Evidence map›Paper›PMID 22323644›Full record

ArticleJournal of the American Society of Nephrology : JASN2012

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

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Review
  7. HO-1 overexpression and underexpression: Clinical implications.Archives of biochemistry and biophysics · 2019
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Proximal tubule-targeted heme oxygenase-1 in cisplatin-induced acute kidney injury.American journal of physiology. Renal physiology · 2016
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Human AKI and heme oxygenase-1.Journal of the American Society of Nephrology : JASN · 2012
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

David E StecDepartment of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, 39216, USA. dstec@umc.edu
Heather A Drummond
Monette U Gousette
Megan V Storm
Nader G Abraham
Eva Csongradi
University of Mississippi Medical Center · USUniversity of Debrecen · HUUniversity of Toledo · US

Funding

Vasoregulatory Function of CYP2E1-Derived EicosanoidsP01HL034300 · NHLBI · NEW YORK MEDICAL COLLEGE · PI JIANG, HOULI · 1985 to 2015
$33.4M
The Renal Medulla and HypertensionR01HL088421 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI STEC, DAVID E · 2008 to 2012
$1.9M
NHLBI NIH HHS HL088421NHLBI NIH HHS HL088421-S1NHLBI NIH HHS P01 HL034300NHLBI NIH HHS P01HL-5197NHLBI NIH HHS R01 HL088421
6 · The paper itself

Abstract

Kidney-specific induction of heme oxygenase-1 (HO-1) attenuates the development of angiotensin II (Ang II) -dependent hypertension, but the relative contribution of vascular versus tubular induction of HO-1 is unknown. 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 transgene to TALH tubule segments. Medullary HO activity, but not cortical HO activity, was significantly higher in transgenic mice than control mice. Enhanced TALH HO-1 attenuated the hypertension induced by Ang II delivered by an osmotic minipump for 10 days (139 ± 3 versus 153 ±2 mmHg in the transgenic and control mice, respectively; P<0.05). The lower blood pressure in transgenic mice associated with a 60% decrease in medullary NKCC2 transporter expression determined by Western blot. Transgenic mice also exhibited a 36% decrease in ouabain-sensitive sodium reabsorption and a significantly attenuated response to furosemide in isolated TALH segments. In summary, these results show that increased levels of HO-1 in the TALH can lower blood pressure by a mechanism that may include alterations in NKCC2-dependent sodium reabsorption.

Indexed as

Angiotensin IIAnimalsBlood PressureFurosemideHeme Oxygenase-1HypertensionLoop of HenleMiceMice, TransgenicOuabainRubidiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1UromodulinAngiotensin IIFurosemideHeme Oxygenase-1HMOX1 protein, humanOuabainRubidiumSLC12A1 protein, humanSlc12a1 protein, mouseSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1Uromodulin

Identifiers

PMID22323644
PMCPMC3338287
OpenAlexW2116594368

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.