Evidence map›Paper›PMID 19136582›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009

Long-term effects of prenatal hypoxia on endothelium-dependent relaxation responses in pulmonary arteries of adult sheep.

Jie Liu, Yuansheng Gao, Sewite Negash, Lawrence D Longo, J Usha Raj

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Long-term hypoxia uncouples CaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. 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

5 authors at 3 institutions in 1 country.

Jie LiuDivision of Neonatology, Harbor-University of California, Los Angeles Medical Center, Geffen School of Medicine at University of California, and Los Angeles Biomedical Research Institute, Los Angeles, California 90502, USA. jliu@labiomed.org
Yuansheng Gao
Sewite Negash
Lawrence D Longo
J Usha Raj
University of California, Los Angeles · USLoma Linda University · USLos Angeles Medical Center · US

Funding

Uterine vascular responses to pregnancy and long term hypoxemiaP01HD031226 · NICHD · LOMA LINDA UNIVERSITY · PI LONGO, LAWRENCE D · 1995 to 2014
$21.4M
Mechanisms of cGMP-Mediated Vasodilation in Perinatal LungR01HL059435 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAJ, J. USHA · 1998 to 2010
$3.9M
Functional Heterogeneity of Pulmonary Arteries and VeinsR01HL075187 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAJ, J. USHA · 2003 to 2011
$3.8M
NHLBI NIH HHS HL 059435NHLBI NIH HHS HL 075187NICHD NIH HHS P01 HD031226NICHD NIH HHS P01 HD31226
6 · The paper itself

Abstract

Chronic hypoxia during the course of pregnancy is a common insult to the fetus. However, its long-term effect on the pulmonary vasculature in adulthood has not been described. In this study, the vasorelaxation responses of conduit pulmonary arteries in adult female sheep that were chronically hypoxic as fetuses and raised postnatally at sea level were investigated. Vessel tension studies revealed that endothelium-dependent relaxation responses were attenuated in pulmonary arteries from adult sheep that experienced prenatal hypoxia. Endothelial nitric oxide synthase (eNOS) protein expression was unchanged, but eNOS activity was significantly decreased in pulmonary arteries from prenatally hypoxic sheep. Protein expression of eNOS partners, caveolin-1, calmodulin, and heat shock protein 90 (Hsp90) did not change following prenatal hypoxia. However, the association between eNOS and caveolin-1, its inhibitory binding partner, was significantly increased, whereas association between eNOS and its stimulatory partners calmodulin and Hsp90 was greatly decreased. Furthermore, phosphorylation of Ser(1177) in eNOS decreased, whereas phosphorylation of Thr(495) increased, in the prenatally hypoxic pulmonary arteries, events that are related to eNOS activity. These data demonstrate that prenatal hypoxia results in persistent abnormalities in endothelium-dependent relaxation responses of pulmonary arteries in adult sheep due to decreased eNOS activity resulting from altered posttranslational regulation.

Indexed as

AcetylcholineAnimalsCalcimycinCalmodulinCaveolin 1Endothelium, VascularFemaleFetal HypoxiaHSP90 Heat-Shock ProteinsIn Vitro TechniquesNitric Oxide Synthase Type IIINitroso CompoundsPhosphorylationPregnancyPrenatal Exposure Delayed EffectsPulmonary Artery2,2'-(hydroxynitrosohydrazono)bis-ethanamineAcetylcholineCalcimycinCalmodulinCaveolin 1HSP90 Heat-Shock ProteinsNitric Oxide Synthase Type IIINitroso CompoundsSerineThreonine

Identifiers

PMID19136582
PMCPMC2660208
OpenAlexW2123229561

What Socratic 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 Socratic graph.