Evidence map›Paper›PMID 20813185›Full record

ArticleThe Journal of steroid biochemistry and molecular biology2010

A role for the cell cycle phosphatase Cdc25a in vitamin D-dependent inhibition of adult rat vascular smooth muscle cell proliferation.

Songcang Chen, Christopher S Law, Christopher L Grigsby, Keith Olsen, David G Gardner

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of steroid biochemistry and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Vitamin D and Arterial Hypertension: Facts and Myths.Current hypertension reports · 2020
    Review
  5. Vitamin D and Cardiovascular Risk: which Implications in Children?International journal of molecular sciences · 2020
    Review
  6. Article
  7. Article
  8. Vitamin D Deficiency Accelerates Coronary Artery Disease Progression in Swine.Arteriosclerosis, thrombosis, and vascular biology · 2016
    Article
  9. Vitamin D deficiency and essential hypertension.Journal of the American Society of Hypertension : JASH · 2015
    Review
  10. Review
  11. Article
  12. Arterial stiffness and vitamin D levels: the Baltimore longitudinal study of aging.The Journal of clinical endocrinology and metabolism · 2012
    Article
  13. Vitamin D deficiency is associated with the development of subclinical coronary artery disease in African Americans with HIV infection: a preliminary study.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2012
    Article
  14. 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

5 authors at 2 institutions in 2 countries.

Songcang ChenDiabetes Center, University of California at San Francisco, CA 94143-0540, United States. schen@diabetes.ucsf.edu
Christopher S Law
Christopher L Grigsby
Keith Olsen
David G Gardner
University of California, San Francisco · USDiabetes Australia · AU

Funding

REGULATION OF ANP RECEPTOR ACTIVITY IN VASCULAR CELLSR01HL045637 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GARDNER, DAVID G · 1992 to 2011
$3.6M
A Role for Non-Hypercalcemic VDR Agonists in the Control of VSMC ProliferationR21HL096047 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHEN, SONGCANG · 2010 to 2011
$425k
NHLBI NIH HHS HL096047NHLBI NIH HHS HL45637NHLBI NIH HHS R01 HL045637NHLBI NIH HHS R21 HL096047
6 · The paper itself

Abstract

We have explored the mechanism(s) underlying 1,25 dihydroxyvitamin D's (1,25(OH)(2)D) suppression of agonist-induced vascular smooth muscle cell (VSMC) proliferation. Quiescent cultured adult rat VSMC were treated with 1,25(OH)(2)D for 48h and endothelin (ET) or angiotensin II (AII) for the final 24h. We show that VSMC responded to 1,25(OH)(2)D or its less hypercalcemic analogue RO 25-6760 with ∼70% inhibition of ET-dependent (3)H-thymidine incorporation. The inhibition was linked to a comparable reduction in ET-stimulated cyclin-dependent kinase 2 (Cdk2) activity and suppression of an ET-induced Cdk2 activator, cell division cycle 25 homolog A (Cdc25A). Both 1,25(OH)(2)D and RO 25-6760 completely inhibited the ET-dependent increase in Cdc25A mRNA and protein levels, phosphatase and promoter activities. 1,25(OH)(2)D also suppressed AII-induced DNA synthesis, Cdk2 activity and Cdc25A gene transcription. Inhibition of Cdc25A gene expression using a siRNA approach resulted in significant inhibition of ET or AII-dependent Cdk2 activity and (3)H-thymidine incorporation. The Cdc25A siRNA-mediated inhibition of ET or AII-induced Cdk2 activity and DNA synthesis was not additive with that produced by 1,25(OH)(2)D treatment. These data demonstrate that 1,25(OH)(2)D inhibits VSMC proliferation through a Cdc25A-dependent mechanism and suggest that this hormone may prove useful in the management of disorders characterized by aberrant proliferation of VSMC in the vascular wall.

Indexed as

Angiotensin IIAnimalsCalcitriolcdc25 PhosphatasesCell ProliferationCells, CulturedCholecalciferolCyclin-Dependent Kinase 2EndothelinsMuscle, Smooth, VascularRatsAngiotensin IICalcitriolcdc25 PhosphatasesCdk2 protein, ratCholecalciferolCyclin-Dependent Kinase 2EndothelinsRo 25-6760

Identifiers

PMID20813185
PMCPMC4143149
OpenAlexW2074530650

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.