Evidence map›Paper›PMID 19841066›Full record

ArticleMolecular and cellular biology2010

Prostaglandin promotion of osteocyte gap junction function through transcriptional regulation of connexin 43 by glycogen synthase kinase 3/beta-catenin signaling.

Xuechun Xia, Nidhi Batra, Qian Shi, Lynda F Bonewald, Eugene Sprague, Jean X Jiang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 141 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Osteocytes and Primary Cilia.Current osteoporosis reports · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Connexin 43 hemichannels and prostaglandin EFrontiers in cell and developmental biology · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Xuechun XiaDepartment of Biochemistry, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Nidhi Batra
Qian Shi
Lynda F Bonewald
Eugene Sprague
Jean X Jiang
The University of Texas Health Science Center at San Antonio · USUniversity of Missouri–Kansas City · US

Funding

Transgenic CoreP01AR046798 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI BONEWALD, LYNDA F · 2001 to 2010
$10.5M
NIAMS NIH HHS AR46798NIAMS NIH HHS P01 AR046798
6 · The paper itself

Abstract

Gap junction intercellular communication in osteocytes plays an important role in bone remodeling in response to mechanical loading; however, the responsible molecular mechanisms remain largely unknown. Here, we show that phosphoinositide-3 kinase (PI3K)/Akt signaling activated by fluid flow shear stress and prostaglandin E(2) (PGE(2)) had a stimulatory effect on both connexin 43 (Cx43) mRNA and protein expression. PGE(2) inactivated glycogen synthase kinase 3 (GSK-3) and promoted nuclear localization and accumulation of beta-catenin. Knockdown of beta-catenin expression resulted in a reduction in Cx43 protein. Furthermore, the chromatin immunoprecipitation (ChIP) assay demonstrated an association of beta-catenin with the Cx43 promoter, suggesting that beta-catenin could regulate Cx43 expression at the level of gene transcription. We have previously reported that PGE(2) activates cyclic AMP (cAMP)-protein kinase A (PKA) signaling and increases Cx43 and gap junctions. Interestingly, the activation of PI3K/Akt appeared to be independent of the activation of PKA, whereas both PI3K/Akt and PKA signaling inactivated GSK-3 and increased beta-catenin translocation. Together, these results suggest that shear stress, through PGE(2) release, activates both PI3K/Akt and cAMP-PKA signaling, which converge through the inactivation of GSK-3, leading to the increase in nuclear accumulation of beta-catenin. beta-Catenin binds to the Cx43 promoter, stimulating Cx43 expression and functional gap junctions between osteocytes.

Indexed as

Transcription, GeneticActive Transport, Cell NucleusAnimalsbeta CateninCell LineCell NucleusConnexin 43Cyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneGap JunctionsGlycogen Synthase Kinase 3MiceOsteocytesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktbeta CateninConnexin 43CTNNB1 protein, mouseCyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneGJA1 protein, mouseGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID19841066
PMCPMC2798309
OpenAlexW2127130496

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.