Advanced Glycation End Products Induce Atherosclerosis via RAGE/TLR4 Signaling Mediated-M1 Macrophage Polarization-Dependent Vascular Smooth Muscle Cell Phenotypic Conversion
Objective. The objective of this study was to investigate the involved mechanisms of advanced glycation end product- (AGE-) exacerbated atherosclerosis (AS). Methods. Toll-like receptor 4 (TLR4) inhibitor was administrated to type 2 diabetes mellitus (T2DM) AS rats. Atherosclerotic plaque, M1 macrop...
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| creator | Xing, Yujie Pan, Shuo Zhu, Ling Cui, Qianwei Tang, Zhiguo Liu, Zhongwei Liu, Fuqiang |
| description | Objective. The objective of this study was to investigate the involved mechanisms of advanced glycation end product- (AGE-) exacerbated atherosclerosis (AS). Methods. Toll-like receptor 4 (TLR4) inhibitor was administrated to type 2 diabetes mellitus (T2DM) AS rats. Atherosclerotic plaque, M1 macrophage infiltration, and VSMCs phenotypes were evaluated. AGE-exposed primary macrophages were treated with specific siRNAs knocking down receptor for AGEs (RAGE) and TLR4. Phenotypes of M1 macrophage and VSMCs were identified by fluorescent stains. Contact and noncontact coculture models were established. VSMCs and macrophages were cocultured in these models. ELISA was used to detect inflammatory cytokine concentrations. Relative mRNA expression levels were determined by real-time PCR. Relative protein expression and phosphorylation levels were evaluated by Western blots assays. Results. TLR4 inhibitor treatment significantly reduced arterial stenosis, infiltration of M1 polarized macrophages, and contractile-to-synthetic phenotype conversion of VSMCs in DM AS animals. RAGE and TLR4 silencing dramatically reduced AGE-induced macrophage M1 polarization, inflammatory cytokine secretion, and RAGE/TLR4/forkhead box protein C2 (FOXC2)/signaling which inhibited delta-like ligand 4 (Dll4) expression in macrophages. AGE-treated macrophages induced VSMC phenotypic conversion via activating Notch pathway in a contact coculture model rather than a noncontact model. The VSMC phenotypic conversion induction capability of macrophages was attenuated by RAGE and TLR4 silencing. Conclusions. AGEs induced activation of RAGE/TLR4/FOXC2 signaling, which featured macrophage with Dll4 high expression during M1 polarization. These macrophages promoted contractile-synthetic phenotypic conversion of VSMCs through the Dll4/Notch pathway after direct cell-to-cell contacts. |
| doi_str_mv | 10.1155/2022/9763377 |
| format | Article |
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The objective of this study was to investigate the involved mechanisms of advanced glycation end product- (AGE-) exacerbated atherosclerosis (AS). Methods. Toll-like receptor 4 (TLR4) inhibitor was administrated to type 2 diabetes mellitus (T2DM) AS rats. Atherosclerotic plaque, M1 macrophage infiltration, and VSMCs phenotypes were evaluated. AGE-exposed primary macrophages were treated with specific siRNAs knocking down receptor for AGEs (RAGE) and TLR4. Phenotypes of M1 macrophage and VSMCs were identified by fluorescent stains. Contact and noncontact coculture models were established. VSMCs and macrophages were cocultured in these models. ELISA was used to detect inflammatory cytokine concentrations. Relative mRNA expression levels were determined by real-time PCR. Relative protein expression and phosphorylation levels were evaluated by Western blots assays. Results. TLR4 inhibitor treatment significantly reduced arterial stenosis, infiltration of M1 polarized macrophages, and contractile-to-synthetic phenotype conversion of VSMCs in DM AS animals. RAGE and TLR4 silencing dramatically reduced AGE-induced macrophage M1 polarization, inflammatory cytokine secretion, and RAGE/TLR4/forkhead box protein C2 (FOXC2)/signaling which inhibited delta-like ligand 4 (Dll4) expression in macrophages. AGE-treated macrophages induced VSMC phenotypic conversion via activating Notch pathway in a contact coculture model rather than a noncontact model. The VSMC phenotypic conversion induction capability of macrophages was attenuated by RAGE and TLR4 silencing. Conclusions. AGEs induced activation of RAGE/TLR4/FOXC2 signaling, which featured macrophage with Dll4 high expression during M1 polarization. These macrophages promoted contractile-synthetic phenotypic conversion of VSMCs through the Dll4/Notch pathway after direct cell-to-cell contacts.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2022/9763377</identifier><identifier>PMID: 35069982</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Age ; Animals ; Antibiotics ; Atherosclerosis ; Atherosclerosis - genetics ; Diabetes ; Glycation End Products, Advanced - metabolism ; Humans ; Kinases ; Macrophages - metabolism ; Male ; Metabolites ; Mice ; Phenotype ; Signal Transduction ; Smooth muscle ; Toll-Like Receptor 4 - metabolism ; Transfection</subject><ispartof>Oxidative medicine and cellular longevity, 2022, Vol.2022, p.9763377-11</ispartof><rights>Copyright © 2022 Yujie Xing et al.</rights><rights>Copyright © 2022 Yujie Xing 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 © 2022 Yujie Xing et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-28b21238b53f50072ee03202ca2dbcae94f4d10ce5329cc2c5a0909dd5bf4faa3</citedby><cites>FETCH-LOGICAL-c448t-28b21238b53f50072ee03202ca2dbcae94f4d10ce5329cc2c5a0909dd5bf4faa3</cites><orcidid>0000-0002-0360-6396 ; 0000-0002-6559-0967 ; 0000-0003-0371-639X ; 0000-0002-0075-9338 ; 0000-0002-0271-5072 ; 0000-0002-5548-5450</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/PMC8776434/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8776434/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35069982$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Lopez Malo, Daniel</contributor><contributor>Daniel Lopez Malo</contributor><creatorcontrib>Xing, Yujie</creatorcontrib><creatorcontrib>Pan, Shuo</creatorcontrib><creatorcontrib>Zhu, Ling</creatorcontrib><creatorcontrib>Cui, Qianwei</creatorcontrib><creatorcontrib>Tang, Zhiguo</creatorcontrib><creatorcontrib>Liu, Zhongwei</creatorcontrib><creatorcontrib>Liu, Fuqiang</creatorcontrib><title>Advanced Glycation End Products Induce Atherosclerosis via RAGE/TLR4 Signaling Mediated-M1 Macrophage Polarization-Dependent Vascular Smooth Muscle Cell Phenotypic Conversion</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Objective. The objective of this study was to investigate the involved mechanisms of advanced glycation end product- (AGE-) exacerbated atherosclerosis (AS). Methods. Toll-like receptor 4 (TLR4) inhibitor was administrated to type 2 diabetes mellitus (T2DM) AS rats. Atherosclerotic plaque, M1 macrophage infiltration, and VSMCs phenotypes were evaluated. AGE-exposed primary macrophages were treated with specific siRNAs knocking down receptor for AGEs (RAGE) and TLR4. Phenotypes of M1 macrophage and VSMCs were identified by fluorescent stains. Contact and noncontact coculture models were established. VSMCs and macrophages were cocultured in these models. ELISA was used to detect inflammatory cytokine concentrations. Relative mRNA expression levels were determined by real-time PCR. Relative protein expression and phosphorylation levels were evaluated by Western blots assays. Results. TLR4 inhibitor treatment significantly reduced arterial stenosis, infiltration of M1 polarized macrophages, and contractile-to-synthetic phenotype conversion of VSMCs in DM AS animals. RAGE and TLR4 silencing dramatically reduced AGE-induced macrophage M1 polarization, inflammatory cytokine secretion, and RAGE/TLR4/forkhead box protein C2 (FOXC2)/signaling which inhibited delta-like ligand 4 (Dll4) expression in macrophages. AGE-treated macrophages induced VSMC phenotypic conversion via activating Notch pathway in a contact coculture model rather than a noncontact model. The VSMC phenotypic conversion induction capability of macrophages was attenuated by RAGE and TLR4 silencing. Conclusions. AGEs induced activation of RAGE/TLR4/FOXC2 signaling, which featured macrophage with Dll4 high expression during M1 polarization. These macrophages promoted contractile-synthetic phenotypic conversion of VSMCs through the Dll4/Notch pathway after direct cell-to-cell contacts.</description><subject>Age</subject><subject>Animals</subject><subject>Antibiotics</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - genetics</subject><subject>Diabetes</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>Humans</subject><subject>Kinases</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Phenotype</subject><subject>Signal Transduction</subject><subject>Smooth muscle</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Transfection</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kk2P0zAQhiMEYpeFG2dkiQsShDq28-ELUlVKWakV1e7C1XLsSeNVagc7KSo_it-IS0sFHLh4LM3jd2ZeT5I8z_DbLMvzCcGETHhZUFqWD5LLjDOSYs7Zw_Md44vkSQj3GBeUsOxxckFzXHBekcvkx1TvpFWg0aLbKzkYZ9HcarT2To9qCOjaxghoOrTgXVDd4TQB7YxEN9PFfHK3vGHo1mys7IzdoBVoIwfQ6SpDK6m861u5AbR2nfTm-y_99D30YDXYAX2RQY0xg263zg0tWo2HCmgGXYfWLVg37Huj0MzZHfgQ3z5NHjWyC_DsFK-Szx_md7OP6fLT4no2XaaKsWpISVWTjNCqzmmTY1wSAEyjUUoSXSsJnDVMZ1hBTglXiqhcRpu41nndsEZKepW8O-r2Y70FrWKzXnai92Yr_V44acTfGWtasXE7UZVlwSiLAq9OAt59HSEMYmuCinNJC24MghSEsCrnhEf05T_ovRt99PNI4argpIjUmyMVPQ3BQ3NuJsPisAjisAjitAgRf_HnAGf4989H4PURaI3V8pv5v9xPt1m-MQ</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Xing, Yujie</creator><creator>Pan, Shuo</creator><creator>Zhu, Ling</creator><creator>Cui, Qianwei</creator><creator>Tang, Zhiguo</creator><creator>Liu, Zhongwei</creator><creator>Liu, Fuqiang</creator><general>Hindawi</general><general>Hindawi Limited</general><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/0000-0002-0360-6396</orcidid><orcidid>https://orcid.org/0000-0002-6559-0967</orcidid><orcidid>https://orcid.org/0000-0003-0371-639X</orcidid><orcidid>https://orcid.org/0000-0002-0075-9338</orcidid><orcidid>https://orcid.org/0000-0002-0271-5072</orcidid><orcidid>https://orcid.org/0000-0002-5548-5450</orcidid></search><sort><creationdate>2022</creationdate><title>Advanced Glycation End Products Induce Atherosclerosis via RAGE/TLR4 Signaling Mediated-M1 Macrophage Polarization-Dependent Vascular Smooth Muscle Cell Phenotypic Conversion</title><author>Xing, Yujie ; 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The objective of this study was to investigate the involved mechanisms of advanced glycation end product- (AGE-) exacerbated atherosclerosis (AS). Methods. Toll-like receptor 4 (TLR4) inhibitor was administrated to type 2 diabetes mellitus (T2DM) AS rats. Atherosclerotic plaque, M1 macrophage infiltration, and VSMCs phenotypes were evaluated. AGE-exposed primary macrophages were treated with specific siRNAs knocking down receptor for AGEs (RAGE) and TLR4. Phenotypes of M1 macrophage and VSMCs were identified by fluorescent stains. Contact and noncontact coculture models were established. VSMCs and macrophages were cocultured in these models. ELISA was used to detect inflammatory cytokine concentrations. Relative mRNA expression levels were determined by real-time PCR. Relative protein expression and phosphorylation levels were evaluated by Western blots assays. Results. TLR4 inhibitor treatment significantly reduced arterial stenosis, infiltration of M1 polarized macrophages, and contractile-to-synthetic phenotype conversion of VSMCs in DM AS animals. RAGE and TLR4 silencing dramatically reduced AGE-induced macrophage M1 polarization, inflammatory cytokine secretion, and RAGE/TLR4/forkhead box protein C2 (FOXC2)/signaling which inhibited delta-like ligand 4 (Dll4) expression in macrophages. AGE-treated macrophages induced VSMC phenotypic conversion via activating Notch pathway in a contact coculture model rather than a noncontact model. The VSMC phenotypic conversion induction capability of macrophages was attenuated by RAGE and TLR4 silencing. Conclusions. AGEs induced activation of RAGE/TLR4/FOXC2 signaling, which featured macrophage with Dll4 high expression during M1 polarization. These macrophages promoted contractile-synthetic phenotypic conversion of VSMCs through the Dll4/Notch pathway after direct cell-to-cell contacts.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>35069982</pmid><doi>10.1155/2022/9763377</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-0360-6396</orcidid><orcidid>https://orcid.org/0000-0002-6559-0967</orcidid><orcidid>https://orcid.org/0000-0003-0371-639X</orcidid><orcidid>https://orcid.org/0000-0002-0075-9338</orcidid><orcidid>https://orcid.org/0000-0002-0271-5072</orcidid><orcidid>https://orcid.org/0000-0002-5548-5450</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Age Animals Antibiotics Atherosclerosis Atherosclerosis - genetics Diabetes Glycation End Products, Advanced - metabolism Humans Kinases Macrophages - metabolism Male Metabolites Mice Phenotype Signal Transduction Smooth muscle Toll-Like Receptor 4 - metabolism Transfection |
| title | Advanced Glycation End Products Induce Atherosclerosis via RAGE/TLR4 Signaling Mediated-M1 Macrophage Polarization-Dependent Vascular Smooth Muscle Cell Phenotypic Conversion |
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