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001-es BibID:BIBFORM097205
035-os BibID:(cikkazonosító)11064 (scopus)85116968958 (wos)000716921300001
Első szerző:Bódi Beáta (molekuláris biológus)
Cím:Alterations in ACE and ACE2 Activities and Cardiomyocyte Signaling Underlie Improved Myocardial Function in a Rat Model of Repeated Remote Ischemic Conditioning / Beáta Bódi, Patrick M. Pilz, Lilla Mártha, Miriam Lang, Ouafa Hamza, Miklós Fagyas, Petra L. Szabó, Dietmar Abraham, Attila Tóth, Bruno K. Podesser, Attila Kiss, Zoltán Papp
Dátum:2021
ISSN:1661-6596 1422-0067
Megjegyzések:Post-ischemic left ventricular (LV) remodeling and its hypothetical prevention by repeated remote ischemic conditioning (rRIC) in male Sprague?Dawley rats were studied. Myocardial infarction (MI) was evoked by permanent ligation of the left anterior descending coronary artery (LAD), and myocardial characteristics were tested in the infarcted anterior and non-infarcted inferior LV re-gions four and/or six weeks later. rRIC was induced by three cycles of five-minute-long unilateral hind limb ischemia and five minutes of reperfusion on a daily basis for a period of two weeks starting four weeks after LAD occlusion. Sham operated animals served as controls. Echocardio-graphic examinations and invasive hemodynamic measurements revealed distinct changes in LV systolic function between four and six weeks after MI induction in the absence of rRIC (i.e., LV ejection fraction (LVEF) decreased from 52.8 ? 2.1% to 50 ? 1.6%, mean ? SEM, p < 0.05) and in the presence of rRIC (i.e., LVEF increased from 48.2 ? 4.8% to 55.2 ? 4.1%, p < 0.05). Angioten-sin-converting enzyme (ACE) activity was about five times higher in the anterior LV wall at six weeks than that in sham animals. Angiotensin-converting enzyme 2 (ACE2) activity roughly doubled in post-ischemic LVs. These increases in ACE and ACE2 activities were effectively miti-gated by rRIC. Ca2+-sensitivities of force production (pCa50) of LV permeabilized cardiomyocytes were increased at six weeks after MI induction together with hypophosphorylation of 1) cardiac troponin I (cTnI) in both LV regions, and 2) cardiac myosin-binding protein C (cMyBP-C) in the anterior wall. rRIC normalized pCa50, cTnI and cMyBP-C phosphorylations. Taken together, post-ischemic LV remodeling involves region-specific alterations in ACE and ACE2 activities to-gether with changes in cardiomyocyte myofilament protein phosphorylation and function. rRIC has the potential to prevent these alterations and to improve LV performance following MI.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
repeated remote ischemic conditioning
cardiomyocyte mechanics
signaling
Megjelenés:International Journal Of Molecular Sciences. - 22 : 20 (2021), p. 1-17. -
További szerzők:Pilz, Patrick M. Mártha Lilla Lang, Miriam Hamza, Ouafa Fagyas Miklós (1984-) (orvos) Szabó Petra L. Abraham, Dietmar Tóth Attila (1971-) (biológus) Podesser, Bruno Karl Kiss Attila Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
Austria-Hungary Action Foundation: 92öu8
Egyéb
Ludwig Boltzmann Society: REM2017-20
Egyéb
2020-4.1.1-TKP2020
Egyéb
TKP2020-IKA-04
Egyéb
TKP2020-NKA04
Egyéb
FK 128809
OTKA
K 132623
OTKA
COST Action EU-CARDIOPROTECTION: CA16225
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

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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