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001-es BibID:	BIBFORM061585
Első szerző:	Csongrádi Éva (szakorvos)
Cím:	Renal Inhibition of Heme Oxygenase-1 Increases Blood Pressure in Angiotensin II-Dependent Hypertension / Csongradi, E., Storm, M. V., Stec, D. E.
Dátum:	2012
Megjegyzések:	The goal of this study was to test the hypothesis that renal medullary heme oxygenase (HO) acts as a buffer against Ang-IIdependent hypertension. To test this hypothesis, renal medullary HO activity was blocked using QC-13, an imidazole-dioxolaneHO-1 inhibitor, or SnMP, a classical porphyrin based HO inhibitor. HO inhibitors were infused via IRMI catheters throughout thestudy starting 3 days prior to implantation of an osmotic minipump which delivered Ang II or saline vehicle. MAP was increasedby Ang II infusion and further increased by IRMI infusion of QC-13 or SnMP.MAP averaged 113?3, 120?7, 141?2, 153?2, and154?3mmHg in vehicle, vehicle + IRMI QC-13, Ang II, Ang II + IRMI QC-13, and Ang II + IRMI SnMP treated mice, respectively(n = 6). Inhibition of renal medullaryHO activity with QC-13 in Ang II infused mice was also associated with a significant increasein superoxide production as well as significant decreases in antioxidant enzymes catalase and MnSOD. These results demonstratethat renal inhibition of HO exacerbates Ang II dependent hypertension through a mechanism which is associated with increasesin superoxide production and decreases in antioxidant enzymes.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Heme Oxygenase-1 Angiotensin II Hypertension
Megjelenés:	International Journal of Hypertension 2012 (2012), p. Article ID 497213. -
További szerzők:	Storm, Megan V. Stec, David E.
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001-es BibID:	BIBFORM061613
Első szerző:	George, Eric M. (tudományos segédmunkatárs)
Cím:	Induction of Heme Oxygenase-1 Attenuates Placental Ischemia-Induced Hypertension / Eric M. George, Kathy Cockrell, Marietta Arany, Eva Csongradi, David E. Stec, Joey P. Granger.
Dátum:	2010
ISSN:	0194-911X
Megjegyzések:	Preeclampsia commonly presents as hypertension and proteinuria after the twentieth week of pregnancy. Recently, it has been recognized that the underlying mechanism in the pathophysiology of the disease is placental insufficiency and ischemia. Two mechanisms believed to be involved are the imbalance of the pro- and anti-angiogenic proteins VEGF and sFlt-1, and the production of ROS in the ischemic placenta. Heme oxygenase-1 (HO-1), a factor in the heme salvage pathway, has been shown to have beneficial effects in several models of hypertension, presumably through the production of biologically active byproducts; the vasodilatory molecule CO and the antioxidant bilirubin. Here we have utilized a rat reduced uterine perfusion pressure (RUPP) model of placental ischemia to determine if HO-1 could have beneficial effects on the disease pathology. At day 19 of pregnancy, RUPP rats showed significantly higher blood e90 Hypertension Vol 56, No 5 November 2010 Downloaded from http://hyper.ahajournals.org/ by guest on December 13, 2015 pressure than controls (1367mmHg vs. 1055mmHg respectively). Induction of HO-1 by administration of cobalt protoporphyrin (COPP) significantly reduced MAP in RUPP rats but not controls (1188 and 1045mmHg respectively). Intriguingly, normalized placental sFlt-1/ VEGF ratio, which is significantly elevated in the RUPP model versus controls (1.24.2 and 11 respectively), is significantly reduced in response to HO-1 induction (0.69.1), indicating a more pro-angiogenic phenotype. Finally, placental ROS production which is elevated nearly 4-fold in RUPP rats (953279 vs. 24471 RLU/min/mg) is significantly attenuated, though not normalized, by COPP administration (617225 RLU/min/mg). Collectively, these results suggest that induction of HO-1 or one of its biologically active metabolites might be a candidate for therapeutic intervention in preeclampsia
Tárgyszavak:	Orvostudományok Egészségtudományok idézhető absztrakt
Megjelenés:	Hypertension 56 : 5 (2010), p. e90. -
További szerzők:	Cockrell, Kathy (tudományos segédmunkatárs) Arany Marietta Csongrádi Éva (1969-) (szakorvos) Stec, David E. Granger, Joey P. (tudományos segédmunkatárs)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM061588
Első szerző:	George, Eric M. (tudományos segédmunkatárs)
Cím:	Induction of Heme Oxygenase-1 Attenuates Placental-Ischemia Induced Hypertension / Eric M. George, Kathy Cockrell, Marietta Aranay, Eva Csongradi, David E. Stec, Joey P. Granger
Dátum:	2011
ISSN:	0194-911X
Megjegyzések:	Recent in vitro studies have reported that heme oxygenase-1 (HO-1) downregulates the angiostaticprotein sFlt-1 from placental villous explants and that the HO-1 metabolites CO and bilirubinnegatively regulates endothelin-1 and reactive oxygen species (ROS). Although sFlt-1, ET-1, andROS have been implicated in the pathophysiology of hypertension during preeclampsia and inresponse to placental ischemia in pregnant rats, it is unknown whether chronic induction of HO-1alters the hypertensive response to placental ischemia. The present study examined the hypothesisthat HO-1 induction in a rat model of placental ischemia would beneficially affect blood pressure,angiogenic balance, superoxide, and ET-1 production in the ischemic placenta. To achieve thisgoal we examined the effects of cobalt protoporphyrin (CoPP), an HO-1 inducer, in the reduceduterine perfusion pressure (RUPP) placental ischemia model and in normal pregnant rats. Inresponse to RUPP treatment, MAP increases 29mmHg (136 ? 7 vs. 106 ? 5 mmHg) which issignificantly attenuated by CoPP (118 ? 5 mmHg). While RUPP treatment causes placental sFlt-1/VEGF ratios to alter significantly to an angiostatic balance (1 ? 0.1 vs 1.27 ? 0.2,), treatment withCoPP causes a significant shift in the ratio to an angiogenic balance (0.68 ? 0.1). Placentalsuperoxide increased in RUPP (952.5 ? 278.8 vs 243.9 ? 70.5 RLU/min/mg), but was significantlyattenuated by HO-1 induction (482.7 ? 117.4 RLU/min/mg). Also, preproendothelin message wassignificantly increased in RUPP, which was prevented by CoPP. These data indicate that HO-1, orits metabolites, are potential therapeutics for the treatment of preeclampsia.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Placental ischemia; sVEGF R1; preeclampsia; reduced uterine perfusion pressure; ET-1
Megjelenés:	Hypertension. - 57 : 5 (2011), p. 941-948. -
További szerzők:	Cockrell, Kathy (tudományos segédmunkatárs) Aranay, Marietta (tudományos segédmunkatárs) Csongrádi Éva (1969-) (szakorvos) Stec, David E. (tudományos segédmunkatárs) Granger, Joey P. (tudományos segédmunkatárs)
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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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