Role of Glutaraldehyde in Calcification of Porcine Aortic Valve Fibroblasts
Glutaraldehyde-treated porcine aortic valve xenografts frequently fail due to calcification. Calcification in the prostheses begins intracellularly. In a previous study, various types of cell injury to canine valvular fibroblasts, including glutaraldehyde treatment, led to calcification. An influx o...
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| Veröffentlicht in: | The American journal of pathology 1999-03, Vol.154 (3), p.843-852 |
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| creator | Kim, Kookmin M. Herrera, Guillermo A. Battarbee, Harold D. |
| description | Glutaraldehyde-treated porcine aortic valve xenografts frequently fail due to calcification. Calcification in the prostheses begins intracellularly. In a previous study, various types of cell injury to canine valvular fibroblasts, including glutaraldehyde treatment, led to calcification. An influx of extracellular Ca
2+ into the phosphate-rich cytosol was theorized to be the mechanism of calcification. To test the Ca
2+ influx theory, cytosolic Ca
2+ and P
i concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied. Glutaraldehyde caused an immediate and sustained massive cytosolic Ca
2+ increase that was dose dependent and a several-fold increase in P
i. Calcification of cells followed within a week. The earliest calcification was observed in blebs formed on glutaraldehyde-treated cells. Live control cells or cells fixed with glutaraldehyde in Ca
2+-free solution did not calcify under the same conditions. Concomitant increases in Ca
2+ and P
i in glutaraldehyde-treated cells appear to underlie the mechanism of calcification, and the presence of extracellular Ca
2+ during glutaraldehyde fixation promotes calcification. |
| doi_str_mv | 10.1016/S0002-9440(10)65331-X |
| format | Article |
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2+ into the phosphate-rich cytosol was theorized to be the mechanism of calcification. To test the Ca
2+ influx theory, cytosolic Ca
2+ and P
i concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied. Glutaraldehyde caused an immediate and sustained massive cytosolic Ca
2+ increase that was dose dependent and a several-fold increase in P
i. Calcification of cells followed within a week. The earliest calcification was observed in blebs formed on glutaraldehyde-treated cells. Live control cells or cells fixed with glutaraldehyde in Ca
2+-free solution did not calcify under the same conditions. Concomitant increases in Ca
2+ and P
i in glutaraldehyde-treated cells appear to underlie the mechanism of calcification, and the presence of extracellular Ca
2+ during glutaraldehyde fixation promotes calcification.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>DOI: 10.1016/S0002-9440(10)65331-X</identifier><identifier>PMID: 10079262</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: Elsevier Inc</publisher><subject>Animals ; Aortic Valve - drug effects ; Aortic Valve - metabolism ; Aortic Valve - pathology ; Aortic Valve - physiopathology ; Biological and medical sciences ; Calcinosis - chemically induced ; Calcinosis - metabolism ; Calcinosis - pathology ; Calcinosis - physiopathology ; Calcium - metabolism ; Cardiology. Vascular system ; Cells, Cultured ; Cytosol - metabolism ; Dose-Response Relationship, Drug ; Endocardial and cardiac valvular diseases ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Fibroblasts - pathology ; Fibroblasts - physiology ; Glutaral - metabolism ; Glutaral - pharmacology ; Heart ; In Vitro Techniques ; Medical sciences ; Microscopy, Electron ; Phosphates - metabolism ; Regular</subject><ispartof>The American journal of pathology, 1999-03, Vol.154 (3), p.843-852</ispartof><rights>1999 American Society for Investigative Pathology</rights><rights>1999 INIST-CNRS</rights><rights>Copyright American Society for Investigative Pathology Mar 1999</rights><rights>Copyright © 1999, American Society for Investigative Pathology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c550t-9f57db07c9bbda4085056523e1c0a7d6ae1d59605ec30ada6b305ac6efa7f4a73</citedby><cites>FETCH-LOGICAL-c550t-9f57db07c9bbda4085056523e1c0a7d6ae1d59605ec30ada6b305ac6efa7f4a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1866403/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0002-9440(10)65331-X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,3550,27924,27925,45995,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1711760$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10079262$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Kookmin M.</creatorcontrib><creatorcontrib>Herrera, Guillermo A.</creatorcontrib><creatorcontrib>Battarbee, Harold D.</creatorcontrib><title>Role of Glutaraldehyde in Calcification of Porcine Aortic Valve Fibroblasts</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>Glutaraldehyde-treated porcine aortic valve xenografts frequently fail due to calcification. Calcification in the prostheses begins intracellularly. In a previous study, various types of cell injury to canine valvular fibroblasts, including glutaraldehyde treatment, led to calcification. An influx of extracellular Ca
2+ into the phosphate-rich cytosol was theorized to be the mechanism of calcification. To test the Ca
2+ influx theory, cytosolic Ca
2+ and P
i concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied. Glutaraldehyde caused an immediate and sustained massive cytosolic Ca
2+ increase that was dose dependent and a several-fold increase in P
i. Calcification of cells followed within a week. The earliest calcification was observed in blebs formed on glutaraldehyde-treated cells. Live control cells or cells fixed with glutaraldehyde in Ca
2+-free solution did not calcify under the same conditions. Concomitant increases in Ca
2+ and P
i in glutaraldehyde-treated cells appear to underlie the mechanism of calcification, and the presence of extracellular Ca
2+ during glutaraldehyde fixation promotes calcification.</description><subject>Animals</subject><subject>Aortic Valve - drug effects</subject><subject>Aortic Valve - metabolism</subject><subject>Aortic Valve - pathology</subject><subject>Aortic Valve - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Calcinosis - chemically induced</subject><subject>Calcinosis - metabolism</subject><subject>Calcinosis - pathology</subject><subject>Calcinosis - physiopathology</subject><subject>Calcium - metabolism</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Cytosol - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endocardial and cardiac valvular diseases</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - pathology</subject><subject>Fibroblasts - physiology</subject><subject>Glutaral - metabolism</subject><subject>Glutaral - pharmacology</subject><subject>Heart</subject><subject>In Vitro Techniques</subject><subject>Medical sciences</subject><subject>Microscopy, Electron</subject><subject>Phosphates - metabolism</subject><subject>Regular</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</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>eNqFkc1u1DAUhS0EokPhEUARQggWgeskdpJNUTWiBVEJxJ-6s27sm45HnniwM4P69jjNqJQVK8v2d46Pz2XsKYc3HLh8-w0AirytKnjF4bUUZcnzy3tswUUh8oK3_D5b3CJH7FGM67SVZQMP2REHqNtCFgv26at3lPk-O3e7EQM6Q6trQ5kdsiU6bXurcbR-mJAvPmg7UHbqw2h19hPdnrIz2wXfOYxjfMwe9OgiPTmsx-zH2fvvyw_5xefzj8vTi1wLAWPe9qI2HdS67TqDFTQChBRFSVwD1kYicSNaCYJ0CWhQdiUI1JJ6rPsK6_KYncy-2123IaNpGFNwtQ12g-FaebTq35vBrtSV3yveSFlBmQyeHwyC_7WjOKq134UhZVYFb1pZtyASJGZIBx9joP72AQ5qGoG6GYGa-p2ObkagLpPu2d10d1Rz5wl4cQAwanR9wEHb-JerOa8lJOzljK3s1eq3DaTiBp1LrlzhestFpUrVVNNv3s0gpc73loKK2tKgySSRHpXx9j-R_wAAELDe</recordid><startdate>19990301</startdate><enddate>19990301</enddate><creator>Kim, Kookmin M.</creator><creator>Herrera, Guillermo A.</creator><creator>Battarbee, Harold D.</creator><general>Elsevier Inc</general><general>ASIP</general><general>American Society for Investigative Pathology</general><scope>IQODW</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8C1</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>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>19990301</creationdate><title>Role of Glutaraldehyde in Calcification of Porcine Aortic Valve Fibroblasts</title><author>Kim, Kookmin M. ; Herrera, Guillermo A. ; Battarbee, Harold D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c550t-9f57db07c9bbda4085056523e1c0a7d6ae1d59605ec30ada6b305ac6efa7f4a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Aortic Valve - drug effects</topic><topic>Aortic Valve - metabolism</topic><topic>Aortic Valve - pathology</topic><topic>Aortic Valve - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Calcinosis - chemically induced</topic><topic>Calcinosis - metabolism</topic><topic>Calcinosis - pathology</topic><topic>Calcinosis - physiopathology</topic><topic>Calcium - metabolism</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Cytosol - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endocardial and cardiac valvular diseases</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - pathology</topic><topic>Fibroblasts - physiology</topic><topic>Glutaral - metabolism</topic><topic>Glutaral - pharmacology</topic><topic>Heart</topic><topic>In Vitro Techniques</topic><topic>Medical sciences</topic><topic>Microscopy, Electron</topic><topic>Phosphates - metabolism</topic><topic>Regular</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Kookmin M.</creatorcontrib><creatorcontrib>Herrera, Guillermo A.</creatorcontrib><creatorcontrib>Battarbee, Harold D.</creatorcontrib><collection>Pascal-Francis</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Public Health 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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The American journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Kookmin M.</au><au>Herrera, Guillermo A.</au><au>Battarbee, Harold D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Glutaraldehyde in Calcification of Porcine Aortic Valve Fibroblasts</atitle><jtitle>The American journal of pathology</jtitle><addtitle>Am J Pathol</addtitle><date>1999-03-01</date><risdate>1999</risdate><volume>154</volume><issue>3</issue><spage>843</spage><epage>852</epage><pages>843-852</pages><issn>0002-9440</issn><eissn>1525-2191</eissn><coden>AJPAA4</coden><abstract>Glutaraldehyde-treated porcine aortic valve xenografts frequently fail due to calcification. Calcification in the prostheses begins intracellularly. In a previous study, various types of cell injury to canine valvular fibroblasts, including glutaraldehyde treatment, led to calcification. An influx of extracellular Ca
2+ into the phosphate-rich cytosol was theorized to be the mechanism of calcification. To test the Ca
2+ influx theory, cytosolic Ca
2+ and P
i concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied. Glutaraldehyde caused an immediate and sustained massive cytosolic Ca
2+ increase that was dose dependent and a several-fold increase in P
i. Calcification of cells followed within a week. The earliest calcification was observed in blebs formed on glutaraldehyde-treated cells. Live control cells or cells fixed with glutaraldehyde in Ca
2+-free solution did not calcify under the same conditions. Concomitant increases in Ca
2+ and P
i in glutaraldehyde-treated cells appear to underlie the mechanism of calcification, and the presence of extracellular Ca
2+ during glutaraldehyde fixation promotes calcification.</abstract><cop>Bethesda, MD</cop><pub>Elsevier Inc</pub><pmid>10079262</pmid><doi>10.1016/S0002-9440(10)65331-X</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present); EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Aortic Valve - drug effects Aortic Valve - metabolism Aortic Valve - pathology Aortic Valve - physiopathology Biological and medical sciences Calcinosis - chemically induced Calcinosis - metabolism Calcinosis - pathology Calcinosis - physiopathology Calcium - metabolism Cardiology. Vascular system Cells, Cultured Cytosol - metabolism Dose-Response Relationship, Drug Endocardial and cardiac valvular diseases Fibroblasts - drug effects Fibroblasts - metabolism Fibroblasts - pathology Fibroblasts - physiology Glutaral - metabolism Glutaral - pharmacology Heart In Vitro Techniques Medical sciences Microscopy, Electron Phosphates - metabolism Regular |
| title | Role of Glutaraldehyde in Calcification of Porcine Aortic Valve Fibroblasts |
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