Evidence map›Paper›PMID 19273721›Full record

ArticleCirculation2009

G-protein-coupled receptor kinase interacting protein-1 is required for pulmonary vascular development.

Jinjiang Pang, Ryan Hoefen, Gloria S Pryhuber, Jing Wang, Guoyong Yin, R James White, Xiangbin Xu, Michael R O'Dell, Amy Mohan, Heidi Michaloski and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.6field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  14. The P2-receptor-mediated CaPurinergic signalling · 2019
    Article
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  17. [Research on influence mechanism of G protein coupled receptor kinase interacting protein 1 on differentiation of bone marrow mesenchymal stem cells into endothelial cells].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2018
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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

13 authors at 1 institution in 1 country.

Jinjiang PangAab Cardiovascular Research Institute and the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Ryan Hoefen
Gloria S Pryhuber
Jing Wang
Guoyong Yin
R James White
Xiangbin Xu
Michael R O'Dell
Amy Mohan
Heidi Michaloski
Michael P Massett
Chen Yan
Bradford C Berk
University of Rochester · US

Funding

Vascular Inflammation and AtherosclerosisP01HL077789 · NHLBI · UNIVERSITY OF ROCHESTER · PI FUJIWARA, KEIGI · 2005 to 2009
$10.1M
ANGIOTENSIN II SIGNAL TRANSDUCTIONR01HL063462 · NHLBI · UNIVERSITY OF ROCHESTER · PI BERK, BRADFORD C · 1999 to 2012
$4.3M
NHLBI NIH HHS HL63462NHLBI NIH HHS HL77789NHLBI NIH HHS P01 HL077789NHLBI NIH HHS R01 HL063462
6 · The paper itself

Abstract

backgroundThe G-protein-coupled receptor kinase interacting protein-1 (GIT1) is a multidomain scaffold protein that participates in many cellular functions including receptor internalization, focal adhesion remodeling, and signaling by both G-protein-coupled receptors and tyrosine kinase receptors. However, there have been no in vivo studies of GIT1 function to date. METHODS AND

resultsTo determine essential functions of GIT1 in vivo, we generated a traditional GIT1 knockout mouse. GIT1 knockout mice exhibited approximately 60% perinatal mortality. Pathological examination showed that the major abnormality in GIT1 knockout mice was impaired lung development characterized by markedly reduced numbers of pulmonary blood vessels and increased alveolar spaces. Given that vascular endothelial growth factor (VEGF) is essential for pulmonary vascular development, we investigated the role of GIT1 in VEGF signaling in the lung and cultured endothelial cells. Because activation of phospholipase-Cgamma (PLCgamma) and extracellular signal-regulated kinases 1/2 (ERK1/2) by angiotensin II requires GIT1, we hypothesized that GIT1 mediates VEGF-dependent pulmonary angiogenesis by modulating PLCgamma and ERK1/2 activity in endothelial cells. In cultured endothelial cells, knockdown of GIT1 decreased VEGF-mediated phosphorylation of PLCgamma and ERK1/2. PLCgamma and ERK1/2 activity in lungs from GIT1 knockout mice was reduced postnatally.

conclusionsOur data support a critical role for GIT1 in pulmonary vascular development by regulating VEGF-induced PLCgamma and ERK1/2 activation.

Indexed as

AnimalsAnimals, NewbornCell Cycle ProteinsCell DivisionCells, CulturedDNAEndothelial CellsGTPase-Activating ProteinsMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neovascularization, PhysiologicPhospholipase C gammaPhosphorylationCell Cycle ProteinsDNAGit1 protein, mouseGTPase-Activating ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phospholipase C gammaVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID19273721
PMCPMC2732662
OpenAlexW2057216996

What OpenQuestion holds

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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.