Evidence map›Paper›PMID 20441584›Full record

ArticleJournal of cardiothoracic surgery2010

Thrombospondin-1 null mice are resistant to hypoxia-induced pulmonary hypertension.

Cristhiaan D Ochoa, Lunyin Yu, Essam Al-Ansari, Charles A Hales, Deborah A Quinn

Open access · goldAbstract read
In one paragraph

Article in Journal of cardiothoracic surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.American journal of physiology. Cell physiology · 2020
    Review
  5. Review
  6. Article
  7. Review
  8. HIF-1α represses the expression of the angiogenesis inhibitor thrombospondin-2.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Article
  9. Thrombospondins: A Role in Cardiovascular Disease.International journal of molecular sciences · 2017
    Review
  10. Review
  11. Article
  12. Article
  13. Observational
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Cristhiaan D OchoaDepartment of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. cdo701@jaguar1.usouthal.edu
Lunyin Yu
Essam Al-Ansari
Charles A Hales
Deborah A Quinn
Harvard University · USMassachusetts General Hospital · US

Funding

HEPARIN ON HYPOXIC PULMONARY HYPERTENSION AND REMODELINGR01HL039150 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HALES, CHARLES A · 1987 to 2011
$4.3M
NHLBI NIH HHS HL39150NHLBI NIH HHS R01 HL039150
6 · The paper itself

Abstract

BACKGROUND AND

objectiveChronic hypoxia induces pulmonary hypertension in mice. Smooth muscle cell hyperplasia and medial thickening characterize the vasculature of these animals. Thrombospondin-1 null (TSP-1(-/-)) mice spontaneously develop pulmonary smooth muscle cell hyperplasia and medial thickening. In addition, TSP-1 produced by the pulmonary endothelium inhibits pulmonary artery smooth muscle cell growth. Based on these observations we sought to describe the pulmonary vascular changes in TSP-1(-/-) mice exposed to chronic hypoxia.

methodsWe exposed TSP-1(-/-) and wild type (WT) mice to a fraction of inspired oxygen (FiO2) of 0.1 for up to six weeks. Pulmonary vascular remodeling was evaluated using tissue morphometrics. Additionally, right ventricle systolic pressures (RVSP) and right ventricular hypertrophy by right ventricle/left ventricle + septum ratios (RV/LV+S) were measured to evaluate pulmonary hypertensive changes. Finally, acute pulmonary vasoconstriction response in both TSP-1(-/-) and WT mice was evaluated by acute hypoxia and U-46619 (a prostaglandin F2 analog) response.

resultsIn hypoxia, TSP-1(-/-) mice had significantly lower RVSP, RV/LV+S ratios and less pulmonary vascular remodeling when compared to WT mice. TSP-1(-/-) mice also had significantly lower RVSP in response to acute pulmonary vasoconstriction challenges than their WT counterparts.

conclusionTSP-1(-/-) mice had diminished pulmonary vasoconstriction response and were less responsive to hypoxia-induced pulmonary hypertension than their wild type counterparts. This observation suggests that TSP-1 could play an active role in the pathogenesis of pulmonary hypertension associated with hypoxia.

Indexed as

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidAnimalsHypertension, PulmonaryHypertrophy, Right VentricularHypoxiaMaleMiceMice, KnockoutMuscle, Smooth, VascularPulmonary ArteryThrombospondin 1VasoconstrictionVasoconstrictor AgentsVentricular Function, Right15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidThrombospondin 1Vasoconstrictor Agents

Identifiers

PMID20441584
PMCPMC2877040
OpenAlexW2113017194

What OpenQuestion holds

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LicenceCC BY
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.