress is one of the major causes to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study showed that maintains the homeostasis of ER could effectively alleviate NAFLD. In this study, we found that the loss of FAM172A increased ER stress.
Aims
The aims of this study were to explore whether FAM172A could improve NAFLD by inhibiting ER stress.
Methods
The expression levels of FAM172A and ER stress were detected by western blot. The method of immunofluorescence was used to determine FAM172A location. The interacted proteins of FAM172A were identified by immunocoprecipitation. The methods of MTS and caspase-3/7 activity were taken to confirm the effect of FAM172A on cell viability and proliferation. The expression levels of inflammation were detected by qPCR.
Results
We confirmed that FAM172A might alleviate NAFLD through inhibiting ER stress. Loss of FAM172A increased the expressions of ATF6, peIF2α, but decreased the expression of IRE1α. Then, it was shown that FAM172A located in ER and FAM172A directly interacted with ATF6 and peIF2α and IRE1α. More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group. However, the binding of FAM172A and ATF6 or IRE1α did not change. Next, we found that the lack of FAM172A could produce more apoptosis and inflammation.
Conclusions
Our results suggest that FAM172A improve steatosis by alleviating ER stress.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1007/s10620-020-06601-y</identifier><identifier>PMID: 32945983</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Antibodies ; Apoptosis ; Automation ; Biochemistry ; Cell Line ; Cell Proliferation ; Cell Survival ; Endoplasmic reticulum ; Endoplasmic Reticulum - physiology ; Endoplasmic Reticulum Stress - genetics ; Gastroenterology ; Gene Deletion ; Gene Expression Profiling - methods ; Gene Expression Regulation ; Hepatology ; Infectious diseases ; Kinases ; Liver ; Liver - metabolism ; Liver - pathology ; Liver diseases ; Medicine ; Medicine & Public Health ; Mice ; Microscopy ; Non-alcoholic Fatty Liver Disease - metabolism ; Oncology ; Original Article ; Proteins ; Proteins - genetics ; Proteins - metabolism ; Reagents ; Transplant Surgery ; Unfolded Protein Response</subject><ispartof>Digestive diseases and sciences, 2021-09, Vol.66 (9), p.3054-3061</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>2020. Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>COPYRIGHT 2021 Springer</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-43b88b31da412206d55294439fd7545ae46c60145083894fcfb8d88e0e7983fd3</citedby><cites>FETCH-LOGICAL-c442t-43b88b31da412206d55294439fd7545ae46c60145083894fcfb8d88e0e7983fd3</cites><orcidid>0000-0001-8893-653X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32945983$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Fan</creatorcontrib><creatorcontrib>Gao, Meixin</creatorcontrib><creatorcontrib>Yang, Junru</creatorcontrib><creatorcontrib>He, Lingling</creatorcontrib><creatorcontrib>Wei, Hongshan</creatorcontrib><title>FAM172A Deletion May Enhance Hepatic Steatosis by Promoting ER Stress</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><addtitle>Dig Dis Sci</addtitle><description>Background
Endoplasmic reticulum (ER) stress is one of the major causes to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study showed that maintains the homeostasis of ER could effectively alleviate NAFLD. In this study, we found that the loss of FAM172A increased ER stress.
Aims
The aims of this study were to explore whether FAM172A could improve NAFLD by inhibiting ER stress.
Methods
The expression levels of FAM172A and ER stress were detected by western blot. The method of immunofluorescence was used to determine FAM172A location. The interacted proteins of FAM172A were identified by immunocoprecipitation. The methods of MTS and caspase-3/7 activity were taken to confirm the effect of FAM172A on cell viability and proliferation. The expression levels of inflammation were detected by qPCR.
Results
We confirmed that FAM172A might alleviate NAFLD through inhibiting ER stress. Loss of FAM172A increased the expressions of ATF6, peIF2α, but decreased the expression of IRE1α. Then, it was shown that FAM172A located in ER and FAM172A directly interacted with ATF6 and peIF2α and IRE1α. More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group. However, the binding of FAM172A and ATF6 or IRE1α did not change. Next, we found that the lack of FAM172A could produce more apoptosis and inflammation.
Conclusions
Our results suggest that FAM172A improve steatosis by alleviating ER stress.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Automation</subject><subject>Biochemistry</subject><subject>Cell Line</subject><subject>Cell Proliferation</subject><subject>Cell Survival</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum - physiology</subject><subject>Endoplasmic Reticulum Stress - genetics</subject><subject>Gastroenterology</subject><subject>Gene Deletion</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation</subject><subject>Hepatology</subject><subject>Infectious diseases</subject><subject>Kinases</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver diseases</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Microscopy</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Proteins</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Reagents</subject><subject>Transplant Surgery</subject><subject>Unfolded Protein Response</subject><issn>0163-2116</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9UU1v1DAQtRCILoU_wAFF4sIlZfwR2zmuypYitQLxcbYcZ7K4SuzFzh7y73G0hQqEkDXyyPPe0xs_Ql5SuKAA6m2mIBnUsJaUQOvlEdnQRvGaNVI_JhugsvSUyjPyLOc7AGgVlU_JGWetaFrNN2R3tb2lim2rdzji7GOobu1S7cJ3GxxW13iws3fVlxntHLPPVbdUn1Kc4uzDvtp9LpOEOT8nTwY7Znxxf5-Tb1e7r5fX9c3H9x8utze1E4LNteCd1h2nvRWUMZB90xQjgrdDrxrRWBTSlT1EA5rrVgxu6HSvNQKqYnbo-Tl5c9I9pPjjiHk2k88Ox9EGjMdsmChqSrZKFOjrv6B38ZhCcWfK73CQnAJ9QO3tiMaHIc7JulXUbBVlLedMNgV18Q9UOT1O3sWAgy_vfxDYieBSzDnhYA7JTzYthoJZszOn7AystWZnlkJ6de_42E3Y_6b8CqsA-AmQyyjsMT2s9B_Zn_7znzY</recordid><startdate>20210901</startdate><enddate>20210901</enddate><creator>Xiao, Fan</creator><creator>Gao, Meixin</creator><creator>Yang, Junru</creator><creator>He, Lingling</creator><creator>Wei, Hongshan</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8893-653X</orcidid></search><sort><creationdate>20210901</creationdate><title>FAM172A Deletion May Enhance Hepatic Steatosis by Promoting ER Stress</title><author>Xiao, Fan ; Gao, Meixin ; Yang, Junru ; He, Lingling ; Wei, Hongshan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-43b88b31da412206d55294439fd7545ae46c60145083894fcfb8d88e0e7983fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Automation</topic><topic>Biochemistry</topic><topic>Cell Line</topic><topic>Cell Proliferation</topic><topic>Cell Survival</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum - physiology</topic><topic>Endoplasmic Reticulum Stress - genetics</topic><topic>Gastroenterology</topic><topic>Gene Deletion</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation</topic><topic>Hepatology</topic><topic>Infectious diseases</topic><topic>Kinases</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver diseases</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Microscopy</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Proteins</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Reagents</topic><topic>Transplant Surgery</topic><topic>Unfolded Protein Response</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Fan</creatorcontrib><creatorcontrib>Gao, Meixin</creatorcontrib><creatorcontrib>Yang, Junru</creatorcontrib><creatorcontrib>He, Lingling</creatorcontrib><creatorcontrib>Wei, Hongshan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Family Health</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiao, Fan</au><au>Gao, Meixin</au><au>Yang, Junru</au><au>He, Lingling</au><au>Wei, Hongshan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FAM172A Deletion May Enhance Hepatic Steatosis by Promoting ER Stress</atitle><jtitle>Digestive diseases and sciences</jtitle><stitle>Dig Dis Sci</stitle><addtitle>Dig Dis Sci</addtitle><date>2021-09-01</date><risdate>2021</risdate><volume>66</volume><issue>9</issue><spage>3054</spage><epage>3061</epage><pages>3054-3061</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><abstract>Background
Endoplasmic reticulum (ER) stress is one of the major causes to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study showed that maintains the homeostasis of ER could effectively alleviate NAFLD. In this study, we found that the loss of FAM172A increased ER stress.
Aims
The aims of this study were to explore whether FAM172A could improve NAFLD by inhibiting ER stress.
Methods
The expression levels of FAM172A and ER stress were detected by western blot. The method of immunofluorescence was used to determine FAM172A location. The interacted proteins of FAM172A were identified by immunocoprecipitation. The methods of MTS and caspase-3/7 activity were taken to confirm the effect of FAM172A on cell viability and proliferation. The expression levels of inflammation were detected by qPCR.
Results
We confirmed that FAM172A might alleviate NAFLD through inhibiting ER stress. Loss of FAM172A increased the expressions of ATF6, peIF2α, but decreased the expression of IRE1α. Then, it was shown that FAM172A located in ER and FAM172A directly interacted with ATF6 and peIF2α and IRE1α. More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group. However, the binding of FAM172A and ATF6 or IRE1α did not change. Next, we found that the lack of FAM172A could produce more apoptosis and inflammation.
Conclusions
Our results suggest that FAM172A improve steatosis by alleviating ER stress.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32945983</pmid><doi>10.1007/s10620-020-06601-y</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-8893-653X</orcidid></addata></record> |
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subjects | Animals Antibodies Apoptosis Automation Biochemistry Cell Line Cell Proliferation Cell Survival Endoplasmic reticulum Endoplasmic Reticulum - physiology Endoplasmic Reticulum Stress - genetics Gastroenterology Gene Deletion Gene Expression Profiling - methods Gene Expression Regulation Hepatology Infectious diseases Kinases Liver Liver - metabolism Liver - pathology Liver diseases Medicine Medicine & Public Health Mice Microscopy Non-alcoholic Fatty Liver Disease - metabolism Oncology Original Article Proteins Proteins - genetics Proteins - metabolism Reagents Transplant Surgery Unfolded Protein Response |
title | FAM172A Deletion May Enhance Hepatic Steatosis by Promoting ER Stress |
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