Evidence map›Paper›PMID 20817051›Full record

ArticleBone2010

Hypoxia increases Annexin A2 expression in osteoblastic cells via VEGF and ERK.

Damian C Genetos, Alice Wong, Shinya Watari, Clare E Yellowley

Abstract read
In one paragraph

Article in Bone, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Annexin A2 in Fibrinolysis, Inflammation and Fibrosis.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Dynamic reciprocity: the role of annexin A2 in tissue integrity.Journal of cell communication and signaling · 2014
    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

4 authors at 1 institution in 1 country.

Damian C GenetosDepartment of Anatomy, Cell Biology, and Physiology, School of Veterinary Medicine, University of California, Davis, Davis, CA, USA.
Alice Wong
Shinya Watari
Clare E Yellowley
University of California, Davis · US

Funding

A role for annexin V in bone cell mechanotransductionR01AG022305 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI YELLOWLEY-GENETOS, CLARE E · 2002 to 2006
$1.4M
Regulation of sclerostin expression by hypoxia: A proposed mechanism to explain hR03AR057547 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GENETOS, DAMIAN C · 2010 to 2012
$224k
NIAMS NIH HHS R03 AR057547NIAMS NIH HHS R03 AR57547NIA NIH HHS R01 AG022305
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF)-stimulated angiogenesis is critical for endochondral ossification that occurs during bone development and bone repair. Under these circumstances, VEGF production appears to be driven by low oxygen tension, under the control of the hypoxia-inducible factor-α family of transcription factors (HIF-α). Annexin 2 (AnxA2) a calcium-dependent phospholipid binding protein has been implicated in VEGF-mediated retinal neovascularization and is upregulated by VEGF in choroid retinal endothelial cells. AnxA2 is also expressed in cells of the osteoblast lineage and chondrocytes and may play a role in matrix mineralization. In this paper, we examined the effects of hypoxia (1% O(2)) and VEGF on the expression of AnxA2 in osteoblastic MC3T3-E1 cells. Hypoxia, desferrioxamine (hypoxia mimetic), and recombinant VEGF all increased AnxA2 mRNA and protein levels in osteoblastic cells. The hypoxia-induced increase in AnxA2 was inhibited by a blocking antibody to VEGF-R1; however, VEGF(120), a VEGF-R1 agonist, demonstrated no influence upon Anxa2 expression. This suggests that VEGF induction of Annexin A2 is not mediated via VEGF-R1 agonism alone but by VEGF-R1 and Neuropilin-1 or Neuropilin-2 heterodimers. In addition, we demonstrated that VEGF-stimulated changes in AnxA2 expression via a pathway involving Src and MEK kinase. These data demonstrate that AnxA2 expression in osteoblasts is under the control of VEGF, which may have implications for both angiogenesis and bone mineralization under low oxygen conditions.

Indexed as

AnimalsAnnexin A2Cell HypoxiaExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHypoxia-Inducible Factor 1, alpha SubunitMaleMiceOsteoblastsOxygenProtein IsoformsProtein StabilityRNA, MessengerSignal Transductionsrc-Family KinasesVascular Endothelial Growth Factor AAnnexin A2Extracellular Signal-Regulated MAP KinasesHypoxia-Inducible Factor 1, alpha SubunitOxygenProtein IsoformsRNA, Messengersrc-Family KinasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID20817051
PMCPMC4420171
OpenAlexW2005612470

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.