Increased expression of calpain and elevated activity of calcineurin in the myocardium of patients with congestive heart failure
The angiotensin (Ang) II/Ang II receptor (ATR)- associated calcium signaling pathway is the major cause of ventricular remodelling in patients with congestive heart failure (CHF). However, the calcium-regulated proteinases responsible for Ang II-induced remodelling are not well understood. We invest...
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| Veröffentlicht in: | International journal of molecular medicine 2010-07, Vol.26 (1), p.159-164 |
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| container_title | International journal of molecular medicine |
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| creator | Yang, Dachun Ma, Shuangtao Tan, Yan Li, De Tang, Bing Zhang, Xin Sun, Meiqin Yang, Yongjian |
| description | The angiotensin (Ang) II/Ang II receptor (ATR)- associated calcium signaling
pathway is the major cause of ventricular remodelling in patients with congestive
heart failure (CHF). However, the calcium-regulated proteinases responsible for
Ang II-induced remodelling are not well understood. We investigated the profiles
of the Ang II/ATR/calpain/calcineurin (CaN) pathway in human failing heart. We
measured both the plasma and cardiac levels of Ang II and cardiac mRNA expression
of ATR in 39 patients with CHF and 38 healthy controls. Importantly, protein expression
of calpains, cleavage of cain/cabin1 and activity of CaN were tested. Both plasma
and cardiac levels of Ang II were significantly increased in patients with CHF
(both p |
| doi_str_mv | 10.3892/ijmm_00000448 |
| format | Article |
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pathway is the major cause of ventricular remodelling in patients with congestive
heart failure (CHF). However, the calcium-regulated proteinases responsible for
Ang II-induced remodelling are not well understood. We investigated the profiles
of the Ang II/ATR/calpain/calcineurin (CaN) pathway in human failing heart. We
measured both the plasma and cardiac levels of Ang II and cardiac mRNA expression
of ATR in 39 patients with CHF and 38 healthy controls. Importantly, protein expression
of calpains, cleavage of cain/cabin1 and activity of CaN were tested. Both plasma
and cardiac levels of Ang II were significantly increased in patients with CHF
(both p<0.01), and the plasma Ang II concentration was closely correlated with
the parameters of ventricular remodelling (r=±0.29-0.65, p<0.05 or <0.01).
In addition, the cardiac level of AT1R but not AT2R was significantly upregulated
in mild failing hearts (p<0.05) but dramatically downregulated in severe failing
ones (p<0.01). CHF was associated with a marked upregulation of calpains, an
increased cleavage of cain/cabin1, and the activation of CaN in the failing ventricular
tissue. In patients with CHF, calpain upregulation was associated with an increase
in cleavage of cain/cabin1 and the activation of CaN, indicating that these changes
in calcium-regulated proteinases contribute to Ang II-induced cardiac remodelling.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm_00000448</identifier><identifier>PMID: 20514436</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adult ; Angiotensin II - blood ; Angiotensin II - metabolism ; Blotting, Western ; Calcineurin - metabolism ; Calpain - biosynthesis ; Calpain - metabolism ; Female ; Gene Expression Profiling ; Heart Failure - blood ; Heart Failure - genetics ; Heart Failure - metabolism ; Humans ; Male ; Middle Aged ; Myocardium - metabolism ; Myocardium - pathology ; Radioimmunoassay ; Receptor, Angiotensin, Type 1 - genetics ; Receptor, Angiotensin, Type 2 - genetics ; Reverse Transcriptase Polymerase Chain Reaction</subject><ispartof>International journal of molecular medicine, 2010-07, Vol.26 (1), p.159-164</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c335t-37441bc67404b74f7b7d7c16de724f4d7f6b823c39512d808062c1fac65818c33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,5573,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20514436$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Dachun</creatorcontrib><creatorcontrib>Ma, Shuangtao</creatorcontrib><creatorcontrib>Tan, Yan</creatorcontrib><creatorcontrib>Li, De</creatorcontrib><creatorcontrib>Tang, Bing</creatorcontrib><creatorcontrib>Zhang, Xin</creatorcontrib><creatorcontrib>Sun, Meiqin</creatorcontrib><creatorcontrib>Yang, Yongjian</creatorcontrib><title>Increased expression of calpain and elevated activity of calcineurin in the myocardium of patients with congestive heart failure</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>The angiotensin (Ang) II/Ang II receptor (ATR)- associated calcium signaling
pathway is the major cause of ventricular remodelling in patients with congestive
heart failure (CHF). However, the calcium-regulated proteinases responsible for
Ang II-induced remodelling are not well understood. We investigated the profiles
of the Ang II/ATR/calpain/calcineurin (CaN) pathway in human failing heart. We
measured both the plasma and cardiac levels of Ang II and cardiac mRNA expression
of ATR in 39 patients with CHF and 38 healthy controls. Importantly, protein expression
of calpains, cleavage of cain/cabin1 and activity of CaN were tested. Both plasma
and cardiac levels of Ang II were significantly increased in patients with CHF
(both p<0.01), and the plasma Ang II concentration was closely correlated with
the parameters of ventricular remodelling (r=±0.29-0.65, p<0.05 or <0.01).
In addition, the cardiac level of AT1R but not AT2R was significantly upregulated
in mild failing hearts (p<0.05) but dramatically downregulated in severe failing
ones (p<0.01). CHF was associated with a marked upregulation of calpains, an
increased cleavage of cain/cabin1, and the activation of CaN in the failing ventricular
tissue. In patients with CHF, calpain upregulation was associated with an increase
in cleavage of cain/cabin1 and the activation of CaN, indicating that these changes
in calcium-regulated proteinases contribute to Ang II-induced cardiac remodelling.</description><subject>Adult</subject><subject>Angiotensin II - blood</subject><subject>Angiotensin II - metabolism</subject><subject>Blotting, Western</subject><subject>Calcineurin - metabolism</subject><subject>Calpain - biosynthesis</subject><subject>Calpain - metabolism</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - genetics</subject><subject>Heart Failure - metabolism</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Radioimmunoassay</subject><subject>Receptor, Angiotensin, Type 1 - genetics</subject><subject>Receptor, Angiotensin, Type 2 - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkMtLAzEQh4MotlaPXiV3Wc1rk92jFB8FwYuCtyWbh03ZF0m22pt_uiltFcNABuabH8wHwCVGN7Qoya1btW2Fto-x4ghMsShxRhh7P049RiKjIucTcBbCCiGSs7I4BROCcswY5VPwveiUNzIYDc3X4E0Iru9gb6GSzSBdB2WXJo1Zy5gQqaJbu7jZA8p1ZvQJShWXBrabXkmv3dhugUFGZ7oY4KeLS6j67sOEtG7g0kgfoZWuGb05BydWNsFc7P8ZeHu4f50_Zc8vj4v53XOmKM1juoIxXCsuGGK1YFbUQguFuTaCMMu0sLwuCFW0zDHRBSoQJwpbqXhe4CJlzEC2y1W-D8EbWw3etdJvKoyqrcnqn8nEX-34Yaxbo3_pg7oEXO-AMCRHTvfhL_HgnXCM8xJzRn8AU7t_Mg</recordid><startdate>20100701</startdate><enddate>20100701</enddate><creator>Yang, Dachun</creator><creator>Ma, Shuangtao</creator><creator>Tan, Yan</creator><creator>Li, De</creator><creator>Tang, Bing</creator><creator>Zhang, Xin</creator><creator>Sun, Meiqin</creator><creator>Yang, Yongjian</creator><general>D.A. Spandidos</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></search><sort><creationdate>20100701</creationdate><title>Increased expression of calpain and elevated activity of calcineurin in the myocardium of patients with congestive heart failure</title><author>Yang, Dachun ; Ma, Shuangtao ; Tan, Yan ; Li, De ; Tang, Bing ; Zhang, Xin ; Sun, Meiqin ; Yang, Yongjian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c335t-37441bc67404b74f7b7d7c16de724f4d7f6b823c39512d808062c1fac65818c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Angiotensin II - blood</topic><topic>Angiotensin II - metabolism</topic><topic>Blotting, Western</topic><topic>Calcineurin - metabolism</topic><topic>Calpain - biosynthesis</topic><topic>Calpain - metabolism</topic><topic>Female</topic><topic>Gene Expression Profiling</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - genetics</topic><topic>Heart Failure - metabolism</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Radioimmunoassay</topic><topic>Receptor, Angiotensin, Type 1 - genetics</topic><topic>Receptor, Angiotensin, Type 2 - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Dachun</creatorcontrib><creatorcontrib>Ma, Shuangtao</creatorcontrib><creatorcontrib>Tan, Yan</creatorcontrib><creatorcontrib>Li, De</creatorcontrib><creatorcontrib>Tang, Bing</creatorcontrib><creatorcontrib>Zhang, Xin</creatorcontrib><creatorcontrib>Sun, Meiqin</creatorcontrib><creatorcontrib>Yang, Yongjian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Dachun</au><au>Ma, Shuangtao</au><au>Tan, Yan</au><au>Li, De</au><au>Tang, Bing</au><au>Zhang, Xin</au><au>Sun, Meiqin</au><au>Yang, Yongjian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased expression of calpain and elevated activity of calcineurin in the myocardium of patients with congestive heart failure</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2010-07-01</date><risdate>2010</risdate><volume>26</volume><issue>1</issue><spage>159</spage><epage>164</epage><pages>159-164</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>The angiotensin (Ang) II/Ang II receptor (ATR)- associated calcium signaling
pathway is the major cause of ventricular remodelling in patients with congestive
heart failure (CHF). However, the calcium-regulated proteinases responsible for
Ang II-induced remodelling are not well understood. We investigated the profiles
of the Ang II/ATR/calpain/calcineurin (CaN) pathway in human failing heart. We
measured both the plasma and cardiac levels of Ang II and cardiac mRNA expression
of ATR in 39 patients with CHF and 38 healthy controls. Importantly, protein expression
of calpains, cleavage of cain/cabin1 and activity of CaN were tested. Both plasma
and cardiac levels of Ang II were significantly increased in patients with CHF
(both p<0.01), and the plasma Ang II concentration was closely correlated with
the parameters of ventricular remodelling (r=±0.29-0.65, p<0.05 or <0.01).
In addition, the cardiac level of AT1R but not AT2R was significantly upregulated
in mild failing hearts (p<0.05) but dramatically downregulated in severe failing
ones (p<0.01). CHF was associated with a marked upregulation of calpains, an
increased cleavage of cain/cabin1, and the activation of CaN in the failing ventricular
tissue. In patients with CHF, calpain upregulation was associated with an increase
in cleavage of cain/cabin1 and the activation of CaN, indicating that these changes
in calcium-regulated proteinases contribute to Ang II-induced cardiac remodelling.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>20514436</pmid><doi>10.3892/ijmm_00000448</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1107-3756 1791-244X |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adult Angiotensin II - blood Angiotensin II - metabolism Blotting, Western Calcineurin - metabolism Calpain - biosynthesis Calpain - metabolism Female Gene Expression Profiling Heart Failure - blood Heart Failure - genetics Heart Failure - metabolism Humans Male Middle Aged Myocardium - metabolism Myocardium - pathology Radioimmunoassay Receptor, Angiotensin, Type 1 - genetics Receptor, Angiotensin, Type 2 - genetics Reverse Transcriptase Polymerase Chain Reaction |
| title | Increased expression of calpain and elevated activity of calcineurin in the myocardium of patients with congestive heart failure |
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