Evidence map›Paper›PMID 12032352›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Corticotropin-releasing factor receptor 2 is a tonic suppressor of vascularization.

Tracy L Bale, Frank J Giordano, Reed P Hickey, Yan Huang, Anjali K Nath, Kirk L Peterson, Wylie W Vale, Kuo-Fen Lee

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. 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
2.4field-weighted citation impact, top 11% 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, 95 citations in OpenAlex.

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  7. Immunolocalization of corticotropin-releasing hormone (CRH) and its receptors (CRHR1 and CRHR2) in human endometrial carcinoma: CRHR1 as a potent prognostic factor.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2014
    Article
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  11. Corticotropin-releasing factor family and its receptors: pro-inflammatory or anti-inflammatory targets in the periphery?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011
    Review
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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

8 authors at 2 institutions in 1 country.

Tracy L BaleClayton Foundation Laboratories for Peptide Biology, The Salk Institute, La Jolla, CA 92037, USA.
Frank J Giordano
Reed P Hickey
Yan Huang
Anjali K Nath
Kirk L Peterson
Wylie W Vale
Kuo-Fen Lee
Salk Institute for Biological Studies · USYale University · US

Funding

TARGETED DISRUPTION OF NEUROENDOCRINE GENESP01DK026741 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI FISCHER, WOLFGANG H, RIVIER, JEAN E · 1986 to 2014
$31.6M
NIDDK NIH HHS DK26741NIDDK NIH HHS P01 DK026741
6 · The paper itself

Abstract

Angiogenesis is regulated by means of a balance between activators and inhibitors. However, little is known regarding the regulation of the quiescent state of adult vessels. Corticotropin-releasing factor receptor 2 (CRFR2) is found in both endothelial and smooth muscle cells (SMCs) in the vasculature, where its function has remained elusive. We have investigated the role of CRFR2 as a determinant of tissue vascularization by comparing control and CRFR2-deficient mice with immunohistological and morphometric techniques. To define the mechanisms responsible for CRFR2 inhibition of angiogenesis, we have also examined in vitro the effect of ligand activation on cell proliferation, cell cycle protein phosphorylation, and capillary tube formation. Our results demonstrate that mice deficient for CRFR2 become hypervascularized postnatally. Activation of this receptor in vitro results in reduced vascular endothelial growth factor (VEGF) release from SMCs, an inhibition of SMC proliferation, and inhibition of capillary tube formation in collagen gels. Treatment of a subcutaneously injected gel matrix with a CRFR2 agonist inhibits growth factor-induced vascularization. Western blots show that cell cycle retinoblastoma protein, which is essential for cell cycle progression, is decreased by CRFR2 agonist treatment in SMCs. These results suggest that CRFR2 is a critical component of a pathway necessary for tonic inhibition of adult neovascularization. CRFR2 may be a potential target for therapeutic modulation of angiogenesis in cancer and ischemic cardiovascular disease.

Indexed as

Angiogenesis InhibitorsAnimalsCapillariesCell DivisionCells, CulturedEndothelial Growth FactorsEndothelium, VascularGene Expression RegulationLymphokinesMiceMice, KnockoutMuscle, Smooth, VascularNeovascularization, PhysiologicReceptors, Corticotropin-Releasing HormoneVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsAngiogenesis InhibitorsCRF receptor type 2Endothelial Growth FactorsLymphokinesReceptors, Corticotropin-Releasing HormoneVascular Endothelial Growth Factor AVascular Endothelial Growth Factors

Identifiers

PMID12032352
PMCPMC124337
OpenAlexW1999524354

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.