Evidence map›Paper›PMID 20056913›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2010

Loss of the serum response factor cofactor, cysteine-rich protein 1, attenuates neointima formation in the mouse.

Brenda Lilly, Kathleen A Clark, Masaaki Yoshigi, Stephen Pronovost, Meng-Ling Wu, Muthu Periasamy, Mei Chi, Richard J Paul, Shaw-Fang Yet, Mary C Beckerle

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

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  13. A Novel Role forFrontiers in genetics · 2017
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  19. CRP1, a protein localized in filopodia of growth cones, is involved in dendritic growth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    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

10 authors at 3 institutions in 2 countries.

Brenda LillyHuntsman Cancer Institute, Department of Biology, University of Utah, 2000 Circle of Hope, Salt Lake City, UT 84112, USA.
Kathleen A Clark
Masaaki Yoshigi
Stephen Pronovost
Meng-Ling Wu
Muthu Periasamy
Mei Chi
Richard J Paul
Shaw-Fang Yet
Mary C Beckerle
University of Utah · USNational Health Research Institutes · TWThe Ohio State University · US

Funding

Structure and function of stress fibers and cell adhesion sitesR01GM050877 · NIGMS · UNIVERSITY OF UTAH · PI BECKERLE, MARY C. · 1994 to 2020
$7.8M
Structure and function of muscleR01HL060591 · NHLBI · UNIVERSITY OF UTAH · PI BECKERLE, MARY C. · 1998 to 2005
$2.0M
NA-PUMP ISOFORM-SPECIFIC REGULATION OF VASCULAR FUNCTIONR01HL066044 · NHLBI · UNIVERSITY OF CINCINNATI · PI PAUL, RICHARD JEROME · 2001 to 2004
$1.5M
Transcriptional regulation of CRP1 in smooth muscleR01HL076428 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI LILLY, BRENDA J · 2006 to 2010
$1.4M
NHLBI NIH HHS HL076428NHLBI NIH HHS HL60591NHLBI NIH HHS HL66044NHLBI NIH HHS R01 HL060591NHLBI NIH HHS R01 HL066044NHLBI NIH HHS R01 HL076428NIGMS NIH HHS GM50877NIGMS NIH HHS R01 GM050877
6 · The paper itself

Abstract

objectiveCysteine-rich protein (CRP) 1 and 2 are cytoskeletal lin-11 isl-1 mec-3 (LIM)-domain proteins thought to be critical for smooth muscle differentiation. Loss of murine CRP2 does not overtly affect smooth muscle differentiation or vascular function but does exacerbate neointima formation in response to vascular injury. Because CRPs 1 and 2 are coexpressed in the vasculature, we hypothesize that CRPs 1 and 2 act redundantly in smooth muscle differentiation. METHODS AND

resultsWe generated Csrp1 (gene name for CRP1) null mice by genetic ablation of the Csrp1 gene and found that mice lacking CRP1 are viable and fertile. Smooth muscle-containing tissues from Csrp1-null mice are morphologically indistinguishable from wild-type mice and have normal contractile properties. Mice lacking CRPs 1 and 2 are viable and fertile, ruling out functional redundancy between these 2 highly related proteins as a cause for the lack of an overt phenotype in the Csrp1-null mice. Csrp1-null mice challenged by wire-induced arterial injury display reduced neointima formation, opposite to that seen in Csrp2-null mice, whereas Csrp1/Csrp2 double-null mice produce a wild-type response.

conclusionsSmooth muscle CRPs are not essential for normal smooth muscle differentiation during development, but may act antagonistically to modulate the smooth muscle response to pathophysiological stress.

Indexed as

Cell DifferentiationCell ProliferationAnimalsApoptosisCell MovementCells, CulturedFemoral ArteryGenotypeHyperplasiaLIM Domain ProteinsMiceMice, Inbred C57BLMice, KnockoutModels, AnimalMuscle ProteinsMuscle, Smooth, VascularCsrp1 protein, mouseCsrp2 protein, mouseLIM Domain ProteinsMuscle ProteinsNuclear Proteins

Identifiers

PMID20056913
PMCPMC2998921
OpenAlexW2123359570

What OpenQuestion holds

Textmetadata
LicenceTDM
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.