Evidence map›Paper›PMID 18787183›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2008

FRNK expression promotes smooth muscle cell maturation during vascular development and after vascular injury.

Rebecca L Sayers, Liisa J Sundberg-Smith, Mauricio Rojas, Haruko Hayasaka, J Thomas Parsons, Christopher P Mack, Joan M Taylor

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. FAK Family Kinases: A Potential Therapeutic Target for Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. FAK Family Kinases in Vascular Diseases.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Signaling mechanisms that regulate smooth muscle cell differentiation.Arteriosclerosis, thrombosis, and vascular biology · 2011
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Rebecca L SayersDepartment of Pathology, University of North Carolina, Chapel Hill, NC 27599-7525, USA.
Liisa J Sundberg-Smith
Mauricio Rojas
Haruko Hayasaka
J Thomas Parsons
Christopher P Mack
Joan M Taylor
Johnson C. Smith University · US

Funding

Regulation of Smooth Muscle Differentiation by RhoAR01HL070953 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MACK, CHRISTOPHER P. · 2002 to 2012
$2.8M
FAK Signaling in cardiac growth and hypertrophyR01HL081844 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TAYLOR, JOAN M · 2005 to 2013
$2.6M
CELL &MOLECULAR BIOLOGY TRAINING PROGRAMT32GM008581 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COX, ADRIENNE D · 1996 to 2008
$1.3M
Adhesion Signaling in Vascular Growth and DevelopmentR01HL071054 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TAYLOR, JOAN M. · 2003 to 2006
$1.2M
NHLBI NIH HHS HL070953NHLBI NIH HHS HL-071054NHLBI NIH HHS HL-081844NHLBI NIH HHS R01 HL070953NHLBI NIH HHS R01 HL071054NHLBI NIH HHS R01 HL081844NIGMS NIH HHS GM008581-06A2NIGMS NIH HHS T32 GM008581
6 · The paper itself

Abstract

objectiveSmooth muscle cell (SMC) differentiation is a dynamic process that must be tightly regulated for proper vascular development and to control the onset of vascular disease. Our laboratory previously reported that a specific focal adhesion kinase (FAK) inhibitor termed FRNK (FAK Related Non-Kinase) is selectively expressed in large arterioles when SMCs are transitioning from a synthetic to contractile phenotype and that FRNK inhibits FAK-dependent SMC proliferation and migration. Herein, we sought to determine whether FRNK expression modulates SMC phenotypes in vivo. METHODS AND

resultsWe present evidence that FRNK(-/-) mice exhibit attenuated SM marker gene expression during postnatal vessel growth and after vascular injury. We also show that FRNK expression is regulated by transforming growth factor (TGF)-beta and that forced expression of FRNK in cultured cells induces serum- and TGF-beta-stimulated SM marker gene expression, whereas FRNK deletion or expression of a constitutively activated FAK variant attenuated SM gene transcription.

conclusionsThese data highlight the possibility that extrinsic signals regulate the SMC gene profile, at least in part, by modulating the expression of FRNK and that tight regulation of FAK activity by FRNK is important for proper SMC differentiation during development and after vascular injury.

Indexed as

AnimalsBlood VesselsCell DifferentiationCells, CulturedFocal Adhesion Protein-Tyrosine KinasesGene ExpressionHumansMiceMice, KnockoutMyocytes, Smooth MuscleProtein-Tyrosine KinasesRatsRNA, MessengerSignal TransductionTransforming Growth Factor betaFAK-related nonkinaseFocal Adhesion Protein-Tyrosine KinasesProtein-Tyrosine KinasesRNA, MessengerTransforming Growth Factor beta

Identifiers

PMID18787183
PMCPMC2785047
OpenAlexW2121456364

What OpenQuestion holds

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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.