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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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001-es BibID:	BIBFORM061587
Első szerző:	Stec, David E.
Cím:	Expression of Heme Oxygenase-1 in Thick Ascending Loop of Henle Attenuates Angiotensin II-Dependent Hypertension / David E. Stec, Heather A. Drummond, Monette U. Gousette, Megan V. Storm, Nader G. Abraham, Eva Csongradi
Dátum:	2012
Megjegyzések:	Kidney-specific induction of heme oxygenase-1 (HO-1) attenuates the development of angiotensin II (AngII) -dependent hypertension, but the relative contribution of vascular versus tubular induction of HO-1 isunknown. To determine the specific contribution of thick ascending loop of Henle (TALH) -derived HO-1,we generated a transgenic mouse in which the uromodulin promoter controlled expression of human HO-1.Quantitative RT-PCR and confocal microscopy confirmed successful localization of the HO-1 transgeneto TALH tubule segments. Medullary HO activity, but not cortical HO activity, was significantly higher intransgenic mice than control mice. Enhanced TALH HO-1 attenuated the hypertension induced by Ang IIdelivered by an osmotic minipump for 10 days (13963 versus 15362 mmHg in the transgenic and controlmice, respectively; P,0.05). The lower blood pressure in transgenic mice associated with a 60% decreasein medullary NKCC2 transporter expression determined by Western blot. Transgenic mice also exhibited a36% decrease in ouabain-sensitive sodium reabsorption and a significantly attenuated response to furosemidein isolated TALH segments,. In summary, these results show that increased levels of HO-1 in theTALH can lower blood pressure by a mechanism that may include alterations in NKCC2-dependent sodiumreabsorption.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Heme Oxygenase-1, Angiotensin II, Hypertension
Megjelenés:	Journal of the American Society of Nephrology. - 23 : 5 (2012), p. 834-841. -
További szerzők:	Drummond, Heather A. (tudományos segédmunkatárs) Gousette, Monette U. (orvos) Storm, Megan V. Abraham, Nader G. (tudományos segédmunkatárs) Csongrádi Éva (1969-) (szakorvos)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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