HMGB1-RAGE Axis Makes No Contribution to Cardiac Remodeling Induced by Pressure-Overload
High-mobility group box1 (HMGB1) exerts effects on inflammation by binding to receptor for advanced glycation end products (RAGE) or Toll-like receptor 4. Considering that inflammation is involved in pressure overload-induced cardiac hypertrophy, we herein attempted to investigate whether HMGB1 play...
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| creator | Lin, Hairuo Shen, Liang Zhang, Xiajun Xie, Jiahe Hao, Huixin Zhang, Yingxue Chen, Zhenhuan Yamamoto, Hiroshi Liao, Wangjun Bin, Jianping Cao, Shiping Huang, Xiaobo Liao, Yulin |
| description | High-mobility group box1 (HMGB1) exerts effects on inflammation by binding to receptor for advanced glycation end products (RAGE) or Toll-like receptor 4. Considering that inflammation is involved in pressure overload-induced cardiac hypertrophy, we herein attempted to investigate whether HMGB1 plays a role in myocardial hypertrophy in RAGE knockout mice as well as in the growth and apoptosis of cardiomyocytes. The myocardial expression of RAGE was not significantly changed while TLR4 mRNA was upregulated in response to transverse aortic constriction (TAC) for 1 week. The myocardial expression of HMGB1 protein was markedly increased in TAC group when compared to the sham group. Heart weight to body weight ratio (HW/BW) and lung weight to body weight ratio (LW/BW) were evaluated in RAGE knockout (KO) and wild-type (WT) mice 1 week after TAC. Significant larger HW/BW and LW/BW ratios were found in TAC groups than the corresponding sham groups, but no significant difference was found between KO and WT TAC mice. Similar results were also found when TAC duration was extended to 4 weeks. Cultured neonatal rat cardiomyocytes were treated with different concentrations of recombinant HMGB1, then cell viability was determined using MTT and CCK8 assays and cell apoptosis was determined by Hoechst staining and TUNEL assay. The results came out that HMGB1 exerted no influence on viability or apoptosis of cardiomyocytes. Besides, the protein expression levels of Bax and Bcl2 in response to different concentrations of HMGB1 were similar. These findings indicate that HMGB1 neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition. |
| doi_str_mv | 10.1371/journal.pone.0158514 |
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Considering that inflammation is involved in pressure overload-induced cardiac hypertrophy, we herein attempted to investigate whether HMGB1 plays a role in myocardial hypertrophy in RAGE knockout mice as well as in the growth and apoptosis of cardiomyocytes. The myocardial expression of RAGE was not significantly changed while TLR4 mRNA was upregulated in response to transverse aortic constriction (TAC) for 1 week. The myocardial expression of HMGB1 protein was markedly increased in TAC group when compared to the sham group. Heart weight to body weight ratio (HW/BW) and lung weight to body weight ratio (LW/BW) were evaluated in RAGE knockout (KO) and wild-type (WT) mice 1 week after TAC. Significant larger HW/BW and LW/BW ratios were found in TAC groups than the corresponding sham groups, but no significant difference was found between KO and WT TAC mice. Similar results were also found when TAC duration was extended to 4 weeks. Cultured neonatal rat cardiomyocytes were treated with different concentrations of recombinant HMGB1, then cell viability was determined using MTT and CCK8 assays and cell apoptosis was determined by Hoechst staining and TUNEL assay. The results came out that HMGB1 exerted no influence on viability or apoptosis of cardiomyocytes. Besides, the protein expression levels of Bax and Bcl2 in response to different concentrations of HMGB1 were similar. These findings indicate that HMGB1 neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0158514</identifier><identifier>PMID: 27355349</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Advanced glycosylation end products ; Animals ; Aorta ; Aorta - pathology ; Apoptosis ; BAX protein ; Binding ; Biology and Life Sciences ; Body weight ; Cardiology ; Cardiomegaly ; Cardiomyocytes ; Cell Survival ; Cells, Cultured ; Chromosomal proteins ; Comparative analysis ; DNA Damage ; Gene expression ; Genetic aspects ; Glycosylation ; Heart ; Heart diseases ; Heart failure ; Heart hypertrophy ; Histamine ; HMGB1 protein ; HMGB1 Protein - metabolism ; Homozygote ; Hypertrophy ; Immune system ; Inflammation ; Ischemia ; Laboratory animals ; Lungs ; Male ; Medicine and Health Sciences ; Mice ; Mice, Knockout ; mRNA ; Myocardium - metabolism ; Myocytes, Cardiac - cytology ; Neonates ; Organ Size ; Pressure ; Proteins ; Rats ; Receptor for Advanced Glycation End Products - metabolism ; Research and Analysis Methods ; Risk factors ; Rodents ; TLR4 protein ; Toll-Like Receptor 4 - metabolism ; Toll-like receptors</subject><ispartof>PloS one, 2016-06, Vol.11 (6), p.e0158514-e0158514</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Lin et al 2016 Lin et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-31dc7bb1d0f6213a330a2424b07222df1545e08da91a920c3d0b1719e342a87f3</citedby><cites>FETCH-LOGICAL-c725t-31dc7bb1d0f6213a330a2424b07222df1545e08da91a920c3d0b1719e342a87f3</cites><orcidid>0000-0001-5961-390X</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/PMC4927190/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927190/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27355349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Minamino, Tohru</contributor><creatorcontrib>Lin, Hairuo</creatorcontrib><creatorcontrib>Shen, Liang</creatorcontrib><creatorcontrib>Zhang, Xiajun</creatorcontrib><creatorcontrib>Xie, Jiahe</creatorcontrib><creatorcontrib>Hao, Huixin</creatorcontrib><creatorcontrib>Zhang, Yingxue</creatorcontrib><creatorcontrib>Chen, Zhenhuan</creatorcontrib><creatorcontrib>Yamamoto, Hiroshi</creatorcontrib><creatorcontrib>Liao, Wangjun</creatorcontrib><creatorcontrib>Bin, Jianping</creatorcontrib><creatorcontrib>Cao, Shiping</creatorcontrib><creatorcontrib>Huang, Xiaobo</creatorcontrib><creatorcontrib>Liao, Yulin</creatorcontrib><title>HMGB1-RAGE Axis Makes No Contribution to Cardiac Remodeling Induced by Pressure-Overload</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>High-mobility group box1 (HMGB1) exerts effects on inflammation by binding to receptor for advanced glycation end products (RAGE) or Toll-like receptor 4. Considering that inflammation is involved in pressure overload-induced cardiac hypertrophy, we herein attempted to investigate whether HMGB1 plays a role in myocardial hypertrophy in RAGE knockout mice as well as in the growth and apoptosis of cardiomyocytes. The myocardial expression of RAGE was not significantly changed while TLR4 mRNA was upregulated in response to transverse aortic constriction (TAC) for 1 week. The myocardial expression of HMGB1 protein was markedly increased in TAC group when compared to the sham group. Heart weight to body weight ratio (HW/BW) and lung weight to body weight ratio (LW/BW) were evaluated in RAGE knockout (KO) and wild-type (WT) mice 1 week after TAC. Significant larger HW/BW and LW/BW ratios were found in TAC groups than the corresponding sham groups, but no significant difference was found between KO and WT TAC mice. Similar results were also found when TAC duration was extended to 4 weeks. Cultured neonatal rat cardiomyocytes were treated with different concentrations of recombinant HMGB1, then cell viability was determined using MTT and CCK8 assays and cell apoptosis was determined by Hoechst staining and TUNEL assay. The results came out that HMGB1 exerted no influence on viability or apoptosis of cardiomyocytes. Besides, the protein expression levels of Bax and Bcl2 in response to different concentrations of HMGB1 were similar. These findings indicate that HMGB1 neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition.</description><subject>Advanced glycosylation end products</subject><subject>Animals</subject><subject>Aorta</subject><subject>Aorta - pathology</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Binding</subject><subject>Biology and Life Sciences</subject><subject>Body weight</subject><subject>Cardiology</subject><subject>Cardiomegaly</subject><subject>Cardiomyocytes</subject><subject>Cell Survival</subject><subject>Cells, Cultured</subject><subject>Chromosomal proteins</subject><subject>Comparative analysis</subject><subject>DNA Damage</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Glycosylation</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart hypertrophy</subject><subject>Histamine</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - metabolism</subject><subject>Homozygote</subject><subject>Hypertrophy</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>Lungs</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>mRNA</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Neonates</subject><subject>Organ Size</subject><subject>Pressure</subject><subject>Proteins</subject><subject>Rats</subject><subject>Receptor for Advanced Glycation End Products - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-like receptors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBEQkJwkeKvxMkNUqlGV2mjqHyIO8uxT1pvaVzsZNr-PW6bTQ3axeQLfz3n9fFrnyh6jdEIU44_XdrONbIebWwDI4TTPMXsSXSMC0qSjCD69GB8FL3w_hKhlOZZ9jw6IpymKWXFcfTn7GL6BSeL8fQ0Ht8YH1_IK_DxNxtPbNM6U3atsU3chrl02kgVL2BtNdSmWcazRncKdFzext8deN85SObX4Gor9cvoWSVrD6_6_iT69fX05-QsOZ9PZ5PxeaI4SduEYq14WWKNqoxgKilFkjDCSsQJIbrCKUsB5VoWWBYEKapRiTkugDIic17Rk-jtXndTWy96U7zAOUIMs4KQQMz2hLbyUmycWUt3K6w0Yrdg3VJI1xpVg9AcoOQ6UynKmVa0RJgpXRBaoaoieHva5_60rlyDVhA8kvVAdLjTmJVY2msRMglZoyDwoRdw9m8HvhVr4xXUtWzAdru8c44pYuwxKGaUF5gH9N1_6MNG9NRShruaprIhRbUVFWOWZsHpFG2p0QNUaBrWRoXPVpmwPgj4OAgITAs37VJ23ovZj8Xj2fnvIfv-gF2BrNuVt_XuQ_ohyPagctZ7B9X9e2AktrVy54bY1oroayWEvTl8y_ugu-Kg_wBYOQts</recordid><startdate>20160629</startdate><enddate>20160629</enddate><creator>Lin, Hairuo</creator><creator>Shen, Liang</creator><creator>Zhang, Xiajun</creator><creator>Xie, Jiahe</creator><creator>Hao, Huixin</creator><creator>Zhang, Yingxue</creator><creator>Chen, Zhenhuan</creator><creator>Yamamoto, Hiroshi</creator><creator>Liao, Wangjun</creator><creator>Bin, Jianping</creator><creator>Cao, Shiping</creator><creator>Huang, Xiaobo</creator><creator>Liao, Yulin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5961-390X</orcidid></search><sort><creationdate>20160629</creationdate><title>HMGB1-RAGE Axis Makes No Contribution to Cardiac Remodeling Induced by Pressure-Overload</title><author>Lin, Hairuo ; Shen, Liang ; Zhang, Xiajun ; Xie, Jiahe ; Hao, Huixin ; Zhang, Yingxue ; Chen, Zhenhuan ; Yamamoto, Hiroshi ; Liao, Wangjun ; Bin, Jianping ; Cao, Shiping ; Huang, Xiaobo ; Liao, Yulin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-31dc7bb1d0f6213a330a2424b07222df1545e08da91a920c3d0b1719e342a87f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Advanced glycosylation end products</topic><topic>Animals</topic><topic>Aorta</topic><topic>Aorta - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Hairuo</au><au>Shen, Liang</au><au>Zhang, Xiajun</au><au>Xie, Jiahe</au><au>Hao, Huixin</au><au>Zhang, Yingxue</au><au>Chen, Zhenhuan</au><au>Yamamoto, Hiroshi</au><au>Liao, Wangjun</au><au>Bin, Jianping</au><au>Cao, Shiping</au><au>Huang, Xiaobo</au><au>Liao, Yulin</au><au>Minamino, Tohru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HMGB1-RAGE Axis Makes No Contribution to Cardiac Remodeling Induced by Pressure-Overload</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-06-29</date><risdate>2016</risdate><volume>11</volume><issue>6</issue><spage>e0158514</spage><epage>e0158514</epage><pages>e0158514-e0158514</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>High-mobility group box1 (HMGB1) exerts effects on inflammation by binding to receptor for advanced glycation end products (RAGE) or Toll-like receptor 4. Considering that inflammation is involved in pressure overload-induced cardiac hypertrophy, we herein attempted to investigate whether HMGB1 plays a role in myocardial hypertrophy in RAGE knockout mice as well as in the growth and apoptosis of cardiomyocytes. The myocardial expression of RAGE was not significantly changed while TLR4 mRNA was upregulated in response to transverse aortic constriction (TAC) for 1 week. The myocardial expression of HMGB1 protein was markedly increased in TAC group when compared to the sham group. Heart weight to body weight ratio (HW/BW) and lung weight to body weight ratio (LW/BW) were evaluated in RAGE knockout (KO) and wild-type (WT) mice 1 week after TAC. Significant larger HW/BW and LW/BW ratios were found in TAC groups than the corresponding sham groups, but no significant difference was found between KO and WT TAC mice. Similar results were also found when TAC duration was extended to 4 weeks. Cultured neonatal rat cardiomyocytes were treated with different concentrations of recombinant HMGB1, then cell viability was determined using MTT and CCK8 assays and cell apoptosis was determined by Hoechst staining and TUNEL assay. The results came out that HMGB1 exerted no influence on viability or apoptosis of cardiomyocytes. Besides, the protein expression levels of Bax and Bcl2 in response to different concentrations of HMGB1 were similar. These findings indicate that HMGB1 neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27355349</pmid><doi>10.1371/journal.pone.0158514</doi><orcidid>https://orcid.org/0000-0001-5961-390X</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-06, Vol.11 (6), p.e0158514-e0158514 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1800414922 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Advanced glycosylation end products Animals Aorta Aorta - pathology Apoptosis BAX protein Binding Biology and Life Sciences Body weight Cardiology Cardiomegaly Cardiomyocytes Cell Survival Cells, Cultured Chromosomal proteins Comparative analysis DNA Damage Gene expression Genetic aspects Glycosylation Heart Heart diseases Heart failure Heart hypertrophy Histamine HMGB1 protein HMGB1 Protein - metabolism Homozygote Hypertrophy Immune system Inflammation Ischemia Laboratory animals Lungs Male Medicine and Health Sciences Mice Mice, Knockout mRNA Myocardium - metabolism Myocytes, Cardiac - cytology Neonates Organ Size Pressure Proteins Rats Receptor for Advanced Glycation End Products - metabolism Research and Analysis Methods Risk factors Rodents TLR4 protein Toll-Like Receptor 4 - metabolism Toll-like receptors |
| title | HMGB1-RAGE Axis Makes No Contribution to Cardiac Remodeling Induced by Pressure-Overload |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-27T19%3A17%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=HMGB1-RAGE%20Axis%20Makes%20No%20Contribution%20to%20Cardiac%20Remodeling%20Induced%20by%20Pressure-Overload&rft.jtitle=PloS%20one&rft.au=Lin,%20Hairuo&rft.date=2016-06-29&rft.volume=11&rft.issue=6&rft.spage=e0158514&rft.epage=e0158514&rft.pages=e0158514-e0158514&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0158514&rft_dat=%3Cgale_plos_%3EA456545502%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1800414922&rft_id=info:pmid/27355349&rft_galeid=A456545502&rft_doaj_id=oai_doaj_org_article_d7eeb7d6c5084dc3b014cd923f0ff21f&rfr_iscdi=true |