Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway
Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on...
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| Veröffentlicht in: | Cellular Physiology and Biochemistry 2015-01, Vol.36 (5), p.2039-2050 |
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| creator | Liu, Lei Geng, Jianqiang Zhao, Hongwei Yun, Fengxiang Wang, Xiaoyu Yan, Sen Ding, Xue Li, Wenpeng Wang, Dingyu Li, Jianqiang Pan, Zhenwei Gong, Yongtai Tan, Xiangyang Li, Yue |
| description | Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway. |
| doi_str_mv | 10.1159/000430171 |
| format | Article |
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Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000430171</identifier><identifier>PMID: 26202363</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Angiotensin II ; Angiotensin II receptor blockers ; Animals ; Atrial fibrillation ; Atrial Fibrillation - prevention & control ; Cellular signal transduction ; Dogs ; Female ; Health aspects ; Male ; MAP Kinase Signaling System ; MAPKs ; Neurturin ; Neurturin - metabolism ; Original Paper ; Parasympathetic remodeling ; Patient outcomes ; Prevention ; Protein kinases ; Rats ; Valsartan ; Valsartan - pharmacology</subject><ispartof>Cellular Physiology and Biochemistry, 2015-01, Vol.36 (5), p.2039-2050</ispartof><rights>2015 S. Karger AG, Basel</rights><rights>2015 S. Karger AG, Basel.</rights><rights>COPYRIGHT 2015 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-4866b2e9c06a0d503d533dec842b63faf7be86286e7c58c50652fb0e8cb637ea3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26202363$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Lei</creatorcontrib><creatorcontrib>Geng, Jianqiang</creatorcontrib><creatorcontrib>Zhao, Hongwei</creatorcontrib><creatorcontrib>Yun, Fengxiang</creatorcontrib><creatorcontrib>Wang, Xiaoyu</creatorcontrib><creatorcontrib>Yan, Sen</creatorcontrib><creatorcontrib>Ding, Xue</creatorcontrib><creatorcontrib>Li, Wenpeng</creatorcontrib><creatorcontrib>Wang, Dingyu</creatorcontrib><creatorcontrib>Li, Jianqiang</creatorcontrib><creatorcontrib>Pan, Zhenwei</creatorcontrib><creatorcontrib>Gong, Yongtai</creatorcontrib><creatorcontrib>Tan, Xiangyang</creatorcontrib><creatorcontrib>Li, Yue</creatorcontrib><title>Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway.</description><subject>Angiotensin II</subject><subject>Angiotensin II receptor blockers</subject><subject>Animals</subject><subject>Atrial fibrillation</subject><subject>Atrial Fibrillation - prevention & control</subject><subject>Cellular signal transduction</subject><subject>Dogs</subject><subject>Female</subject><subject>Health aspects</subject><subject>Male</subject><subject>MAP Kinase Signaling System</subject><subject>MAPKs</subject><subject>Neurturin</subject><subject>Neurturin - metabolism</subject><subject>Original Paper</subject><subject>Parasympathetic remodeling</subject><subject>Patient outcomes</subject><subject>Prevention</subject><subject>Protein kinases</subject><subject>Rats</subject><subject>Valsartan</subject><subject>Valsartan - pharmacology</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNptkUtv1DAUhSMEog9YsEcoEhtYpPUjduLldERhRIERr23k2DcZlyQOtqMqe344HtJmhbyw7_V3jo7uTZIXGF1gzMQlQiinCBf4UXKKc4IzURTl4_hGmGWlKIuT5Mz7WxTLQpCnyQnhBBHK6Wny56fsvHRBDulX0JMCnW6CM7JLr03tTNfJYOyQfpu8gjGY2nQmzGk9p7vhEKtghvZBsJdO-rkfZThAMCr69VZDdyTCwdmpPaSfNvuP_vIzTC5MzgxREg53cn6WPGliDHh-f58nP67ffd9-yG6-vN9tNzeZYoiELC85rwkIhbhEmiGqGaUaVJmTmtNGNkUNJSclh0KxMmo4I02NoFTxuwBJz5Pd4qutvK1GZ3rp5spKU_1rWNdWcRRGdVBRLGpRgJYqxzliROBG6UYSXSpgjOvo9WbxGp39PYEPVW_ijOLABrCTrzAXIj_OnkX0YkFbGZ3N0NjgpIpHQ2-UHaAxsb-JGRnCmBwFbxeBctZ7B82aFaPquPFq3XhkX93nmOoe9Eo-rDgCLxfgl3QtuBVY9a__-73dXy1ENeqG_gXX3rx7</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Liu, Lei</creator><creator>Geng, Jianqiang</creator><creator>Zhao, Hongwei</creator><creator>Yun, Fengxiang</creator><creator>Wang, Xiaoyu</creator><creator>Yan, Sen</creator><creator>Ding, Xue</creator><creator>Li, Wenpeng</creator><creator>Wang, Dingyu</creator><creator>Li, Jianqiang</creator><creator>Pan, Zhenwei</creator><creator>Gong, Yongtai</creator><creator>Tan, Xiangyang</creator><creator>Li, Yue</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>IAO</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20150101</creationdate><title>Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway</title><author>Liu, Lei ; Geng, Jianqiang ; Zhao, Hongwei ; Yun, Fengxiang ; Wang, Xiaoyu ; Yan, Sen ; Ding, Xue ; Li, Wenpeng ; Wang, Dingyu ; Li, Jianqiang ; Pan, Zhenwei ; Gong, Yongtai ; Tan, Xiangyang ; Li, Yue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c502t-4866b2e9c06a0d503d533dec842b63faf7be86286e7c58c50652fb0e8cb637ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiotensin II</topic><topic>Angiotensin II receptor blockers</topic><topic>Animals</topic><topic>Atrial fibrillation</topic><topic>Atrial Fibrillation - prevention & control</topic><topic>Cellular signal transduction</topic><topic>Dogs</topic><topic>Female</topic><topic>Health aspects</topic><topic>Male</topic><topic>MAP Kinase Signaling System</topic><topic>MAPKs</topic><topic>Neurturin</topic><topic>Neurturin - metabolism</topic><topic>Original Paper</topic><topic>Parasympathetic remodeling</topic><topic>Patient outcomes</topic><topic>Prevention</topic><topic>Protein kinases</topic><topic>Rats</topic><topic>Valsartan</topic><topic>Valsartan - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Lei</creatorcontrib><creatorcontrib>Geng, Jianqiang</creatorcontrib><creatorcontrib>Zhao, Hongwei</creatorcontrib><creatorcontrib>Yun, Fengxiang</creatorcontrib><creatorcontrib>Wang, Xiaoyu</creatorcontrib><creatorcontrib>Yan, Sen</creatorcontrib><creatorcontrib>Ding, Xue</creatorcontrib><creatorcontrib>Li, Wenpeng</creatorcontrib><creatorcontrib>Wang, Dingyu</creatorcontrib><creatorcontrib>Li, Jianqiang</creatorcontrib><creatorcontrib>Pan, Zhenwei</creatorcontrib><creatorcontrib>Gong, Yongtai</creatorcontrib><creatorcontrib>Tan, Xiangyang</creatorcontrib><creatorcontrib>Li, Yue</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular Physiology and Biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Lei</au><au>Geng, Jianqiang</au><au>Zhao, Hongwei</au><au>Yun, Fengxiang</au><au>Wang, Xiaoyu</au><au>Yan, Sen</au><au>Ding, Xue</au><au>Li, Wenpeng</au><au>Wang, Dingyu</au><au>Li, Jianqiang</au><au>Pan, Zhenwei</au><au>Gong, Yongtai</au><au>Tan, Xiangyang</au><au>Li, Yue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>36</volume><issue>5</issue><spage>2039</spage><epage>2050</epage><pages>2039-2050</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>26202363</pmid><doi>10.1159/000430171</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin II Angiotensin II receptor blockers Animals Atrial fibrillation Atrial Fibrillation - prevention & control Cellular signal transduction Dogs Female Health aspects Male MAP Kinase Signaling System MAPKs Neurturin Neurturin - metabolism Original Paper Parasympathetic remodeling Patient outcomes Prevention Protein kinases Rats Valsartan Valsartan - pharmacology |
| title | Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway |
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