Mechanism of agonistic angiotensin Ⅱ type Ⅰ receptor autoantibody-amplified contractile response to Ang Ⅱ in the isolated rat thoracic aorta
Agonistic autoantibody to the angiotensin Ⅱ type Ⅰ receptor （AT1-AA） is highly associated with preeclampsia by increasing the sensitivity of Ang Ⅱ during pregnancy in rats, thus leading to a preeclampsia-like syndrome. However, the mechanism underlying this phenomenon remains unclear. The purpose of...
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| Veröffentlicht in: | Acta biochimica et biophysica Sinica 2015-10, Vol.47 (10), p.851-856 |
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| creator | Zhang, Wenhui Zheng, Yanqian Liu, Fang Wang, Xiaofang Jin, Zhu Zhi, Jianming |
| description | Agonistic autoantibody to the angiotensin Ⅱ type Ⅰ receptor （AT1-AA） is highly associated with preeclampsia by increasing the sensitivity of Ang Ⅱ during pregnancy in rats, thus leading to a preeclampsia-like syndrome. However, the mechanism underlying this phenomenon remains unclear. The purpose of this study was to observe AT1-AA amplification of Ang Ⅱ-induced vasocon- striction in rat thoracic aortic rings. It was found that exposure to low concentrations of AT1-AA （0.4 nM） caused a contraction of 〈5% of the maximal response to 60 mM KCI. In addition, the Ang Ⅱ-induced contractile response was amplified in the presence of a threshold contraction to AT1- AA, as manifested by a leftward shift of the midpoint of the concentration-response curve with no change in the maximal response. These results showed that preincubation with low AT1-AA could amplify the Ang Ⅱ dose-response curve, and this amplification could be attenuated markedly by 0.1 μM heptapeptide AFHYESQ. In calcium-free Krebs solution, 10 μM of 2-aminoethoxydiphenyl borate （an IP3 receptor inhibitor） both blocked the AT1-AA base contraction and completely abolished the amplification. Both 5 μM of U-73122 （a phospholipase C inhibitor） and 10μM of εV1-2 （an εPKC inhibitor） could partially inhibit the Ang Ⅱ-induced contractile response. εV1-2, but not U-73122, could completely inhibit the amplification response of AT1-AA to Ang Ⅱ. These results suggest that AT1-AA is able to cause amplification response to Ang Ⅱ probably via the calcium-independent protein kinase C pathway, which may provide a new therapy strategy for preeclampsia. |
| doi_str_mv | 10.1093/abbs/gmv088 |
| format | Article |
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However, the mechanism underlying this phenomenon remains unclear. The purpose of this study was to observe AT1-AA amplification of Ang Ⅱ-induced vasocon- striction in rat thoracic aortic rings. It was found that exposure to low concentrations of AT1-AA （0.4 nM） caused a contraction of 〈5% of the maximal response to 60 mM KCI. In addition, the Ang Ⅱ-induced contractile response was amplified in the presence of a threshold contraction to AT1- AA, as manifested by a leftward shift of the midpoint of the concentration-response curve with no change in the maximal response. These results showed that preincubation with low AT1-AA could amplify the Ang Ⅱ dose-response curve, and this amplification could be attenuated markedly by 0.1 μM heptapeptide AFHYESQ. In calcium-free Krebs solution, 10 μM of 2-aminoethoxydiphenyl borate （an IP3 receptor inhibitor） both blocked the AT1-AA base contraction and completely abolished the amplification. Both 5 μM of U-73122 （a phospholipase C inhibitor） and 10μM of εV1-2 （an εPKC inhibitor） could partially inhibit the Ang Ⅱ-induced contractile response. εV1-2, but not U-73122, could completely inhibit the amplification response of AT1-AA to Ang Ⅱ. These results suggest that AT1-AA is able to cause amplification response to Ang Ⅱ probably via the calcium-independent protein kinase C pathway, which may provide a new therapy strategy for preeclampsia.</description><identifier>ISSN: 1672-9145</identifier><identifier>EISSN: 1745-7270</identifier><identifier>DOI: 10.1093/abbs/gmv088</identifier><identifier>PMID: 26350097</identifier><language>eng</language><publisher>China</publisher><subject>Angiotensin II - administration & dosage ; Animals ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - immunology ; Autoantibodies - immunology ; Dose-Response Relationship, Drug ; In Vitro Techniques ; Muscle Contraction - drug effects ; Muscle Contraction - immunology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - immunology ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1 - immunology ; Vasoconstriction - drug effects ; Vasoconstriction - immunology ; 主动脉 ; 受体抑制剂 ; 大鼠 ; 放大 ; 机制 ; 缩反应 ; 自身抗体</subject><ispartof>Acta biochimica et biophysica Sinica, 2015-10, Vol.47 (10), p.851-856</ispartof><rights>The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-784c045d2e70b9e822b6a28eb3f5e84058ee301f937bc4efe43684111d55e9db3</citedby><cites>FETCH-LOGICAL-c386t-784c045d2e70b9e822b6a28eb3f5e84058ee301f937bc4efe43684111d55e9db3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/90160X/90160X.jpg</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26350097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Wenhui</creatorcontrib><creatorcontrib>Zheng, Yanqian</creatorcontrib><creatorcontrib>Liu, Fang</creatorcontrib><creatorcontrib>Wang, Xiaofang</creatorcontrib><creatorcontrib>Jin, Zhu</creatorcontrib><creatorcontrib>Zhi, Jianming</creatorcontrib><title>Mechanism of agonistic angiotensin Ⅱ type Ⅰ receptor autoantibody-amplified contractile response to Ang Ⅱ in the isolated rat thoracic aorta</title><title>Acta biochimica et biophysica Sinica</title><addtitle>Acta Biochimica et Biophysica Sinica</addtitle><description>Agonistic autoantibody to the angiotensin Ⅱ type Ⅰ receptor （AT1-AA） is highly associated with preeclampsia by increasing the sensitivity of Ang Ⅱ during pregnancy in rats, thus leading to a preeclampsia-like syndrome. However, the mechanism underlying this phenomenon remains unclear. The purpose of this study was to observe AT1-AA amplification of Ang Ⅱ-induced vasocon- striction in rat thoracic aortic rings. It was found that exposure to low concentrations of AT1-AA （0.4 nM） caused a contraction of 〈5% of the maximal response to 60 mM KCI. In addition, the Ang Ⅱ-induced contractile response was amplified in the presence of a threshold contraction to AT1- AA, as manifested by a leftward shift of the midpoint of the concentration-response curve with no change in the maximal response. These results showed that preincubation with low AT1-AA could amplify the Ang Ⅱ dose-response curve, and this amplification could be attenuated markedly by 0.1 μM heptapeptide AFHYESQ. In calcium-free Krebs solution, 10 μM of 2-aminoethoxydiphenyl borate （an IP3 receptor inhibitor） both blocked the AT1-AA base contraction and completely abolished the amplification. Both 5 μM of U-73122 （a phospholipase C inhibitor） and 10μM of εV1-2 （an εPKC inhibitor） could partially inhibit the Ang Ⅱ-induced contractile response. εV1-2, but not U-73122, could completely inhibit the amplification response of AT1-AA to Ang Ⅱ. These results suggest that AT1-AA is able to cause amplification response to Ang Ⅱ probably via the calcium-independent protein kinase C pathway, which may provide a new therapy strategy for preeclampsia.</description><subject>Angiotensin II - administration & dosage</subject><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - immunology</subject><subject>Autoantibodies - immunology</subject><subject>Dose-Response Relationship, Drug</subject><subject>In Vitro Techniques</subject><subject>Muscle Contraction - drug effects</subject><subject>Muscle Contraction - immunology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - immunology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Angiotensin, Type 1 - immunology</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstriction - immunology</subject><subject>主动脉</subject><subject>受体抑制剂</subject><subject>大鼠</subject><subject>放大</subject><subject>机制</subject><subject>缩反应</subject><subject>自身抗体</subject><issn>1672-9145</issn><issn>1745-7270</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtuFDEQhluIiITAij2yWCGhTvy2exlFvKREbGDdst3VPUbddsf2RJoDcAFOAFfjJHiYIdus6lfpq68Wf9O8IviC4I5dGmvz5bTcY62fNGdEcdEqqvDTmqWibUe4OG2e5_wdYyYlwc-aUyqZwLhTZ83PW3AbE3xeUByRmWKNxTtkwuRjgZB9QH9-_EZlt0INv1ACB2uJCZltiSYUb-Owa82yzn70MCAXQ0nGFT9DZfMaQwZUIroK0z9R9ZUNIJ_jbErlkyl1EevJ_mtMxbxoTkYzZ3h5nOfNtw_vv15_am--fPx8fXXTOqZlaZXmDnMxUFDYdqAptdJQDZaNAjTHQgMwTMaOKes4jMCZ1JwQMggB3WDZefP24F1TvNtCLv3is4N5NgHiNvdEU9ZxUs8eRxWRHceYsIq-O6AuxZwTjP2a_GLSrie43_fV7_vqD31V-vVRvLULDA_s_4Iq8Oao28Qw3fkwPTBSSiUokZr9Bf3-opg</recordid><startdate>20151001</startdate><enddate>20151001</enddate><creator>Zhang, Wenhui</creator><creator>Zheng, Yanqian</creator><creator>Liu, Fang</creator><creator>Wang, Xiaofang</creator><creator>Jin, Zhu</creator><creator>Zhi, Jianming</creator><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</scope><scope>~WA</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>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20151001</creationdate><title>Mechanism of agonistic angiotensin Ⅱ type Ⅰ receptor autoantibody-amplified contractile response to Ang Ⅱ in the isolated rat thoracic aorta</title><author>Zhang, Wenhui ; Zheng, Yanqian ; Liu, Fang ; Wang, Xiaofang ; Jin, Zhu ; Zhi, Jianming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-784c045d2e70b9e822b6a28eb3f5e84058ee301f937bc4efe43684111d55e9db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiotensin II - administration & dosage</topic><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - immunology</topic><topic>Autoantibodies - immunology</topic><topic>Dose-Response Relationship, Drug</topic><topic>In Vitro Techniques</topic><topic>Muscle Contraction - drug effects</topic><topic>Muscle Contraction - immunology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - immunology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Angiotensin, Type 1 - immunology</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstriction - immunology</topic><topic>主动脉</topic><topic>受体抑制剂</topic><topic>大鼠</topic><topic>放大</topic><topic>机制</topic><topic>缩反应</topic><topic>自身抗体</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Wenhui</creatorcontrib><creatorcontrib>Zheng, Yanqian</creatorcontrib><creatorcontrib>Liu, Fang</creatorcontrib><creatorcontrib>Wang, Xiaofang</creatorcontrib><creatorcontrib>Jin, Zhu</creatorcontrib><creatorcontrib>Zhi, Jianming</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-自然科学</collection><collection>中文科技期刊数据库-自然科学-生物科学</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Acta biochimica et biophysica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Wenhui</au><au>Zheng, Yanqian</au><au>Liu, Fang</au><au>Wang, Xiaofang</au><au>Jin, Zhu</au><au>Zhi, Jianming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism of agonistic angiotensin Ⅱ type Ⅰ receptor autoantibody-amplified contractile response to Ang Ⅱ in the isolated rat thoracic aorta</atitle><jtitle>Acta biochimica et biophysica Sinica</jtitle><addtitle>Acta Biochimica et Biophysica Sinica</addtitle><date>2015-10-01</date><risdate>2015</risdate><volume>47</volume><issue>10</issue><spage>851</spage><epage>856</epage><pages>851-856</pages><issn>1672-9145</issn><eissn>1745-7270</eissn><abstract>Agonistic autoantibody to the angiotensin Ⅱ type Ⅰ receptor （AT1-AA） is highly associated with preeclampsia by increasing the sensitivity of Ang Ⅱ during pregnancy in rats, thus leading to a preeclampsia-like syndrome. However, the mechanism underlying this phenomenon remains unclear. The purpose of this study was to observe AT1-AA amplification of Ang Ⅱ-induced vasocon- striction in rat thoracic aortic rings. It was found that exposure to low concentrations of AT1-AA （0.4 nM） caused a contraction of 〈5% of the maximal response to 60 mM KCI. In addition, the Ang Ⅱ-induced contractile response was amplified in the presence of a threshold contraction to AT1- AA, as manifested by a leftward shift of the midpoint of the concentration-response curve with no change in the maximal response. These results showed that preincubation with low AT1-AA could amplify the Ang Ⅱ dose-response curve, and this amplification could be attenuated markedly by 0.1 μM heptapeptide AFHYESQ. In calcium-free Krebs solution, 10 μM of 2-aminoethoxydiphenyl borate （an IP3 receptor inhibitor） both blocked the AT1-AA base contraction and completely abolished the amplification. Both 5 μM of U-73122 （a phospholipase C inhibitor） and 10μM of εV1-2 （an εPKC inhibitor） could partially inhibit the Ang Ⅱ-induced contractile response. εV1-2, but not U-73122, could completely inhibit the amplification response of AT1-AA to Ang Ⅱ. These results suggest that AT1-AA is able to cause amplification response to Ang Ⅱ probably via the calcium-independent protein kinase C pathway, which may provide a new therapy strategy for preeclampsia.</abstract><cop>China</cop><pmid>26350097</pmid><doi>10.1093/abbs/gmv088</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin II - administration & dosage Animals Aorta, Thoracic - drug effects Aorta, Thoracic - immunology Autoantibodies - immunology Dose-Response Relationship, Drug In Vitro Techniques Muscle Contraction - drug effects Muscle Contraction - immunology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - immunology Rats Rats, Wistar Receptor, Angiotensin, Type 1 - immunology Vasoconstriction - drug effects Vasoconstriction - immunology 主动脉 受体抑制剂 大鼠 放大 机制 缩反应 自身抗体 |
| title | Mechanism of agonistic angiotensin Ⅱ type Ⅰ receptor autoantibody-amplified contractile response to Ang Ⅱ in the isolated rat thoracic aorta |
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