HMGB1 Silencing Potentiates the Anti-inflammatory Effects of Sodium Ferulate in ox-LDL-Stimulated Vascular Smooth Muscle Cells
Atherosclerosis is a sustained inflammatory disease of the arterial wall. The purpose of the current study is to investigate the effect of sodium ferulate on the proliferation and migration of human vascular smooth muscle cells (hVSMCs). In addition, we also sought to determine whether HMGB1 knockdo...
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| Veröffentlicht in: | Cell biochemistry and biophysics 2015-05, Vol.72 (1), p.297-304 |
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| creator | Hu, Nan Kong, Lingshang Qian, Aimin Meng, Qingyou Li, Chenglong Yu, Xiaobin Chen, Hong Du, Xiaolong Li, Xiaoqiang |
| description | Atherosclerosis is a sustained inflammatory disease of the arterial wall. The purpose of the current study is to investigate the effect of sodium ferulate on the proliferation and migration of human vascular smooth muscle cells (hVSMCs). In addition, we also sought to determine whether
HMGB1
knockdown could potentiate the anti-inflammatory effects of sodium ferulate. hVSMCs were treated with oxidized lower-density lipoprotein (ox-LDL, 50 mg/l) to induce inflammation. Cells were then treated with sodium ferulate and HMGB1 silencing (SiHMGB1) individually or in combination. The phenotypes of the treated cells including proliferation, cell cycle profile, apoptosis, and gene expression were analyzed. Results showed that sodium ferulate or SiHMGB1 treatment inhibited ox-LDL-induced inflammation in hVSMCs. Furthermore, the combination of SiHMGB1 plus sodium ferulate treatment displayed an additive effect in inhibiting the proliferation and migration of hVSMCs. Consistently, the suppression of receptor for advanced glycation end products expression was also observed. ICAM-1 and transforming growth factor-β suggest that these signaling components were involved in the anti-inflammatory effect. Our study confirms the anti-inflammatory function of sodium ferulate, and uncovered the potentiating effect of HMGB1 knockdown in suppressing ox-LDL-induced proliferation and migration of hVSMCs. Inhibition of
HMGB1
expression in addition to sodium ferulate treatment might be a more effective therapeutic approach for atherosclerosis. |
| doi_str_mv | 10.1007/s12013-014-0455-x |
| format | Article |
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HMGB1
knockdown could potentiate the anti-inflammatory effects of sodium ferulate. hVSMCs were treated with oxidized lower-density lipoprotein (ox-LDL, 50 mg/l) to induce inflammation. Cells were then treated with sodium ferulate and HMGB1 silencing (SiHMGB1) individually or in combination. The phenotypes of the treated cells including proliferation, cell cycle profile, apoptosis, and gene expression were analyzed. Results showed that sodium ferulate or SiHMGB1 treatment inhibited ox-LDL-induced inflammation in hVSMCs. Furthermore, the combination of SiHMGB1 plus sodium ferulate treatment displayed an additive effect in inhibiting the proliferation and migration of hVSMCs. Consistently, the suppression of receptor for advanced glycation end products expression was also observed. ICAM-1 and transforming growth factor-β suggest that these signaling components were involved in the anti-inflammatory effect. Our study confirms the anti-inflammatory function of sodium ferulate, and uncovered the potentiating effect of HMGB1 knockdown in suppressing ox-LDL-induced proliferation and migration of hVSMCs. Inhibition of
HMGB1
expression in addition to sodium ferulate treatment might be a more effective therapeutic approach for atherosclerosis.</description><identifier>ISSN: 1085-9195</identifier><identifier>EISSN: 1559-0283</identifier><identifier>DOI: 10.1007/s12013-014-0455-x</identifier><identifier>PMID: 25561283</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Anti-Inflammatory Agents - chemistry ; Apoptosis ; Atherosclerosis - metabolism ; Biochemistry ; Biological and Medical Physics ; Biomedical and Life Sciences ; Biophysics ; Biotechnology ; Cell Biology ; Cell Cycle ; Cell Movement ; Cell Proliferation ; Coumaric Acids - chemistry ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Silencing ; Glycation End Products, Advanced - metabolism ; HMGB1 Protein - genetics ; HMGB1 Protein - physiology ; Humans ; Inflammation ; Life Sciences ; Lipoproteins, LDL - chemistry ; Muscle, Smooth, Vascular - cytology ; Myocytes, Smooth Muscle - cytology ; Myocytes, Smooth Muscle - drug effects ; Original Paper ; Pharmacology/Toxicology ; Phenotype ; Sodium</subject><ispartof>Cell biochemistry and biophysics, 2015-05, Vol.72 (1), p.297-304</ispartof><rights>Springer Science+Business Media New York 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-69b4b3605aeefe6fc8f5b84f512dbfc4688cd7f5a376459774793e9d8b20d09e3</citedby><cites>FETCH-LOGICAL-c442t-69b4b3605aeefe6fc8f5b84f512dbfc4688cd7f5a376459774793e9d8b20d09e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12013-014-0455-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12013-014-0455-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25561283$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Nan</creatorcontrib><creatorcontrib>Kong, Lingshang</creatorcontrib><creatorcontrib>Qian, Aimin</creatorcontrib><creatorcontrib>Meng, Qingyou</creatorcontrib><creatorcontrib>Li, Chenglong</creatorcontrib><creatorcontrib>Yu, Xiaobin</creatorcontrib><creatorcontrib>Chen, Hong</creatorcontrib><creatorcontrib>Du, Xiaolong</creatorcontrib><creatorcontrib>Li, Xiaoqiang</creatorcontrib><title>HMGB1 Silencing Potentiates the Anti-inflammatory Effects of Sodium Ferulate in ox-LDL-Stimulated Vascular Smooth Muscle Cells</title><title>Cell biochemistry and biophysics</title><addtitle>Cell Biochem Biophys</addtitle><addtitle>Cell Biochem Biophys</addtitle><description>Atherosclerosis is a sustained inflammatory disease of the arterial wall. The purpose of the current study is to investigate the effect of sodium ferulate on the proliferation and migration of human vascular smooth muscle cells (hVSMCs). In addition, we also sought to determine whether
HMGB1
knockdown could potentiate the anti-inflammatory effects of sodium ferulate. hVSMCs were treated with oxidized lower-density lipoprotein (ox-LDL, 50 mg/l) to induce inflammation. Cells were then treated with sodium ferulate and HMGB1 silencing (SiHMGB1) individually or in combination. The phenotypes of the treated cells including proliferation, cell cycle profile, apoptosis, and gene expression were analyzed. Results showed that sodium ferulate or SiHMGB1 treatment inhibited ox-LDL-induced inflammation in hVSMCs. Furthermore, the combination of SiHMGB1 plus sodium ferulate treatment displayed an additive effect in inhibiting the proliferation and migration of hVSMCs. Consistently, the suppression of receptor for advanced glycation end products expression was also observed. ICAM-1 and transforming growth factor-β suggest that these signaling components were involved in the anti-inflammatory effect. Our study confirms the anti-inflammatory function of sodium ferulate, and uncovered the potentiating effect of HMGB1 knockdown in suppressing ox-LDL-induced proliferation and migration of hVSMCs. Inhibition of
HMGB1
expression in addition to sodium ferulate treatment might be a more effective therapeutic approach for atherosclerosis.</description><subject>Anti-Inflammatory Agents - chemistry</subject><subject>Apoptosis</subject><subject>Atherosclerosis - metabolism</subject><subject>Biochemistry</subject><subject>Biological and Medical Physics</subject><subject>Biomedical and Life Sciences</subject><subject>Biophysics</subject><subject>Biotechnology</subject><subject>Cell Biology</subject><subject>Cell Cycle</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Coumaric Acids - chemistry</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Gene Silencing</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>HMGB1 Protein - genetics</subject><subject>HMGB1 Protein - physiology</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Life Sciences</subject><subject>Lipoproteins, LDL - chemistry</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Myocytes, Smooth Muscle - cytology</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Original Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Phenotype</subject><subject>Sodium</subject><issn>1085-9195</issn><issn>1559-0283</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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><recordid>eNp1kU9v1DAQxSMEoqXwAbggS1y4GMaOHTvHsvQP0lZFWuBqOc64TZXExXak7aWfvV62IITU08zYv_dmpFdVbxl8ZADqU2IcWE2BCQpCSrp9Vh0yKVsKXNfPSw9a0pa18qB6ldINAOcgxMvqgEvZsMIcVvfnF2efGdkMI85umK_It5BxzoPNmEi-RnJcBjrMfrTTZHOId-TEe3Q5keDJJvTDMpFTjMtYFGSYSdjS9Zc13eRh-v3Wk582udJGsplCyNfkYkluRLLCcUyvqxfejgnfPNaj6sfpyffVOV1fnn1dHa-pE4Jn2rSd6OoGpEX02Hinvey08JLxvvNONFq7Xnlpa9UI2SolVFtj2-uOQw8t1kfVh73vbQy_FkzZTENy5QI7Y1iSYUppBUoAFPT9f-hNWOJcrjOs0Q1rNegdxfaUiyGliN7cxmGy8c4wMLtwzD4cU8Ixu3DMtmjePTov3YT9X8WfNArA90AqX_MVxn9WP-n6AJMdmnM</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Hu, Nan</creator><creator>Kong, Lingshang</creator><creator>Qian, Aimin</creator><creator>Meng, Qingyou</creator><creator>Li, Chenglong</creator><creator>Yu, Xiaobin</creator><creator>Chen, Hong</creator><creator>Du, Xiaolong</creator><creator>Li, Xiaoqiang</creator><general>Springer US</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>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</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>C1K</scope><scope>CCPQU</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20150501</creationdate><title>HMGB1 Silencing Potentiates the Anti-inflammatory Effects of Sodium Ferulate in ox-LDL-Stimulated Vascular Smooth Muscle Cells</title><author>Hu, Nan ; Kong, Lingshang ; Qian, Aimin ; Meng, Qingyou ; Li, Chenglong ; Yu, Xiaobin ; Chen, Hong ; Du, Xiaolong ; Li, Xiaoqiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-69b4b3605aeefe6fc8f5b84f512dbfc4688cd7f5a376459774793e9d8b20d09e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Anti-Inflammatory Agents - chemistry</topic><topic>Apoptosis</topic><topic>Atherosclerosis - metabolism</topic><topic>Biochemistry</topic><topic>Biological and Medical Physics</topic><topic>Biomedical and Life Sciences</topic><topic>Biophysics</topic><topic>Biotechnology</topic><topic>Cell Biology</topic><topic>Cell Cycle</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Coumaric Acids - chemistry</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Gene Silencing</topic><topic>Glycation End Products, Advanced - metabolism</topic><topic>HMGB1 Protein - genetics</topic><topic>HMGB1 Protein - physiology</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Life Sciences</topic><topic>Lipoproteins, LDL - chemistry</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Myocytes, Smooth Muscle - cytology</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Original Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Phenotype</topic><topic>Sodium</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Nan</creatorcontrib><creatorcontrib>Kong, Lingshang</creatorcontrib><creatorcontrib>Qian, Aimin</creatorcontrib><creatorcontrib>Meng, Qingyou</creatorcontrib><creatorcontrib>Li, Chenglong</creatorcontrib><creatorcontrib>Yu, Xiaobin</creatorcontrib><creatorcontrib>Chen, Hong</creatorcontrib><creatorcontrib>Du, Xiaolong</creatorcontrib><creatorcontrib>Li, Xiaoqiang</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Nan</au><au>Kong, Lingshang</au><au>Qian, Aimin</au><au>Meng, Qingyou</au><au>Li, Chenglong</au><au>Yu, Xiaobin</au><au>Chen, Hong</au><au>Du, Xiaolong</au><au>Li, Xiaoqiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HMGB1 Silencing Potentiates the Anti-inflammatory Effects of Sodium Ferulate in ox-LDL-Stimulated Vascular Smooth Muscle Cells</atitle><jtitle>Cell biochemistry and biophysics</jtitle><stitle>Cell Biochem Biophys</stitle><addtitle>Cell Biochem Biophys</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>72</volume><issue>1</issue><spage>297</spage><epage>304</epage><pages>297-304</pages><issn>1085-9195</issn><eissn>1559-0283</eissn><abstract>Atherosclerosis is a sustained inflammatory disease of the arterial wall. The purpose of the current study is to investigate the effect of sodium ferulate on the proliferation and migration of human vascular smooth muscle cells (hVSMCs). In addition, we also sought to determine whether
HMGB1
knockdown could potentiate the anti-inflammatory effects of sodium ferulate. hVSMCs were treated with oxidized lower-density lipoprotein (ox-LDL, 50 mg/l) to induce inflammation. Cells were then treated with sodium ferulate and HMGB1 silencing (SiHMGB1) individually or in combination. The phenotypes of the treated cells including proliferation, cell cycle profile, apoptosis, and gene expression were analyzed. Results showed that sodium ferulate or SiHMGB1 treatment inhibited ox-LDL-induced inflammation in hVSMCs. Furthermore, the combination of SiHMGB1 plus sodium ferulate treatment displayed an additive effect in inhibiting the proliferation and migration of hVSMCs. Consistently, the suppression of receptor for advanced glycation end products expression was also observed. ICAM-1 and transforming growth factor-β suggest that these signaling components were involved in the anti-inflammatory effect. Our study confirms the anti-inflammatory function of sodium ferulate, and uncovered the potentiating effect of HMGB1 knockdown in suppressing ox-LDL-induced proliferation and migration of hVSMCs. Inhibition of
HMGB1
expression in addition to sodium ferulate treatment might be a more effective therapeutic approach for atherosclerosis.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>25561283</pmid><doi>10.1007/s12013-014-0455-x</doi><tpages>8</tpages></addata></record> |
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| subjects | Anti-Inflammatory Agents - chemistry Apoptosis Atherosclerosis - metabolism Biochemistry Biological and Medical Physics Biomedical and Life Sciences Biophysics Biotechnology Cell Biology Cell Cycle Cell Movement Cell Proliferation Coumaric Acids - chemistry Gene Expression Profiling Gene Expression Regulation Gene Silencing Glycation End Products, Advanced - metabolism HMGB1 Protein - genetics HMGB1 Protein - physiology Humans Inflammation Life Sciences Lipoproteins, LDL - chemistry Muscle, Smooth, Vascular - cytology Myocytes, Smooth Muscle - cytology Myocytes, Smooth Muscle - drug effects Original Paper Pharmacology/Toxicology Phenotype Sodium |
| title | HMGB1 Silencing Potentiates the Anti-inflammatory Effects of Sodium Ferulate in ox-LDL-Stimulated Vascular Smooth Muscle Cells |
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