CCL

Összesen 2 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM055181
035-os BibID:PMID: 25097723 Article ID: 976394
Első szerző:Bányai Emese (orvos)
Cím:Novel functional changes during podocyte differentiation : increase of oxidative resistance and H-ferritin expression / Emese Bányai, Enikő Balogh, Miklós Fagyas, Paolo Arosio, Zoltán Hendrik, Gábor Király, Gábor Nagy, Bence Tánczos, István Pócsi, György Balla, József Balla, Gáspár Bánfalvi, Viktória Jeney
Dátum:2014
ISSN:1942-0900 1942-0994
Megjegyzések:Podocytes are highly specialized, arborized epithelial cells covering the outer surface of the glomerular tuft in the kidney. Terminally differentiated podocytes are unable to go through cell division and hereby they are lacking a key property for regeneration after a toxic injury. Podocytes are long-lived cells but, to date, little is known about the mechanisms that support their stress resistance. Our aim was to investigate whether the well-known morphological changes during podocyte differentiation are accompanied by changes in oxidative resistance in a manner that could support their long-term survival. We used a conditionally immortalized human podocyte cell line to study the morphological and functional changes during differentiation. We followed the differentiation process for 14 days by time-lapse microscopy. During this period nondifferentiated podocytes gradually transformed into large, nonproliferating, frequently multinucleated cells, with enlarged nuclei and opened chromatin structure. We observed that differentiated podocytes were highly resistant to oxidants such as H2O2 and heme when applied separately or in combination, whereas undifferentiated cells were prone to such challenges. Elevated oxidative resistance of differentiated podocytes was associated with increased activities of antioxidant enzymes and H-ferritin expression. Immunohistochemical analysis of normal human kidney specimens revealed that podocytes highly express H-ferritin in vivo as well.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Oxidative Medicine and Cellular Longevity 2014 (2014), p. 1-10. -
További szerzők:Balogh Enikő (1987-) (molekuláris biológus) Fagyas Miklós (1984-) (orvos) Arosio, Paolo Hendrik Zoltán (1986-) (orvos) Király Gábor (1988-) (biológus) Szemán-Nagy Gábor (1975-) (biológia tanár-molekuláris biológus) Tánczos Bence (1987-) (biológus) Pócsi István (1961-) (vegyész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus) Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész) Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Belgyógyászat Kutatócsoport
TÁMOP-4.2.4.A/2-11-1-2012-0001
TÁMOP
OTKA-K83478
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM064197
Első szerző:Kovács Árpád (kardiológus)
Cím:Renin overexpression leads to increased titin-based stiffness contributing to diastolic dysfunction in hypertensive mRen2 rats / Árpád Kovács, Gábor Á. Fülöp, Andrea Kovács, Tamás Csípő, Beáta Bódi, Dániel Priksz, Béla Juhász, Lívia Beke, Zoltán Hendrik, Gábor Méhes, Henk L. Granzier, István Édes, Miklós Fagyas, Zoltán Papp, Judit Barta, Attila Tóth
Dátum:2016
ISSN:0363-6135
Megjegyzések:Hypertension (HTN) is a major risk factor for heart failure. We investigated the influence of HTN on cardiac contraction and relaxation in transgenic renin overexpressing rats (carrying mouse Ren-2 renin gene, mRen2, n = 6). Blood pressure (BP) was measured. Cardiac contractility was characterized by echocardiography, cellular force measurements, and biochemical assays were applied to reveal molecular mechanisms. Sprague-Dawley (SD) rats (n = 6) were used as controls. Transgenic rats had higher circulating renin activity and lower cardiac angiotensin-converting enzyme two levels. Systolic BP was elevated in mRen2 rats (235.11 ? 5.32 vs. 127.03 ? 7.56 mmHg in SD, P < 0.05), resulting in increased left ventricular (LV) weight/body weight ratio (4.05 ? 0.09 vs. 2.77 ? 0.08 mg/g in SD, P < 0.05). Transgenic renin expression had no effect on the systolic parameters, such as LV ejection fraction, cardiomyocyte Ca(2+)-activated force, and Ca(2+) sensitivity of force production. In contrast, diastolic dysfunction was observed in mRen2 compared with SD rats: early and late LV diastolic filling ratio (E/A) was lower (1.14 ? 0.04 vs. 1.87 ? 0.08, P < 0.05), LV isovolumetric relaxation time was longer (43.85 ? 0.89 vs. 28.55 ? 1.33 ms, P < 0.05), cardiomyocyte passive tension was higher (1.74 ? 0.06 vs. 1.28 ? 0.18 kN/m(2), P < 0.05), and lung weight/body weight ratio was increased (6.47 ? 0.24 vs. 5.78 ? 0.19 mg/g, P < 0.05), as was left atrial weight/body weight ratio (0.21 ? 0.03 vs. 0.14 ? 0.03 mg/g, P < 0.05). Hyperphosphorylation of titin at Ser-12742 within the PEVK domain and a twofold overexpression of protein kinase C-? in mRen2 rats were detected. Our data suggest a link between the activation of renin-angiotensin-aldosterone system and increased titin-based stiffness through phosphorylation of titin's PEVK element, contributing to diastolic dysfunction.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
hypertension
passive stiffness
renin-angiotensin-aldosterone system
RAAS
diastolic dysfunction
titin phosphorylation
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 310 : 11 (2016), p. H1671-H1682. -
További szerzők:Fülöp Gábor Áron (1988-) (általános orvos) Kovács Andrea (1974-) (neurológus) Csípő Tamás (1990-) Bódi Beáta (1989-) (molekuláris biológus) Priksz Dániel (1989-) (farmakológus) Juhász Béla (1978-) (kísérletes farmakológus) Beke Lívia Hendrik Zoltán (1986-) (orvos) Méhes Gábor (1966-) (patológus) Granzier, Henk L. Édes István (1952-) (kardiológus) Fagyas Miklós (1984-) (orvos) Papp Zoltán (1965-) (kardiológus, élettanász) Barta Judit (1975-) (kardiológus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:PD116212
OTKA
K109083
OTKA
K116940
OTKA
MEDIA
FP7
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1