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001-es BibID:BIBFORM049141
Első szerző:Balogh Ágnes (kardiológus)
Cím:Myofilament protein carbonylation contributes to the contractile dysfunction in the infarcted LV region of mouse hearts / Ágnes Balogh, David Santer, Enikő T. Pásztor, Attila Tóth, Dániel Czuriga, Bruno K. Podesser, Karola Trescher, Kornelia Jaquet, Ferenc Erdődi, István Édes, Zoltán Papp
Dátum:2014
ISSN:0008-6363
Megjegyzések:Aims: The region-specific mechanical function of left ventricular (LV) murinecardiomyocytes and the role of phosphorylation and oxidative modifications of myofilamentproteins were investigated in the process of post-myocardial infarction (MI) remodeling 10weeks after ligation of the left anterior descending (LAD) coronary artery. Methods andResults: Permeabilized murine cardiomyocytes from the remaining anterior and a remotenoninfarcted inferior LV area were compared with those of noninfarcted age-matchedcontrols. Myofilament phosphorylation, sulfhydryl (SH) oxidation and carbonylation werealso assayed. The Ca2+ sensitivity of force production was significantly lower in the anteriorwall (pCa50:5.81?0.03, mean?SEM, at 2.3 ?m sarcomere length) than that in the controls(pCa50:5.91?0.02) or in the MI inferior area (pCa50:5.88?0.02). The level of troponin Iphosphorylation was lower and that of myofilament protein SH oxidation was higher in theanterior location relative to controls, but these changes did not explain the differences in Ca2+sensitivities. On the other hand, significantly higher carbonylation levels [e.g. in myosinheavy chain (MHC) and actin] were observed in the MI anterior wall [carbonylation index(CI), CIMHC:2.06?0.46, CIactin:1.46?0.18] than in the controls (CI:1). In vitro Fenton-basedmyofilament carbonylation in the control cardiomyocytes also decreased the Ca2+ sensitivityof force production irrespective of the phosphorylation status of the myofilaments.Furthermore, the Ca2+ sensitivity correlated strongly with myofilament carbonylation levels inall investigated samples. Conclusions: Post-MI myocardial remodeling involves increasedmyofibrillar protein carbonylation and decreased Ca2+ sensitivity of force production, leadingpotentially to contractile dysfunction in the remaining cardiomyocytes of the infarcted area.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
contractile function
infarction
myocytes
remodeling
sarcomere
Megjelenés:Cardiovascular Research. - 101 : 1 (2014), p. 108-119. -
További szerzők:Santer, David Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Tóth Attila (1971-) (biológus) Czuriga Dániel (1982-) (kardiológus) Podesser, Bruno Karl Trescher, Karola Jaquet, Kornelia Erdődi Ferenc (1953-) (biokémikus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
K 109083
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Biomolekuláris interakciók jellemzőinek kvantitatív meghatározása
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001-es BibID:BIBFORM086997
Első szerző:Santer, David
Cím:Tenascin-C aggravates ventricular dilatation and angiotensin-converting enzyme activity after myocardial infarction in mice / David Santer, Felix Nagel, Inês Fonseca Gonçalves, Christoph Kaun, Johann Wojta, Miklós Fagyas, Martin Krššák, Ágnes Balogh, Zoltán Papp, Attila Tóth, Viktor Bánhegyi, Karola Trescher, Attila Kiss, Bruno K. Podesser
Dátum:2020
ISSN:2055-5822
Megjegyzések:Abstract Aims Tenascin?C (TN?C) is suggested to be detrimental in cardiac remodelling after myocardial infarction (MI). The aim of this study is to reveal the effects of TN?C on extracellular matrix organization and its haemodynamic influence in an experimental mouse model of MI and in myocardial cell culture during hypoxic conditions. Methods and results Myocardial infarction was induced in TN?C knockout (TN?C KO) and wild?type mice. Six weeks later, cardiac function was studied by magnetic resonance imaging and under isolated working heart conditions. Myocardial mRNA levels and immunoreactivity of TN?C, TIMP?1, TIMP?3, and matrix metalloproteinase (MMP)?9, as well as serum and tissue activities of angiotensin?converting enzyme (ACE), were determined at 1 and 6 weeks after infarction. Cardiac output and external heart work were higher, while left ventricular wall stress and collagen expression were decreased (P < 0.05) in TN?C KO mice as compared with age?matched controls at 6 weeks after infarction. TIMP?1 expression was down?regulated at 1 and 6 weeks, and TIMP?3 expression was up?regulated at 1 week (P < 0.01) after infarction in knockout mice. MMP?9 level was lower in TN?C KO at 6 weeks after infarction (P < 0.05). TIMP?3/MMP?9 ratio was higher in knockout mice at 1 and 6 weeks after infarction (P < 0.01). ACE activity in the myocardial border zone (i.e. between scar and free wall) was significantly lower in knockout than in wild?type mice 1 week after MI (P < 0.05). Conclusions Tenascin?C expression is induced by hypoxia in association with ACE activity and MMP?2 and MMP?9 elevations, thereby promoting left ventricular dilatation after MI.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:ESC Heart Failure. - 7 : 5 (2020), p. 2113-2122. -
További szerzők:Nagel, Felix Gonçalves, Inês Fonseca Kaun, Christoph Wojta, Johann Fagyas Miklós (1984-) (orvos) Krššák, Martin Balogh Ágnes (1984-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus) Bánhegyi Viktor (1991-) (kardiológus) Trescher, Karola Kiss Attila Podesser, Bruno Karl
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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