Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease
The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR − ...
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| Veröffentlicht in: | Journal of cardiovascular translational research 2015-12, Vol.8 (9), p.554-566 |
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| creator | Horgan, Stephen J. Watson, Chris J. Glezeva, Nadia Collier, Pat Neary, Roisin Tea, Isaac J. Corrigan, Niamh Ledwidge, Mark McDonald, Ken Baugh, John A. |
| description | The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR − SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (
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| doi_str_mv | 10.1007/s12265-015-9661-1 |
| format | Article |
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p
< 0.01), perivascular collagen (
p
< 0.01), and cardiomyocyte size (
p
< 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (
p
< 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.</description><identifier>ISSN: 1937-5387</identifier><identifier>EISSN: 1937-5395</identifier><identifier>DOI: 10.1007/s12265-015-9661-1</identifier><identifier>PMID: 26577946</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biomedical Engineering and Bioengineering ; Biomedicine ; Biopsy, Needle ; Cardiology ; Cells, Cultured ; Disease Models, Animal ; Human Genetics ; Humans ; Hypertension - complications ; Hypertension - drug therapy ; Hypertension - physiopathology ; Hypertrophy, Left Ventricular - drug therapy ; Hypertrophy, Left Ventricular - etiology ; Hypertrophy, Left Ventricular - pathology ; Immunohistochemistry ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Medicine ; Medicine & Public Health ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Random Allocation ; Rats, Inbred SHR ; Rats, Inbred WKY ; Reference Values ; Serum Amyloid P-Component - administration & dosage ; Ventricular Remodeling - drug effects</subject><ispartof>Journal of cardiovascular translational research, 2015-12, Vol.8 (9), p.554-566</ispartof><rights>Springer Science+Business Media New York 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c344t-e10fc3a772917e3e212b072295f05e513f1e03a893a434eae37cf9a579ddc6b33</citedby><cites>FETCH-LOGICAL-c344t-e10fc3a772917e3e212b072295f05e513f1e03a893a434eae37cf9a579ddc6b33</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/s12265-015-9661-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12265-015-9661-1$$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/26577946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Horgan, Stephen J.</creatorcontrib><creatorcontrib>Watson, Chris J.</creatorcontrib><creatorcontrib>Glezeva, Nadia</creatorcontrib><creatorcontrib>Collier, Pat</creatorcontrib><creatorcontrib>Neary, Roisin</creatorcontrib><creatorcontrib>Tea, Isaac J.</creatorcontrib><creatorcontrib>Corrigan, Niamh</creatorcontrib><creatorcontrib>Ledwidge, Mark</creatorcontrib><creatorcontrib>McDonald, Ken</creatorcontrib><creatorcontrib>Baugh, John A.</creatorcontrib><title>Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease</title><title>Journal of cardiovascular translational research</title><addtitle>J. of Cardiovasc. Trans. Res</addtitle><addtitle>J Cardiovasc Transl Res</addtitle><description>The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR − SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (
p
< 0.01), perivascular collagen (
p
< 0.01), and cardiomyocyte size (
p
< 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (
p
< 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.</description><subject>Animals</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Biomedicine</subject><subject>Biopsy, Needle</subject><subject>Cardiology</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hypertension - complications</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Hypertrophy, Left Ventricular - drug therapy</subject><subject>Hypertrophy, Left Ventricular - etiology</subject><subject>Hypertrophy, Left Ventricular - pathology</subject><subject>Immunohistochemistry</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Random Allocation</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Reference Values</subject><subject>Serum Amyloid P-Component - administration & dosage</subject><subject>Ventricular Remodeling - drug effects</subject><issn>1937-5387</issn><issn>1937-5395</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LAzEQhoMotlZ_gBfJ0ctqJtlsmmOpHxUKFqvnkO7OlpT9Mtkt9N-7ZatHTzMwz_vCPITcAnsAxtRjAM4TGTGQkU4SiOCMjEELFUmh5fnfPlUjchXCjrGEM6UuyahPKaXjZEzWa_RdSWfloahdRlfRvC6busKqpSuP-34GOrc-czalH1jWGRau2lJX0cWhQd9iFdwe6QKtb-mTC2gDXpOL3BYBb05zQr5enj_ni2j5_vo2ny2jVMRxGyGwPBVWKa5BoUAOfMMU51rmTKIEkQMyYada2FjEaFGoNNdWKp1labIRYkLuh97G198dhtaULqRYFLbCugsGVKyEgFgcURjQ1NcheMxN411p_cEAM0eXZnBpepfm6NJAn7k71XebErO_xK-8HuADEPpTtUVvdnXnq_7lf1p_AAiDfp4</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Horgan, Stephen J.</creator><creator>Watson, Chris J.</creator><creator>Glezeva, Nadia</creator><creator>Collier, Pat</creator><creator>Neary, Roisin</creator><creator>Tea, Isaac J.</creator><creator>Corrigan, Niamh</creator><creator>Ledwidge, Mark</creator><creator>McDonald, Ken</creator><creator>Baugh, John A.</creator><general>Springer US</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>7X8</scope></search><sort><creationdate>20151201</creationdate><title>Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease</title><author>Horgan, Stephen J. ; Watson, Chris J. ; Glezeva, Nadia ; Collier, Pat ; Neary, Roisin ; Tea, Isaac J. ; Corrigan, Niamh ; Ledwidge, Mark ; McDonald, Ken ; Baugh, John A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c344t-e10fc3a772917e3e212b072295f05e513f1e03a893a434eae37cf9a579ddc6b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Biomedicine</topic><topic>Biopsy, Needle</topic><topic>Cardiology</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Hypertension - complications</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - physiopathology</topic><topic>Hypertrophy, Left Ventricular - drug therapy</topic><topic>Hypertrophy, Left Ventricular - etiology</topic><topic>Hypertrophy, Left Ventricular - pathology</topic><topic>Immunohistochemistry</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Random Allocation</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Reference Values</topic><topic>Serum Amyloid P-Component - administration & dosage</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Horgan, Stephen J.</creatorcontrib><creatorcontrib>Watson, Chris J.</creatorcontrib><creatorcontrib>Glezeva, Nadia</creatorcontrib><creatorcontrib>Collier, Pat</creatorcontrib><creatorcontrib>Neary, Roisin</creatorcontrib><creatorcontrib>Tea, Isaac J.</creatorcontrib><creatorcontrib>Corrigan, Niamh</creatorcontrib><creatorcontrib>Ledwidge, Mark</creatorcontrib><creatorcontrib>McDonald, Ken</creatorcontrib><creatorcontrib>Baugh, John A.</creatorcontrib><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><jtitle>Journal of cardiovascular translational research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Horgan, Stephen J.</au><au>Watson, Chris J.</au><au>Glezeva, Nadia</au><au>Collier, Pat</au><au>Neary, Roisin</au><au>Tea, Isaac J.</au><au>Corrigan, Niamh</au><au>Ledwidge, Mark</au><au>McDonald, Ken</au><au>Baugh, John A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease</atitle><jtitle>Journal of cardiovascular translational research</jtitle><stitle>J. of Cardiovasc. Trans. Res</stitle><addtitle>J Cardiovasc Transl Res</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>8</volume><issue>9</issue><spage>554</spage><epage>566</epage><pages>554-566</pages><issn>1937-5387</issn><eissn>1937-5395</eissn><abstract>The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR − SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (
p
< 0.01), perivascular collagen (
p
< 0.01), and cardiomyocyte size (
p
< 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (
p
< 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26577946</pmid><doi>10.1007/s12265-015-9661-1</doi><tpages>13</tpages></addata></record> |
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| subjects | Animals Biomedical Engineering and Bioengineering Biomedicine Biopsy, Needle Cardiology Cells, Cultured Disease Models, Animal Human Genetics Humans Hypertension - complications Hypertension - drug therapy Hypertension - physiopathology Hypertrophy, Left Ventricular - drug therapy Hypertrophy, Left Ventricular - etiology Hypertrophy, Left Ventricular - pathology Immunohistochemistry Macrophages - drug effects Macrophages - metabolism Male Medicine Medicine & Public Health Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Random Allocation Rats, Inbred SHR Rats, Inbred WKY Reference Values Serum Amyloid P-Component - administration & dosage Ventricular Remodeling - drug effects |
| title | Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease |
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