Interaction of TPPP3 with VDAC1 Promotes Endothelial Injury through Activation of Reactive Oxygen Species
Endothelial injury plays a critical role in the pathogenesis of cardiovascular disorders and metabolic-associated vascular complications which are the leading cause of death worldwide. However, the mechanism underlying endothelial dysfunction is not completely understood. The study is aimed at inves...
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| creator | Hu, Renming Li, Rumei Huang, Jinya Zhou, Wenbai Nan, Wu Li, Yintao Liu, Naijia Zhou, Linuo |
| description | Endothelial injury plays a critical role in the pathogenesis of cardiovascular disorders and metabolic-associated vascular complications which are the leading cause of death worldwide. However, the mechanism underlying endothelial dysfunction is not completely understood. The study is aimed at investigating the role of tubulin polymerization-promoting protein family member 3 (TPPP3) in palmitic acid- (PA-) induced endothelial injury. The effect of TPPP3 on human umbilical vein endothelial cells (HUVECs) was determined by evaluating apoptosis, tube formation, and reactive oxygen species (ROS) production. TPPP3 silencing inhibited PA overload-induced apoptosis and production of ROS, along with the alteration of apoptosis-related key proteins such as BCL-2 and Bax. Mechanically, voltage-dependent anion channel 1 (VDAC1) was identified as a novel functional binding partner of TPPP3, and TPPP3 promoted VDAC1 protein stability and its activity. Further studies indicated that TPPP3 could promote apoptosis, ROS production, tube formation, and proapoptotic protein expression and reduce antiapoptotic protein expression through increasing VDAC1 expression under mildly elevated levels of PA. Collectively, these results demonstrated that TPPP3 could promote PA-induced oxidative damage in HUVECs via a VDAC1-dependent pathway, suggesting that TPPP3 might be considered as a potential therapeutic target in vascular disease. |
| doi_str_mv | 10.1155/2020/5950195 |
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However, the mechanism underlying endothelial dysfunction is not completely understood. The study is aimed at investigating the role of tubulin polymerization-promoting protein family member 3 (TPPP3) in palmitic acid- (PA-) induced endothelial injury. The effect of TPPP3 on human umbilical vein endothelial cells (HUVECs) was determined by evaluating apoptosis, tube formation, and reactive oxygen species (ROS) production. TPPP3 silencing inhibited PA overload-induced apoptosis and production of ROS, along with the alteration of apoptosis-related key proteins such as BCL-2 and Bax. Mechanically, voltage-dependent anion channel 1 (VDAC1) was identified as a novel functional binding partner of TPPP3, and TPPP3 promoted VDAC1 protein stability and its activity. Further studies indicated that TPPP3 could promote apoptosis, ROS production, tube formation, and proapoptotic protein expression and reduce antiapoptotic protein expression through increasing VDAC1 expression under mildly elevated levels of PA. Collectively, these results demonstrated that TPPP3 could promote PA-induced oxidative damage in HUVECs via a VDAC1-dependent pathway, suggesting that TPPP3 might be considered as a potential therapeutic target in vascular disease.</description><identifier>ISSN: 1942-0900</identifier><identifier>ISSN: 1942-0994</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2020/5950195</identifier><identifier>PMID: 33082910</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antibodies ; Apoptosis ; Apoptosis - drug effects ; bcl-2-Associated X Protein - metabolism ; Blood circulation disorders ; Cytoskeletal Proteins - antagonists & inhibitors ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Endothelium ; Experiments ; Flow cytometry ; Health aspects ; Human Umbilical Vein Endothelial Cells ; Humans ; Injuries ; Metabolism ; Neovascularization, Physiologic - drug effects ; Oxidative stress ; Oxidative Stress - drug effects ; Palmitic Acid - pharmacology ; Polymerization ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; RNA Interference ; RNA, Small Interfering - metabolism ; Saturated fatty acids ; Statistical analysis ; Up-Regulation - drug effects ; Voltage-Dependent Anion Channel 1 - antagonists & inhibitors ; Voltage-Dependent Anion Channel 1 - genetics ; Voltage-Dependent Anion Channel 1 - metabolism</subject><ispartof>Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-13</ispartof><rights>Copyright © 2020 Naijia Liu et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Naijia Liu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Naijia Liu et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-cae8d742fc5ab8b4fadd389f6292edf223db7a634350af713db685e399e6ba103</citedby><cites>FETCH-LOGICAL-c499t-cae8d742fc5ab8b4fadd389f6292edf223db7a634350af713db685e399e6ba103</cites><orcidid>0000-0002-8558-1347 ; 0000-0002-7742-2602</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7556057/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7556057/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33082910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>de Oliveira, Marcos R.</contributor><contributor>Marcos R de Oliveira</contributor><creatorcontrib>Hu, Renming</creatorcontrib><creatorcontrib>Li, Rumei</creatorcontrib><creatorcontrib>Huang, Jinya</creatorcontrib><creatorcontrib>Zhou, Wenbai</creatorcontrib><creatorcontrib>Nan, Wu</creatorcontrib><creatorcontrib>Li, Yintao</creatorcontrib><creatorcontrib>Liu, Naijia</creatorcontrib><creatorcontrib>Zhou, Linuo</creatorcontrib><title>Interaction of TPPP3 with VDAC1 Promotes Endothelial Injury through Activation of Reactive Oxygen Species</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Endothelial injury plays a critical role in the pathogenesis of cardiovascular disorders and metabolic-associated vascular complications which are the leading cause of death worldwide. However, the mechanism underlying endothelial dysfunction is not completely understood. The study is aimed at investigating the role of tubulin polymerization-promoting protein family member 3 (TPPP3) in palmitic acid- (PA-) induced endothelial injury. The effect of TPPP3 on human umbilical vein endothelial cells (HUVECs) was determined by evaluating apoptosis, tube formation, and reactive oxygen species (ROS) production. TPPP3 silencing inhibited PA overload-induced apoptosis and production of ROS, along with the alteration of apoptosis-related key proteins such as BCL-2 and Bax. Mechanically, voltage-dependent anion channel 1 (VDAC1) was identified as a novel functional binding partner of TPPP3, and TPPP3 promoted VDAC1 protein stability and its activity. Further studies indicated that TPPP3 could promote apoptosis, ROS production, tube formation, and proapoptotic protein expression and reduce antiapoptotic protein expression through increasing VDAC1 expression under mildly elevated levels of PA. Collectively, these results demonstrated that TPPP3 could promote PA-induced oxidative damage in HUVECs via a VDAC1-dependent pathway, suggesting that TPPP3 might be considered as a potential therapeutic target in vascular disease.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Blood circulation disorders</subject><subject>Cytoskeletal Proteins - antagonists & inhibitors</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Endothelium</subject><subject>Experiments</subject><subject>Flow cytometry</subject><subject>Health aspects</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>Injuries</subject><subject>Metabolism</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Palmitic Acid - pharmacology</subject><subject>Polymerization</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Saturated fatty acids</subject><subject>Statistical analysis</subject><subject>Up-Regulation - drug effects</subject><subject>Voltage-Dependent Anion Channel 1 - antagonists & inhibitors</subject><subject>Voltage-Dependent Anion Channel 1 - genetics</subject><subject>Voltage-Dependent Anion Channel 1 - metabolism</subject><issn>1942-0900</issn><issn>1942-0994</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkc9v0zAUxy3ExMbgxhlZ4oIE3fwjTuILUlUGVJq0CgZXy0meG1epXeyko_89jtp1bCdOfpY_7_P89EXoDSUXlApxyQgjl0IKQqV4hs6ozNiESJk9P9aEnKKXMa4IyTnL6At0yjkpmaTkDNm56yHourfeYW_w7WKx4PjO9i3-9Xk6o3gR_Nr3EPGVa3zfQmd1h-duNYQd7tvgh2WLp6l9q-8V32HUbQHf_NktweEfG6gtxFfoxOguwuvDeY5-frm6nX2bXN98nc-m15M6k7Kf1BrKpsiYqYWuyiozuml4KU3OJIPGMMabqtA5z7gg2hQ0XfNSAJcS8kpTws_Rp713M1RraGpwfdCd2gS71mGnvLbq8YuzrVr6rSqEyIkokuD9QRD87wFir9Y21tB12oEfomKZYLKkhNKEvnuCrvwQXFpvpGgheJ4VD9RSd6CsMz7NrUepmuayIGXJRJmoj3uqDj7GAOb4ZUrUmLQak1aHpBP-9t81j_B9tAn4sAda6xp9Z_9TB4kBox9oRlIunP8FwDi56w</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Hu, Renming</creator><creator>Li, Rumei</creator><creator>Huang, Jinya</creator><creator>Zhou, Wenbai</creator><creator>Nan, Wu</creator><creator>Li, Yintao</creator><creator>Liu, Naijia</creator><creator>Zhou, Linuo</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</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><orcidid>https://orcid.org/0000-0002-8558-1347</orcidid><orcidid>https://orcid.org/0000-0002-7742-2602</orcidid></search><sort><creationdate>2020</creationdate><title>Interaction of TPPP3 with VDAC1 Promotes Endothelial Injury through Activation of Reactive Oxygen Species</title><author>Hu, Renming ; Li, Rumei ; Huang, Jinya ; Zhou, Wenbai ; Nan, Wu ; Li, Yintao ; Liu, Naijia ; Zhou, Linuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-cae8d742fc5ab8b4fadd389f6292edf223db7a634350af713db685e399e6ba103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Blood circulation disorders</topic><topic>Cytoskeletal Proteins - antagonists & inhibitors</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Endothelium</topic><topic>Experiments</topic><topic>Flow cytometry</topic><topic>Health aspects</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>Injuries</topic><topic>Metabolism</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Palmitic Acid - pharmacology</topic><topic>Polymerization</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Saturated fatty acids</topic><topic>Statistical analysis</topic><topic>Up-Regulation - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Renming</au><au>Li, Rumei</au><au>Huang, Jinya</au><au>Zhou, Wenbai</au><au>Nan, Wu</au><au>Li, Yintao</au><au>Liu, Naijia</au><au>Zhou, Linuo</au><au>de Oliveira, Marcos R.</au><au>Marcos R de Oliveira</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction of TPPP3 with VDAC1 Promotes Endothelial Injury through Activation of Reactive Oxygen Species</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>13</epage><pages>1-13</pages><issn>1942-0900</issn><issn>1942-0994</issn><eissn>1942-0994</eissn><abstract>Endothelial injury plays a critical role in the pathogenesis of cardiovascular disorders and metabolic-associated vascular complications which are the leading cause of death worldwide. However, the mechanism underlying endothelial dysfunction is not completely understood. The study is aimed at investigating the role of tubulin polymerization-promoting protein family member 3 (TPPP3) in palmitic acid- (PA-) induced endothelial injury. The effect of TPPP3 on human umbilical vein endothelial cells (HUVECs) was determined by evaluating apoptosis, tube formation, and reactive oxygen species (ROS) production. TPPP3 silencing inhibited PA overload-induced apoptosis and production of ROS, along with the alteration of apoptosis-related key proteins such as BCL-2 and Bax. Mechanically, voltage-dependent anion channel 1 (VDAC1) was identified as a novel functional binding partner of TPPP3, and TPPP3 promoted VDAC1 protein stability and its activity. Further studies indicated that TPPP3 could promote apoptosis, ROS production, tube formation, and proapoptotic protein expression and reduce antiapoptotic protein expression through increasing VDAC1 expression under mildly elevated levels of PA. Collectively, these results demonstrated that TPPP3 could promote PA-induced oxidative damage in HUVECs via a VDAC1-dependent pathway, suggesting that TPPP3 might be considered as a potential therapeutic target in vascular disease.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>33082910</pmid><doi>10.1155/2020/5950195</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-8558-1347</orcidid><orcidid>https://orcid.org/0000-0002-7742-2602</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-13 |
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| source | MEDLINE; Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access |
| subjects | Antibodies Apoptosis Apoptosis - drug effects bcl-2-Associated X Protein - metabolism Blood circulation disorders Cytoskeletal Proteins - antagonists & inhibitors Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Endothelium Experiments Flow cytometry Health aspects Human Umbilical Vein Endothelial Cells Humans Injuries Metabolism Neovascularization, Physiologic - drug effects Oxidative stress Oxidative Stress - drug effects Palmitic Acid - pharmacology Polymerization Proteins Proto-Oncogene Proteins c-bcl-2 - metabolism Reactive oxygen species Reactive Oxygen Species - metabolism RNA Interference RNA, Small Interfering - metabolism Saturated fatty acids Statistical analysis Up-Regulation - drug effects Voltage-Dependent Anion Channel 1 - antagonists & inhibitors Voltage-Dependent Anion Channel 1 - genetics Voltage-Dependent Anion Channel 1 - metabolism |
| title | Interaction of TPPP3 with VDAC1 Promotes Endothelial Injury through Activation of Reactive Oxygen Species |
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