Evidence map›Paper›PMID 18079198›Full record

ArticleEndocrinology2008

Dehydroepiandrosterone stimulates endothelial proliferation and angiogenesis through extracellular signal-regulated kinase 1/2-mediated mechanisms.

Dongmin Liu, Mary Iruthayanathan, Laurie L Homan, Yiqiang Wang, Lingling Yang, Yao Wang, Joseph S Dillon

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. 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
3.3field-weighted citation impact, top 8% 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, 91 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Menopause, androgens, and cardiovascular ageing: a narrative review.Therapeutic advances in endocrinology and metabolism · 2022
    Review
  10. Deletion ofFrontiers in endocrinology · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Dehydroepiandrosterone and Erectile Function: A Review.The world journal of men's health · 2018
    Review
  15. Article
  16. Inhibition of Osteoblast Function byFrontiers in immunology · 2018
    Article
  17. Article
  18. Article
  19. Androgen receptor in human endothelial cells.The Journal of endocrinology · 2015
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Dongmin LiuDivision of Endocrinology, Veterans Affairs Medical Center, University of Iowa,Iowa City, Iowa 52242, USA. doliu@vt.edu
Mary Iruthayanathan
Laurie L Homan
Yiqiang Wang
Lingling Yang
Yao Wang
Joseph S Dillon
University of Iowa · USShandong Eye Institute & Hospital · CN

Funding

DEHYDROEPIANDROSTERONE SULFATE AND INSULIN SECRETIONR01AG018928 · NIA · UNIVERSITY OF IOWA · PI DILLON, JOSEPH S · 2000 to 2004
$968k
NIA NIH HHS AG55741NIA NIH HHS R01 AG018928
6 · The paper itself

Abstract

Dehydroepiandrosterone (DHEA) activates a plasma membrane receptor on vascular endothelial cells and phosphorylates ERK 1/2. We hypothesize that ERK1/2-dependent vascular endothelial proliferation underlies part of the beneficial vascular effect of DHEA. DHEA (0.1-10 nm) activated ERK1/2 in bovine aortic endothelial cells (BAECs) by 15 min, causing nuclear translocation of phosphorylated ERK1/2 and phosphorylation of nuclear p90 ribosomal S6 kinase. ERK1/2 phosphorylation was dependent on plasma membrane-initiated activation of Gi/o proteins and the upstream MAPK kinase because the effect was seen with albumin-conjugated DHEA and was blocked by pertussis toxin or PD098059. A 15-min incubation of BAECs with 1 nm DHEA (or albumin-conjugated DHEA) increased endothelial proliferation by 30% at 24 h. This effect was not altered by inhibition of estrogen or androgen receptors or nitric oxide production. There was a similar effect of DHEA to increase endothelial migration. DHEA also increased the formation of primitive capillary tubes of BAECs in vitro in solubilized basement membrane. These rapid DHEA-induced effects were reversed by the inhibition of either Gi/o-proteins or ERK1/2. Additionally, DHEA enhanced angiogenesis in vivo in a chick embryo chorioallantoic membrane assay. These findings indicate that exposure to DHEA, at concentrations found in human blood, causes vascular endothelial proliferation by a plasma membrane-initiated activity that is Gi/o and ERK1/2 dependent. These data, along with previous findings, define an important vascular endothelial cell signaling pathway that is activated by DHEA and suggest that this steroid may play a role in vascular function.

Indexed as

Cell ProliferationAnimalsAortaCattleCell MovementCells, CulturedDehydroepiandrosteroneEndothelium, VascularEnzyme ActivationGTP-Binding Protein alpha Subunits, Gi-GoMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neovascularization, PhysiologicSignal TransductionDehydroepiandrosteroneGTP-Binding Protein alpha Subunits, Gi-GoMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3

Identifiers

PMID18079198
PMCPMC2275364
OpenAlexW2080953895

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.