Evidence map›Paper›PMID 11806997›Full record

ArticleBlood2002

Cyclin A transcriptional suppression is the major mechanism mediating homocysteine-induced endothelial cell growth inhibition.

Hong Wang, XiaoHua Jiang, Fan Yang, Gary B Chapman, William Durante, Nicholas E S Sibinga, Andrew I Schafer

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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  6. Article
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  9. Article
  10. Article
  11. Review
  12. Prolonged cyclic strain inhibits human endothelial cell growth.Frontiers in bioscience (Elite edition) · 2016
    Article
  13. Article
  14. Article
  15. Homocysteine induces inflammatory transcriptional signaling in monocytes.Frontiers in bioscience (Landmark edition) · 2013
    Article
  16. Article
  17. Homocysteine inhibits adipogenesis in 3T3-L1 preadipocytes.Experimental biology and medicine (Maywood, N.J.) · 2011
    Article
  18. Article
  19. Review
  20. Regulation of homocysteine metabolism and methylation in human and mouse tissues.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010
    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

7 authors at 1 institution in 1 country.

Hong WangDepartment of Medicine, Baylor College of Medicine, 2002 Holcombe Ave 109-129, Houston, TX 77030, USA. hongw@bcm.tmc.edu
XiaoHua Jiang
Fan Yang
Gary B Chapman
William Durante
Nicholas E S Sibinga
Andrew I Schafer
Albert Einstein College of Medicine · US

Funding

Atherogenic mechanisms with homocysteineR01HL077288 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2004 to 2014
$3.8M
CARBON MONOXIDE AND VASCULAR SMOOTH MUSCLE CELL FUNCTIONR01HL059976 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DURANTE, WILLIAM · 1999 to 2013
$3.3M
Inhibition of Endothelial Growth by HomocysteineR01HL067033 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2002 to 2011
$3.0M
VASCULAR CELL CATIONIC AMINO ACID TRANSPORT &METABOLISMR01HL062467 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI SCHAFER, ANDREW I · 1999 to 2002
$926k
Homocysteine-induced Endothelial Cell Growth InhibitionK02HL074925 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2004 to 2008
$527k
NHLBI NIH HHS HL-59976NHLBI NIH HHS HL-62467NHLBI NIH HHS K02 HL074925NHLBI NIH HHS R01 HL059976NHLBI NIH HHS R01 HL067033NHLBI NIH HHS R01 HL077288
6 · The paper itself

Abstract

Previously, it was reported that homocysteine (Hcy) specifically inhibits the growth of endothelial cells (ECs), suppresses Ras/mitogen-activated protein (MAP) signaling, and arrests cell growth at the G(1)/S transition of the cell cycle. The present study investigated the molecular mechanisms underlying this cell-cycle effect. Results showed that clinically relevant concentrations (50 microM) of Hcy significantly inhibited the expression of cyclin A messenger RNA (mRNA) in ECs in a dose- and time-dependent manner. G(1)/S-associated molecules that might account for this block were not changed, because Hcy did not affect mRNA and protein expression of cyclin D1 and cyclin E. Cyclin D1- and E-associated kinase activities were unchanged. In contrast, cyclin A-associated kinase activity and CDK2 kinase activity were markedly suppressed. Nuclear run-on assay demonstrated that Hcy decreased the transcription rate of the cyclin A gene but had no effect on the half-life of cyclin A mRNA. In transient transfection experiments, Hcy significantly inhibited cyclin A promoter activity in endothelial cells, but not in vascular smooth muscle cells. Finally, adenovirus-transduced cyclin A expression restored EC growth inhibition and overcame the S phase block imposed by Hcy. Taken together, these findings indicate that cyclin A is a critical functional target of Hcy-mediated EC growth inhibition.

Indexed as

AnimalsAortaCell CycleCell DivisionCells, CulturedCyclin ADown-RegulationEndothelium, VascularHomocysteineHumansMuscle, Smooth, VascularPromoter Regions, GeneticRatsRNA, MessengerTranscription, GeneticUmbilical VeinsCyclin AHomocysteineRNA, Messenger

Identifiers

PMID11806997
PMCPMC5539868
OpenAlexW1555819284

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.