Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation
Elevated cardiac troponin-I (cTnI) levels have been demonstrated in serum of patients without acute coronary syndromes, potentially via a stretch-related process. We hypothesize that this cTnI release from viable cardiomyocytes is mediated by stimulation of stretch-responsive integrins. Cultured car...
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| Veröffentlicht in: | Pflügers Archiv 2008-03, Vol.455 (6), p.979-986 |
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| description | Elevated cardiac troponin-I (cTnI) levels have been demonstrated in serum of patients without acute coronary syndromes, potentially via a stretch-related process. We hypothesize that this cTnI release from viable cardiomyocytes is mediated by stimulation of stretch-responsive integrins. Cultured cardiomyocytes were treated with (1) Gly–Arg–Gly–Asp–Ser (
GRGDS
,
n
= 22) to stimulate integrins, (2) Ser–Asp–Gly–Arg–Gly (
SDGRG
,
n
= 8) that does not stimulate integrins, or (3) phosphate-buffered saline (control,
n
= 38). Cells and media were analyzed for intact cTnI, cTnI degradation products, and matrix metalloproteinase (MMP)-2. Cell viability was examined by assay of lactate dehydrogenase (LDH) activity and by nuclear staining with propidium iodide.
GRGDS
-induced integrin stimulation caused increased release of intact cTnI (9.6 ± 3.0%) as compared to
SDGRG
-treated cardiomyocytes (4.5 ± 0.8%,
p
|
| doi_str_mv | 10.1007/s00424-007-0354-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2226063</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1998446281</sourcerecordid><originalsourceid>FETCH-LOGICAL-c581t-1baee533f29737a2761adba31e5905ff6c185a924e426a146dbfe028fc737c113</originalsourceid><addsrcrecordid>eNp1kUGLFDEQhYMo7uzoD_AiwYO31lSSTqcvgizqLiwIojchpDPVY5buZEzSC_PvzdCDq4KnFNT3XqrqEfIC2BtgrHubGZNcNrVsmGhlox-RDUjBG85APCYbxgQ0qlP6glzmfMcY41Lzp-QCup71WuoN-f4FJ7QZaRyps2nnraMlxUMMPtAbOqY403tvhwnXdpyP0R0LZuoznbHyBXd0OFIfCu5TFeXi52WyxcfwjDwZ7ZTx-fndkm8fP3y9um5uP3-6uXp_27hWQ2lgsIitECPvO9FZ3imwu8EKwLZn7TgqB7q1PZcoubIg1W4YkXE9uoo7ALEl71bfwzLUmRyGkuxkDsnPNh1NtN783Qn-h9nHe8M5V0yJavD6bJDizwVzMbPPDqfJBoxLNh3jQgA_ga_-Ae_ikkJdzvB63Q5UJbcEVsilmHPC8fckwMwpOLMGZ07lKTijq-blnys8KM5JVYCvQK6tsMf08PP_XX8BED-k1g</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>200271602</pqid></control><display><type>article</type><title>Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Hessel, M. H. M. ; Atsma, D. E. ; van der Valk, E. J. M. ; Bax, W. H. ; Schalij, M. J. ; van der Laarse, A.</creator><creatorcontrib>Hessel, M. H. M. ; Atsma, D. E. ; van der Valk, E. J. M. ; Bax, W. H. ; Schalij, M. J. ; van der Laarse, A.</creatorcontrib><description>Elevated cardiac troponin-I (cTnI) levels have been demonstrated in serum of patients without acute coronary syndromes, potentially via a stretch-related process. We hypothesize that this cTnI release from viable cardiomyocytes is mediated by stimulation of stretch-responsive integrins. Cultured cardiomyocytes were treated with (1) Gly–Arg–Gly–Asp–Ser (
GRGDS
,
n
= 22) to stimulate integrins, (2) Ser–Asp–Gly–Arg–Gly (
SDGRG
,
n
= 8) that does not stimulate integrins, or (3) phosphate-buffered saline (control,
n
= 38). Cells and media were analyzed for intact cTnI, cTnI degradation products, and matrix metalloproteinase (MMP)-2. Cell viability was examined by assay of lactate dehydrogenase (LDH) activity and by nuclear staining with propidium iodide.
GRGDS
-induced integrin stimulation caused increased release of intact cTnI (9.6 ± 3.0%) as compared to
SDGRG
-treated cardiomyocytes (4.5 ± 0.8%,
p
< 0.001) and control (3.0 ± 3.4%,
p
< 0.001). LDH release from
GRGDS
-treated cardiomyocytes (15.9 ± 3.8%) equalled that from controls (15.2 ± 2.3%,
p
= n.s.), indicating that the
GRGDS
-induced release of cTnI is not due to cell necrosis. This result was confirmed by nuclear staining with propidium iodide. Integrin stimulation increased the intracellular and extracellular MMP2 activity as compared to controls (both
p
< 0.05). However, despite the ability of active MMP2 to degrade cTnI in vitro, integrin stimulation in cardiomyocytes was not associated with cTnI degradation. The present study demonstrates that intact cTnI can be released from viable cardiomyocytes by stimulation of stretch-responsive integrins.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-007-0354-8</identifier><identifier>PMID: 17909848</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Acute coronary syndromes ; Animals ; Bacteria ; Biomedical and Life Sciences ; Biomedicine ; Blotting, Western ; Cardiomyocytes ; Cardiovascular System ; Cell Biology ; Cell Death - drug effects ; Cell Nucleus - drug effects ; Cell Nucleus - ultrastructure ; Coloring Agents ; Enzyme-Linked Immunosorbent Assay ; Human Physiology ; In Vitro Techniques ; Integrins - agonists ; L-Lactate Dehydrogenase - metabolism ; Matrix Metalloproteinase 2 - metabolism ; Molecular Medicine ; Myocardium - cytology ; Myocardium - metabolism ; Myocytes, Cardiac - metabolism ; Necrosis ; Neurosciences ; Oligopeptides - pharmacology ; Propidium ; Rats ; Rats, Wistar ; Receptors ; Stimulation, Chemical ; Troponin I - metabolism</subject><ispartof>Pflügers Archiv, 2008-03, Vol.455 (6), p.979-986</ispartof><rights>Springer-Verlag 2007</rights><rights>Springer-Verlag 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c581t-1baee533f29737a2761adba31e5905ff6c185a924e426a146dbfe028fc737c113</citedby><cites>FETCH-LOGICAL-c581t-1baee533f29737a2761adba31e5905ff6c185a924e426a146dbfe028fc737c113</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/s00424-007-0354-8$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00424-007-0354-8$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,315,781,785,886,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17909848$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hessel, M. H. M.</creatorcontrib><creatorcontrib>Atsma, D. E.</creatorcontrib><creatorcontrib>van der Valk, E. J. M.</creatorcontrib><creatorcontrib>Bax, W. H.</creatorcontrib><creatorcontrib>Schalij, M. J.</creatorcontrib><creatorcontrib>van der Laarse, A.</creatorcontrib><title>Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>Elevated cardiac troponin-I (cTnI) levels have been demonstrated in serum of patients without acute coronary syndromes, potentially via a stretch-related process. We hypothesize that this cTnI release from viable cardiomyocytes is mediated by stimulation of stretch-responsive integrins. Cultured cardiomyocytes were treated with (1) Gly–Arg–Gly–Asp–Ser (
GRGDS
,
n
= 22) to stimulate integrins, (2) Ser–Asp–Gly–Arg–Gly (
SDGRG
,
n
= 8) that does not stimulate integrins, or (3) phosphate-buffered saline (control,
n
= 38). Cells and media were analyzed for intact cTnI, cTnI degradation products, and matrix metalloproteinase (MMP)-2. Cell viability was examined by assay of lactate dehydrogenase (LDH) activity and by nuclear staining with propidium iodide.
GRGDS
-induced integrin stimulation caused increased release of intact cTnI (9.6 ± 3.0%) as compared to
SDGRG
-treated cardiomyocytes (4.5 ± 0.8%,
p
< 0.001) and control (3.0 ± 3.4%,
p
< 0.001). LDH release from
GRGDS
-treated cardiomyocytes (15.9 ± 3.8%) equalled that from controls (15.2 ± 2.3%,
p
= n.s.), indicating that the
GRGDS
-induced release of cTnI is not due to cell necrosis. This result was confirmed by nuclear staining with propidium iodide. Integrin stimulation increased the intracellular and extracellular MMP2 activity as compared to controls (both
p
< 0.05). However, despite the ability of active MMP2 to degrade cTnI in vitro, integrin stimulation in cardiomyocytes was not associated with cTnI degradation. The present study demonstrates that intact cTnI can be released from viable cardiomyocytes by stimulation of stretch-responsive integrins.</description><subject>Acute coronary syndromes</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Western</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular System</subject><subject>Cell Biology</subject><subject>Cell Death - drug effects</subject><subject>Cell Nucleus - drug effects</subject><subject>Cell Nucleus - ultrastructure</subject><subject>Coloring Agents</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Human Physiology</subject><subject>In Vitro Techniques</subject><subject>Integrins - agonists</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Molecular Medicine</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Necrosis</subject><subject>Neurosciences</subject><subject>Oligopeptides - pharmacology</subject><subject>Propidium</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors</subject><subject>Stimulation, Chemical</subject><subject>Troponin I - metabolism</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNp1kUGLFDEQhYMo7uzoD_AiwYO31lSSTqcvgizqLiwIojchpDPVY5buZEzSC_PvzdCDq4KnFNT3XqrqEfIC2BtgrHubGZNcNrVsmGhlox-RDUjBG85APCYbxgQ0qlP6glzmfMcY41Lzp-QCup71WuoN-f4FJ7QZaRyps2nnraMlxUMMPtAbOqY403tvhwnXdpyP0R0LZuoznbHyBXd0OFIfCu5TFeXi52WyxcfwjDwZ7ZTx-fndkm8fP3y9um5uP3-6uXp_27hWQ2lgsIitECPvO9FZ3imwu8EKwLZn7TgqB7q1PZcoubIg1W4YkXE9uoo7ALEl71bfwzLUmRyGkuxkDsnPNh1NtN783Qn-h9nHe8M5V0yJavD6bJDizwVzMbPPDqfJBoxLNh3jQgA_ga_-Ae_ikkJdzvB63Q5UJbcEVsilmHPC8fckwMwpOLMGZ07lKTijq-blnys8KM5JVYCvQK6tsMf08PP_XX8BED-k1g</recordid><startdate>20080301</startdate><enddate>20080301</enddate><creator>Hessel, M. H. M.</creator><creator>Atsma, D. E.</creator><creator>van der Valk, E. J. M.</creator><creator>Bax, W. H.</creator><creator>Schalij, M. J.</creator><creator>van der Laarse, A.</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>C6C</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>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</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>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20080301</creationdate><title>Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation</title><author>Hessel, M. H. M. ; Atsma, D. E. ; van der Valk, E. J. M. ; Bax, W. H. ; Schalij, M. J. ; van der Laarse, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c581t-1baee533f29737a2761adba31e5905ff6c185a924e426a146dbfe028fc737c113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acute coronary syndromes</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Western</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular System</topic><topic>Cell Biology</topic><topic>Cell Death - drug effects</topic><topic>Cell Nucleus - drug effects</topic><topic>Cell Nucleus - ultrastructure</topic><topic>Coloring Agents</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Human Physiology</topic><topic>In Vitro Techniques</topic><topic>Integrins - agonists</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Molecular Medicine</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Necrosis</topic><topic>Neurosciences</topic><topic>Oligopeptides - pharmacology</topic><topic>Propidium</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors</topic><topic>Stimulation, Chemical</topic><topic>Troponin I - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hessel, M. H. M.</creatorcontrib><creatorcontrib>Atsma, D. E.</creatorcontrib><creatorcontrib>van der Valk, E. J. M.</creatorcontrib><creatorcontrib>Bax, W. H.</creatorcontrib><creatorcontrib>Schalij, M. 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H. M.</au><au>Atsma, D. E.</au><au>van der Valk, E. J. M.</au><au>Bax, W. H.</au><au>Schalij, M. J.</au><au>van der Laarse, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2008-03-01</date><risdate>2008</risdate><volume>455</volume><issue>6</issue><spage>979</spage><epage>986</epage><pages>979-986</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>Elevated cardiac troponin-I (cTnI) levels have been demonstrated in serum of patients without acute coronary syndromes, potentially via a stretch-related process. We hypothesize that this cTnI release from viable cardiomyocytes is mediated by stimulation of stretch-responsive integrins. Cultured cardiomyocytes were treated with (1) Gly–Arg–Gly–Asp–Ser (
GRGDS
,
n
= 22) to stimulate integrins, (2) Ser–Asp–Gly–Arg–Gly (
SDGRG
,
n
= 8) that does not stimulate integrins, or (3) phosphate-buffered saline (control,
n
= 38). Cells and media were analyzed for intact cTnI, cTnI degradation products, and matrix metalloproteinase (MMP)-2. Cell viability was examined by assay of lactate dehydrogenase (LDH) activity and by nuclear staining with propidium iodide.
GRGDS
-induced integrin stimulation caused increased release of intact cTnI (9.6 ± 3.0%) as compared to
SDGRG
-treated cardiomyocytes (4.5 ± 0.8%,
p
< 0.001) and control (3.0 ± 3.4%,
p
< 0.001). LDH release from
GRGDS
-treated cardiomyocytes (15.9 ± 3.8%) equalled that from controls (15.2 ± 2.3%,
p
= n.s.), indicating that the
GRGDS
-induced release of cTnI is not due to cell necrosis. This result was confirmed by nuclear staining with propidium iodide. Integrin stimulation increased the intracellular and extracellular MMP2 activity as compared to controls (both
p
< 0.05). However, despite the ability of active MMP2 to degrade cTnI in vitro, integrin stimulation in cardiomyocytes was not associated with cTnI degradation. The present study demonstrates that intact cTnI can be released from viable cardiomyocytes by stimulation of stretch-responsive integrins.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>17909848</pmid><doi>10.1007/s00424-007-0354-8</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Pflügers Archiv, 2008-03, Vol.455 (6), p.979-986 |
| issn | 0031-6768 1432-2013 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Acute coronary syndromes Animals Bacteria Biomedical and Life Sciences Biomedicine Blotting, Western Cardiomyocytes Cardiovascular System Cell Biology Cell Death - drug effects Cell Nucleus - drug effects Cell Nucleus - ultrastructure Coloring Agents Enzyme-Linked Immunosorbent Assay Human Physiology In Vitro Techniques Integrins - agonists L-Lactate Dehydrogenase - metabolism Matrix Metalloproteinase 2 - metabolism Molecular Medicine Myocardium - cytology Myocardium - metabolism Myocytes, Cardiac - metabolism Necrosis Neurosciences Oligopeptides - pharmacology Propidium Rats Rats, Wistar Receptors Stimulation, Chemical Troponin I - metabolism |
| title | Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation |
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