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001-es BibID:	BIBFORM061586
Első szerző:	Csongrádi Éva (szakorvos)
Cím:	In Vivo Inhibition of Renal Heme Oxygenase with an Imidazole- Dioxolane Inhibitor / Csongradi, E., Vera, T., Rimoldi, J. M., Gadepalli, R. S.V., Stec, D. E.
Dátum:	2010
Megjegyzések:	Recent studies have indentified imidazole-dioxolane based compounds as novel heme oxyenase(HO) inhibitors. While these compounds have been demonstrated to be specific HO inhibitors invitro, they have yet to be used to inhibit renal HO activity in vivo. The goal of this study was todetermine the effectiveness of the imidazole-dioxolane HO-1 inhibitor, QC-13, in the inhibition ofrenal HO activity in vivo. HO-1 was induced in mice by treatment with cobalt protoporphyrin(CoPP). After 5 days, QC-13 was delivered either by continuous intrarenal medullay interstitialinfusion (IRMI) into one kidney at several concentrations for 72 hours or by two intraperitonealinjections over a 48 hour period. IRMI infusion of QC-13 at a concentration of 25 ?M resulted in asignificant decrease in medullary but not cortical HO activity as compared to CoPP treatedkidneys. IRMI infusion of QC-13 at a lower concentration (2.5 ?M) had no effect on eithermedullary or cortical HO activity in CoPP treated mice. In contrast, administration of QC-13 at ahigher concentration (250 ?M) resulted in a significant decrease in both medullary and corticalHO activity in CoPP treated mice. Systemic administration of QC-13 resulted in significantdecrease both renal cortical and medullary HO activity in CoPP treated mice. In contrast toclassical porphyrin based HO inhibitors, IRMI infusion of QC-13 did not induce HO-1 proteinlevels as determined by Western blot analysis of medullary protein samples. Our resultsdemonstrated that imidazole-dioxolane inhibitors are renal HO inhibitors in vivo and can inhibitHO activity independent of HO-1 induction. These inhibitors may be useful tools to elucidate therole of renal HO-1 in numerous physiologic and pathophysiologic conditions.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Kidney Carbon Monoxide Cobalt Protoporyphrin Heme Oxygenase-1 Mouse
Megjelenés:	Pharmacological research 61 : 6 (2010), p. 525-530. -
További szerzők:	Vera, Trinity Rimoldi, John M. Gadepalli, Rama S.V. Stec, David E.
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001-es BibID:	BIBFORM061583
Első szerző:	Csongrádi Éva (szakorvos)
Cím:	Role of carbon monoxide in kidney function : is a little carbon monoxide good for the kidney? / Csongradi, E., Juncos, L. A., Drummond, H. A., Vera, T., Stec, D. E.
Dátum:	2012
Megjegyzések:	Carbon monoxide (CO) is an endogenously produced gas resulting from the degradation of hemeby heme oxygense or from fatty acid oxidation. Heme oxygenase (HO) enzymes are constitutivelyexpressed in the kidney (HO-2) and HO-1 is induced in the kidney in response to severalphysiological and pathological stimuli. While the beneficial actions of HO in the kidney have beenrecognized for some time, the important role of CO in mediating these effects has not been fullyexamined. Recent studies using CO inhalation therapy and carbon monoxide releasing molecules(CORMs) are demonstrating that increases in CO alone can be beneficial to the kidney in severalforms of acute renal injury by limiting oxidative injury, decreasing cell apoptosis, and promotingcell survival pathways. Renal CO is also emerging as a major regulator of renal vascular andtubular function acting to protect the renal vasculature against excessive vasoconstriction and topromote natriuresis by limiting sodium reabsorption in tubule cells. Within this review, recentstudies on the physiological actions of CO in the kidney will be explored as well as the potentialtherapeutic avenues that are being developed targeting CO in the kidney which may be beneficialin diseases such as acute renal failure and hypertension.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Heme oxygenase renal failure blood pressure bilirubin acute renal injury
Megjelenés:	Current pharmaceutical biotechnology 13 : 6 (2012), p.819-826. -
További szerzők:	Juncos, Luis A. Drummond, Heather A. Vera, Trinity Stec, David E.
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM061581
Első szerző:	Csongrádi Éva (szakorvos)
Cím:	Chronic HO-1 induction with cobalt protoporphyrin (CoPP) treatment increases oxygen consumption, activity, heat production and lowers body weight in obese melanocortin-4 receptor-deficient mice / Csongradi Eva, Docarmo, J. M., Dubinion, John H., Vera, Trinity, Stec, David E.
Dátum:	2012
Megjegyzések:	Objective?Heme oxygenase-1 induction (HO-1) elicits chronic weight loss in several rodentmodels of obesity. Despite these findings, the mechanism by which HO-1 induction reduces bodyweight is unclear. Chronic HO-1 induction does not alter food intake suggesting other mechanismssuch as increases in metabolism and activity may be responsible for the observed reduction ofbody weight. In this study, we investigated the mechanism of weight loss elicited by chronic HO-1induction in a model of genetic obesity due to melanocortin-4 receptor (MC4R) deficiency.Design?Experiments were performed on loxTB MC4R deficient mice as well as lean controls.Mice were administered cobalt protoporphyrin (CoPP, 5 mg/kg), an inducer of HO-1, once weeklyfrom 4 to 23 weeks of age. Body weights were measured weekly and fasted blood glucose andinsulin as well as food intake were determined at 18 weeks of age. O2 consumption, CO2production, activity, and body heat production were measured at 20 weeks of age.Results?Chronic CoPP treatment resulted in a significant decrease in body weight from 5weeks on in loxTB mice. Chronic CoPP treatment resulted in a significant decrease in fasted bloodglucose levels, plasma insulin, and a significant increase in plasma adiponectin levels in MC4Rdeficient mice. Chronic CoPP treatment increased O2 consumption (47 ? 4 vs. 38 ? 3 ml/kg/min,P<0.05) and CO2 production (44 ? 7 vs. 34 ? 4 ml/kg/min, P<0.05) in treated versus non-treated,MC4R deficient mice (n=4). Heat production (10%) and activity (18%) were also significantly(P<0.05) increased in CoPP treated MC4R deficient mice.Conclusion?Our results suggest that chronic HO-1 induction with CoPP induction elicitsweight loss by increasing metabolism and activity by an MC4R independent pathway.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Heme oxygenase adiponectin metabolism gene knockout diabetes leptin
Megjelenés:	International journal of obesity. - 36 : 2 (2012), p. 244-253. -
További szerzők:	DoCarmo, Jussara M. Dubinion, John H. Vera, Trinity Stec, David E.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM061612
Első szerző:	Stec, David E.
Cím:	Thick Ascending Loop of Henle (talh) Specific Expression of Ho-1 Attenuates the Development of Ang II-Dependent Hypertension / David E. Stec, Eva Csongradi, Trinity Vera, Heather A. Drummond, Nader G. Abraham
Dátum:	2010
ISSN:	0194-911X
Megjegyzések:	Recent studies have demonstrated an important antihypertensive action of renal heme oxygenase-1 (HO-1) induction; however, the specific contribution of thick ascending loop of Henle (TALH) derived HO-1 to this response is unknown. We generated a transgenic mouse model in which expression of the human HO-1 cDNA was controlled by the uromodulin (Tamm-Horsfall protein, THP) promoter (TALH-HHO1). Expression of the HO-1 transgene was only detected in isolated microdissected TALH tubule segments by rt-PCR. TALH-HHO1 mice exhibited a significant increase in medullary HO-1 protein which co-localized with endogenous THP protein as determined by confocal microscopy. HO activity was significantly increased in the medulla of TALH-HHO1 mice as compared to controls (25?7 vs. 151 30 pmoles/bilirubin/ mg/hr, n=6, p0.05), however, no difference in cortical HO activity was observed between TALH-HHO1 and non-transgenic mice. The effect of enhanced TALH HO-1 on the blood pressure response to increased Angiotensin II (Ang II) was determined in mice in which Ang II (1 g/min/kg. s.c.) was infused via an osmotic minipump for 10 days. Conscious blood pressures were measured over the last five days using implanted catheters. Ang II hypertension was significantly attenuated in TALH-HHO1 mice as compared to non-transgenic mice and averaged 139?3 vs. 153?2 mmHg (n=5, p0.05) in each group respectively. The decrease in blood pressure in TALH-HHO1 transgenic mice was associated with a 60% decrease in the level of the NKCC2 transporter in the medulla as determined by Western blot. TALH-HHO1 mice also exhibited a 36% decrease in sodium reabsorption measure in isolated TAHL tubule segments by ouabain sensitive rubidium (Rb) uptake. Our results demonstrate that increased levels of HO-1 in the TALH can lower blood pressure via a mechanism that may include alterations in NKCC2 dependent sodium reabsorption.
Tárgyszavak:	Orvostudományok Egészségtudományok idézhető absztrakt
Megjelenés:	Hypertension 56 : 5 (2010), p. e60. -
További szerzők:	Csongrádi Éva (1969-) (szakorvos) Vera, Trinity Drummond, Heather A. Abraham, Nader G. (tudományos segédmunkatárs)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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