Evidence map›Paper›PMID 18387947›Full record

ArticleThe Journal of biological chemistry2008

Transforming growth factor beta up-regulates cysteine-rich protein 2 in vascular smooth muscle cells via activating transcription factor 2.

Da-Wei Lin, Il-Chi Chang, Alan Tseng, Meng-Ling Wu, Chung-Huang Chen, Cassandra A Patenaude, Matthew D Layne, Shaw-Fang Yet

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The TGFβ superfamily in cardiac dysfunction.Acta biochimica et biophysica Sinica · 2018
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Can proteomics yield insight into aging aorta?Proteomics. Clinical applications · 2013
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

8 authors at 4 institutions in 2 countries.

Da-Wei LinDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Il-Chi Chang
Alan Tseng
Meng-Ling Wu
Chung-Huang Chen
Cassandra A Patenaude
Matthew D Layne
Shaw-Fang Yet
National Health Research Institutes · TWBoston University · USHarvard University · USBrigham and Women's Hospital · US

Funding

Role of ACLP in Vascular Smooth Muscle BiologyR01HL078869 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LAYNE, MATTHEW D · 2007 to 2011
$2.2M
SMLIM, A VASCULAR SMOOTH MUSCLE LIM PROTEINR01HL057977 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI YET, SHAW-FANG · 1997 to 2005
$1.8M
NHLBI NIH HHS HL 057977NHLBI NIH HHS HL 078869NHLBI NIH HHS R01 HL057977NHLBI NIH HHS R01 HL078869
6 · The paper itself

Abstract

CRP2 (cysteine-rich protein) is a vascular smooth muscle cell (VSMC)-expressed LIM-only protein. CRP2 associates with the actin cytoskeleton and interacts with transcription factors in the nucleus to mediate smooth muscle cell gene expression. Using Csrp2 (gene symbol of the mouse CRP2 gene)-deficient mice, we previously demonstrated that an absence of CRP2 enhances VSMC migration and increases neointima formation following arterial injury. Despite its importance in vascular injury, the molecular mechanisms controlling CRP2 expression in VSMC are largely unknown. Transforming growth factor beta (TGFbeta), a key factor present in the vessel wall in the early phases of arterial response to injury, plays an important role in modulating lesion formation. Because both CRP2 and TGFbeta are mediators of VSMC responses, we examined the possibility that TGFbeta might regulate CRP2 expression. TGFbeta significantly induced CRP2 mRNA and protein expression in VSMCs. Promoter analysis identified a conserved cAMP-responsive element (CRE)-like site (TAACGTCA) in the Csrp2 promoter that was critical for basal promoter activity and response to TGFbeta. Gel mobility shift assays revealed that mainly ATF2 bound to this CRE-like element, and mutation of the CRE sequences abolished binding. TGFbeta enhanced the activation of ATF2, leading to increased phospho-ATF2 levels within the DNA-protein complexes. Furthermore, ATF2-transactivated Csrp2 promoter activity and TGFbeta enhanced this activation. In addition, a phosphorylation-negative ATF2 mutant construct decreased basal and TGFbeta-mediated Csrp2 promoter activity. Our results show for the first time in VSMC that TGFbeta activates ATF2 phosphorylation and Csrp2 gene expression via a CRE promoter element.

Indexed as

Transcriptional ActivationActinsActivating Transcription Factor 2AnimalsArteriesCell MovementCell NucleusCells, CulturedCytoskeletonLIM Domain ProteinsMiceMuscle ProteinsMuscle, Smooth, VascularMutationMyocytes, Smooth MuscleNuclear ProteinsActinsActivating Transcription Factor 2Atf2 protein, mouseAtf2 protein, ratCsrp2 protein, mouseCsrp2 protein, ratLIM Domain ProteinsMuscle ProteinsNuclear ProteinsTransforming Growth Factor beta

Identifiers

PMID18387947
PMCPMC2397482
OpenAlexW1985638610

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.