Deubiquitination of CD36 by UCHL1 promotes foam cell formation
Atherosclerosis-associated cardiovascular diseases are main causes leading to high mortality worldwide. Macrophage-derived foam cell formation via uptaking modified lipoproteins is the initial and core step in the process of atherosclerosis. Meanwhile, scavenger receptor is indispensable for the for...
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| Veröffentlicht in: | Cell death & disease 2020-08, Vol.11 (8), p.636-636, Article 636 |
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| creator | Xia, Xiaohong Xu, Qiong Liu, Mingke Chen, Xuke Liu, Xiaolin He, Jinchan Hu, Tumei Yu, Cuifu Huang, Hongbiao Liu, Shiming Liu, Ningning |
| description | Atherosclerosis-associated cardiovascular diseases are main causes leading to high mortality worldwide. Macrophage-derived foam cell formation via uptaking modified lipoproteins is the initial and core step in the process of atherosclerosis. Meanwhile, scavenger receptor is indispensable for the formation of foam cells. UCHL1, a deubiquitinase, has been widely studied in multiple cancers. UCHL1 could be an oncogene or a tumor suppressor in dependent of tumor types. It remains unknown whether UCHL1 influences cellular oxLDL uptake. Herein we show that UCHL1 deletion significantly inhibits lipid accumulation and foam cell formation. Subsequently, we found that UCHL1 inhibitor or siRNA downregulates the expression of CD36 protein whereas SR-A, ABCA1, ABCG1, Lox-1, and SR-B1 have no significant change. Furthermore, the treatment of UCHL1 inhibition increases the abundance of K48-polyubiquitin on CD36 and the suppression of lipid uptake induced by UCHL1 deficiency is attenuated by blocking CD36 activation. Our study concluded that UCHL1 deletion decreases foam cell formation by promoting the degradation of CD36 protein, indicating UCHL1 may be a potential target for atherosclerosis treatment. |
| doi_str_mv | 10.1038/s41419-020-02888-x |
| format | Article |
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Macrophage-derived foam cell formation via uptaking modified lipoproteins is the initial and core step in the process of atherosclerosis. Meanwhile, scavenger receptor is indispensable for the formation of foam cells. UCHL1, a deubiquitinase, has been widely studied in multiple cancers. UCHL1 could be an oncogene or a tumor suppressor in dependent of tumor types. It remains unknown whether UCHL1 influences cellular oxLDL uptake. Herein we show that UCHL1 deletion significantly inhibits lipid accumulation and foam cell formation. Subsequently, we found that UCHL1 inhibitor or siRNA downregulates the expression of CD36 protein whereas SR-A, ABCA1, ABCG1, Lox-1, and SR-B1 have no significant change. Furthermore, the treatment of UCHL1 inhibition increases the abundance of K48-polyubiquitin on CD36 and the suppression of lipid uptake induced by UCHL1 deficiency is attenuated by blocking CD36 activation. Our study concluded that UCHL1 deletion decreases foam cell formation by promoting the degradation of CD36 protein, indicating UCHL1 may be a potential target for atherosclerosis treatment.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-02888-x</identifier><identifier>PMID: 32801299</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/2 ; 13/31 ; 13/89 ; 13/95 ; 14/63 ; 692/308/575 ; 692/699/75/593/2100 ; 96/35 ; ABCA1 protein ; Animals ; Antibodies ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - pathology ; ATP Binding Cassette Transporter 1 - metabolism ; ATP-Binding Cassette Transporters - genetics ; ATP-binding protein ; Biochemistry ; Biological Transport ; Biomedical and Life Sciences ; Cardiovascular diseases ; CD36 antigen ; CD36 Antigens - metabolism ; Cell Biology ; Cell Culture ; Cell Line ; Cholesterol - metabolism ; Clonal deletion ; Deubiquitinating Enzymes - metabolism ; Foam Cells - metabolism ; Humans ; Immunology ; Life Sciences ; Lipid Metabolism - physiology ; Lipids ; Lipoproteins ; Lipoproteins, LDL - metabolism ; LOX-1 protein ; Macrophages ; Macrophages - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Scavenger receptors ; Scavenger Receptors, Class A - metabolism ; siRNA ; Tumor suppressor genes ; Ubiquitin Thiolesterase - genetics ; Ubiquitin Thiolesterase - metabolism ; Ubiquitination</subject><ispartof>Cell death & disease, 2020-08, Vol.11 (8), p.636-636, Article 636</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-854fc38b54a715a4170d7609f3adb09e02b1ae05170c97785bd2a306c0af8f2d3</citedby><cites>FETCH-LOGICAL-c502t-854fc38b54a715a4170d7609f3adb09e02b1ae05170c97785bd2a306c0af8f2d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7429868/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7429868/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32801299$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xia, Xiaohong</creatorcontrib><creatorcontrib>Xu, Qiong</creatorcontrib><creatorcontrib>Liu, Mingke</creatorcontrib><creatorcontrib>Chen, Xuke</creatorcontrib><creatorcontrib>Liu, Xiaolin</creatorcontrib><creatorcontrib>He, Jinchan</creatorcontrib><creatorcontrib>Hu, Tumei</creatorcontrib><creatorcontrib>Yu, Cuifu</creatorcontrib><creatorcontrib>Huang, Hongbiao</creatorcontrib><creatorcontrib>Liu, Shiming</creatorcontrib><creatorcontrib>Liu, Ningning</creatorcontrib><title>Deubiquitination of CD36 by UCHL1 promotes foam cell formation</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Atherosclerosis-associated cardiovascular diseases are main causes leading to high mortality worldwide. Macrophage-derived foam cell formation via uptaking modified lipoproteins is the initial and core step in the process of atherosclerosis. Meanwhile, scavenger receptor is indispensable for the formation of foam cells. UCHL1, a deubiquitinase, has been widely studied in multiple cancers. UCHL1 could be an oncogene or a tumor suppressor in dependent of tumor types. It remains unknown whether UCHL1 influences cellular oxLDL uptake. Herein we show that UCHL1 deletion significantly inhibits lipid accumulation and foam cell formation. Subsequently, we found that UCHL1 inhibitor or siRNA downregulates the expression of CD36 protein whereas SR-A, ABCA1, ABCG1, Lox-1, and SR-B1 have no significant change. Furthermore, the treatment of UCHL1 inhibition increases the abundance of K48-polyubiquitin on CD36 and the suppression of lipid uptake induced by UCHL1 deficiency is attenuated by blocking CD36 activation. Our study concluded that UCHL1 deletion decreases foam cell formation by promoting the degradation of CD36 protein, indicating UCHL1 may be a potential target for atherosclerosis treatment.</description><subject>13/1</subject><subject>13/2</subject><subject>13/31</subject><subject>13/89</subject><subject>13/95</subject><subject>14/63</subject><subject>692/308/575</subject><subject>692/699/75/593/2100</subject><subject>96/35</subject><subject>ABCA1 protein</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - pathology</subject><subject>ATP Binding Cassette Transporter 1 - metabolism</subject><subject>ATP-Binding Cassette Transporters - genetics</subject><subject>ATP-binding protein</subject><subject>Biochemistry</subject><subject>Biological Transport</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiovascular diseases</subject><subject>CD36 antigen</subject><subject>CD36 Antigens - metabolism</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Line</subject><subject>Cholesterol - metabolism</subject><subject>Clonal deletion</subject><subject>Deubiquitinating Enzymes - metabolism</subject><subject>Foam Cells - metabolism</subject><subject>Humans</subject><subject>Immunology</subject><subject>Life Sciences</subject><subject>Lipid Metabolism - physiology</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>LOX-1 protein</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Scavenger receptors</subject><subject>Scavenger Receptors, Class A - metabolism</subject><subject>siRNA</subject><subject>Tumor suppressor genes</subject><subject>Ubiquitin Thiolesterase - genetics</subject><subject>Ubiquitin Thiolesterase - metabolism</subject><subject>Ubiquitination</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kUtLAzEUhYMoWqp_wIUMuHEzevOaJBtB6qNCwY1dh8xMRqd0Jm0yI_bfG9v6XDQQcsn97kkOB6FTDJcYqLwKDDOsUiAQt5Qyfd9DAwIMp0xKtf-rPkInIcwgLkqB8OwQHVEiAROlBuj61vZ5vezrrm5NV7s2cVUyuqVZkq-S6Wg8wcnCu8Z1NiSVM01S2Pk8Vr5Z08fooDLzYE-25xBN7--eR-N08vTwOLqZpAUH0qWSs6qgMufMCMwNwwJKkYGqqClzUBZIjo0FHu8LJYTkeUkMhawAU8mKlHSIrje6iz5vbFnYtvNmrhe-boxfaWdq_bfT1q_6xb1pwYiSmYwCF1sB75a9DZ1u6vDpxbTW9UETRpngGaM4ouf_0JnrfRvtRUqKjCucwW6KMiokZSxSZEMV3oXgbfX9ZQz6M0e9yVHHHPU6R_0eh85-m_0e-UotAnQDhNhqX6z_eXuH7AfwxaaS</recordid><startdate>20200815</startdate><enddate>20200815</enddate><creator>Xia, Xiaohong</creator><creator>Xu, Qiong</creator><creator>Liu, Mingke</creator><creator>Chen, Xuke</creator><creator>Liu, Xiaolin</creator><creator>He, Jinchan</creator><creator>Hu, Tumei</creator><creator>Yu, Cuifu</creator><creator>Huang, Hongbiao</creator><creator>Liu, Shiming</creator><creator>Liu, Ningning</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><scope>C6C</scope><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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200815</creationdate><title>Deubiquitination of CD36 by UCHL1 promotes foam cell formation</title><author>Xia, Xiaohong ; Xu, Qiong ; Liu, Mingke ; Chen, Xuke ; Liu, Xiaolin ; He, Jinchan ; Hu, Tumei ; Yu, Cuifu ; Huang, Hongbiao ; Liu, Shiming ; Liu, Ningning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c502t-854fc38b54a715a4170d7609f3adb09e02b1ae05170c97785bd2a306c0af8f2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/1</topic><topic>13/2</topic><topic>13/31</topic><topic>13/89</topic><topic>13/95</topic><topic>14/63</topic><topic>692/308/575</topic><topic>692/699/75/593/2100</topic><topic>96/35</topic><topic>ABCA1 protein</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xia, Xiaohong</au><au>Xu, Qiong</au><au>Liu, Mingke</au><au>Chen, Xuke</au><au>Liu, Xiaolin</au><au>He, Jinchan</au><au>Hu, Tumei</au><au>Yu, Cuifu</au><au>Huang, Hongbiao</au><au>Liu, Shiming</au><au>Liu, Ningning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deubiquitination of CD36 by UCHL1 promotes foam cell formation</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-08-15</date><risdate>2020</risdate><volume>11</volume><issue>8</issue><spage>636</spage><epage>636</epage><pages>636-636</pages><artnum>636</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Atherosclerosis-associated cardiovascular diseases are main causes leading to high mortality worldwide. Macrophage-derived foam cell formation via uptaking modified lipoproteins is the initial and core step in the process of atherosclerosis. Meanwhile, scavenger receptor is indispensable for the formation of foam cells. UCHL1, a deubiquitinase, has been widely studied in multiple cancers. UCHL1 could be an oncogene or a tumor suppressor in dependent of tumor types. It remains unknown whether UCHL1 influences cellular oxLDL uptake. Herein we show that UCHL1 deletion significantly inhibits lipid accumulation and foam cell formation. Subsequently, we found that UCHL1 inhibitor or siRNA downregulates the expression of CD36 protein whereas SR-A, ABCA1, ABCG1, Lox-1, and SR-B1 have no significant change. Furthermore, the treatment of UCHL1 inhibition increases the abundance of K48-polyubiquitin on CD36 and the suppression of lipid uptake induced by UCHL1 deficiency is attenuated by blocking CD36 activation. Our study concluded that UCHL1 deletion decreases foam cell formation by promoting the degradation of CD36 protein, indicating UCHL1 may be a potential target for atherosclerosis treatment.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32801299</pmid><doi>10.1038/s41419-020-02888-x</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/2 13/31 13/89 13/95 14/63 692/308/575 692/699/75/593/2100 96/35 ABCA1 protein Animals Antibodies Arteriosclerosis Atherosclerosis Atherosclerosis - pathology ATP Binding Cassette Transporter 1 - metabolism ATP-Binding Cassette Transporters - genetics ATP-binding protein Biochemistry Biological Transport Biomedical and Life Sciences Cardiovascular diseases CD36 antigen CD36 Antigens - metabolism Cell Biology Cell Culture Cell Line Cholesterol - metabolism Clonal deletion Deubiquitinating Enzymes - metabolism Foam Cells - metabolism Humans Immunology Life Sciences Lipid Metabolism - physiology Lipids Lipoproteins Lipoproteins, LDL - metabolism LOX-1 protein Macrophages Macrophages - metabolism Male Mice Mice, Inbred C57BL Scavenger receptors Scavenger Receptors, Class A - metabolism siRNA Tumor suppressor genes Ubiquitin Thiolesterase - genetics Ubiquitin Thiolesterase - metabolism Ubiquitination |
| title | Deubiquitination of CD36 by UCHL1 promotes foam cell formation |
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