Evidence map›Paper›PMID 20881097›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2010

ID family protein expression and regulation in hypoxic pulmonary hypertension.

Jonathan W Lowery, Andrea L Frump, Lynda Anderson, Gabriella E DiCarlo, Mark T Jones, Mark P de Caestecker

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. The role of Id genes on pulmonary hypertension development in left heart failure.American heart journal plus : cardiology research and practice · 2026
    Article
  4. AFrontiers in cardiovascular medicine · 2024
    Article
  5. Review
  6. Review
  7. Hearing Loss in Id1Frontiers in genetics · 2021
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Molecular mechanisms of pulmonary arterial remodeling.Molecular medicine (Cambridge, Mass.) · 2014
    Review
  15. Id proteins are critical downstream effectors of BMP signaling in human pulmonary arterial smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  16. Article
  17. Article
  18. Genome-scale study of transcription factor expression in the branching mouse lung.Developmental dynamics : an official publication of the American Association of Anatomists · 2012
    Article
  19. A brief overview of mouse models of pulmonary arterial hypertension: problems and prospects.American journal of physiology. Lung cellular and molecular physiology · 2012
    Review
  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

6 authors at 1 institution in 1 country.

Jonathan W LoweryVanderbilt Univ. Medical Center, Department of Cell and Developmental Biology, Nashville, TN 37232, USA.
Andrea L Frump
Lynda Anderson
Gabriella E DiCarlo
Mark T Jones
Mark P de Caestecker
Vanderbilt University Medical Center · US

Funding

TRAINING GRANT IN MECHANISMS OF VASCULAR DISEASET32HL007751 · NHLBI · VANDERBILT UNIVERSITY · PI BOCK, PAUL E · 1994 to 2014
$6.6M
NHLBI NIH HHS T32HL007751
6 · The paper itself

Abstract

Bone morphogenetic protein (BMP) signaling has been linked to the development of pulmonary hypertension (PH). Inhibitors of differentiation (ID) proteins (ID1-4) are a family of basic helix-loop-helix transcription factors that are downstream targets of the BMP signaling pathway, but the role that ID proteins play in the development of PH is unknown. To address this, we evaluated pulmonary expression of ID proteins in a mouse model of hypoxia-induced PH. There is selective induction of ID1 and ID3 expression in hypoxic pulmonary vascular smooth muscle cells (VSMCs) in vivo, and ID1 and ID3 expression are increased by hypoxia in cultured pulmonary VSMCs in a BMP-dependent fashion. ID4 protein is barely detectable in the mouse lung, and while ID2 is induced in hypoxic peripheral VSMCs in vivo, it is not increased by hypoxia or BMP signaling in cultured pulmonary VSMCs. In addition, the PH response to chronic hypoxia is indistinguishable between wild type and Id1 null mice. This is associated with a compensatory increase in ID3 but not ID2 expression in pulmonary VSMCs of Id1 null mice. These findings indicate that ID1 is dispensable for mounting a normal pulmonary vascular response to hypoxia, but suggest that ID3 may compensate for loss of ID1 expression in pulmonary VSMCs. Taken together, these findings indicate that ID1 and ID3 expression are regulated in a BMP-dependent fashion in hypoxic pulmonary VSMCs, and that ID1 and ID3 may play a cooperative role in regulating BMP-dependent VSMC responses to chronic hypoxia.

Indexed as

Analysis of VarianceAnimalsBlotting, WesternCells, CulturedHypertension, PulmonaryHypoxiaImmunohistochemistryInhibitor of Differentiation ProteinsLungMiceMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphorylationInhibitor of Differentiation Proteins

Identifiers

PMID20881097
PMCPMC3007180
OpenAlexW2031454522

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.