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Specific enhancement of sarcomeric response to Ca2+ protects murine myocardium against ischemia-reperfusion dysfunction
dc.creator | Arteaga, GM | |
dc.creator | Warren, CM | |
dc.creator | Milutinović-Smiljanić, Sanja | |
dc.creator | Martin, AF | |
dc.creator | Solaro, RJ | |
dc.date.accessioned | 2020-07-02T12:08:20Z | |
dc.date.available | 2020-07-02T12:08:20Z | |
dc.date.issued | 2005 | |
dc.identifier.issn | 0363-6135 | |
dc.identifier.uri | https://smile.stomf.bg.ac.rs/handle/123456789/1249 | |
dc.description.abstract | Alteration in myofilament response to Ca2+ is a major mechanism for depressed cardiac function after ischemia-reperfusion (I/R) dysfunction. We tested the hypothesis that hearts with increased myofilament response to Ca2+ are less susceptible to I/R. In one approach, we studied transgenic (TG) mice with a constitutive increase in myofilament Ca2+ sensitivity in which the adult form of cardiac troponin I (cTnI) is stoichiometrically replaced with the embryonic/neonatal isoform, slow skeletal TnI (ssTnI). We also studied mouse hearts with EMD-57033, which acts specifically to enhance myofilament response to Ca2+. We subjected isolated, perfused hearts to an I/R protocol consisting of 25 min of no-flow ischemia followed by 30 min of reperfusion. After I/R, developed pressure and rates of pressure change were significantly depressed and end-diastolic pressure was significantly elevated in nontransgenic (NTG) control hearts. These changes were significantly blunted in TG hearts and in NTG hearts perfused with EMD-57033 during reperfusion, with function returning to nearly baseline levels. Ca2+- and cross bridge-dependent activation, protein breakdown, and phosphorylation in detergent-extracted fiber bundles were also investigated. After I/R NTG fiber bundles exhibited a significant depression of cross bridge-dependent activation and Ca2+-activated tension and length dependence of activation that were not evident in TG preparations. Only NTG hearts demonstrated a significant increase in cTnI phosphorylation. Our results support the hypothesis that specific increases in myofilament Ca2+ sensitivity are able to diminish the effect of I/R on cardiac function. | en |
dc.publisher | Amer Physiological Soc, Bethesda | |
dc.relation | NHLBI NIH HHSUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI) [KO1-HL-67709, P01-HL-62426, R37-HL-22231] | |
dc.rights | restrictedAccess | |
dc.source | American Journal of Physiology - Heart & Circulatory Physiology | |
dc.subject | troponin I | en |
dc.subject | calcium sensitizers | en |
dc.subject | phosphorylation | en |
dc.subject | stunning | en |
dc.subject | cross bridge-dependent activation | en |
dc.title | Specific enhancement of sarcomeric response to Ca2+ protects murine myocardium against ischemia-reperfusion dysfunction | en |
dc.type | article | |
dc.rights.license | ARR | |
dcterms.abstract | Мартин, AФ; Милутиновић-Смиљанић, Сања; Соларо, РЈ; Wаррен, ЦМ; Aртеага, ГМ; | |
dc.citation.volume | 289 | |
dc.citation.issue | 5 | |
dc.citation.spage | H2183 | |
dc.citation.epage | H2192 | |
dc.citation.other | 289(5): H2183-H2192 | |
dc.citation.rank | M21 | |
dc.identifier.wos | 000232497500052 | |
dc.identifier.doi | 10.1152/ajpheart.00520.2005 | |
dc.identifier.pmid | 16024565 | |
dc.identifier.scopus | 2-s2.0-27144551306 | |
dc.type.version | publishedVersion |