Evidence map›Paper›PMID 11076975›Full record

ArticleThe Journal of cell biology2000

Connexin43 deficiency causes delayed ossification, craniofacial abnormalities, and osteoblast dysfunction.

F Lecanda, P M Warlow, S Sheikh, F Furlan, T H Steinberg, R Civitelli

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
5.6field-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

162 citing papers in PubMed, 397 citations in OpenAlex.

  1. Article
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  7. Article
  8. Article
  9. Mechanosignaling in Osteoporosis: When Cells Feel the Force.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Calcium Regulation of Connexin Hemichannels.International journal of molecular sciences · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

102 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.

F LecandaDivisions of Bone and Mineral and Infectious Diseases, Department of Internal Medicine, Washington University School of Medicine, Barnes-Jewish Hospital, St. Louis, Missouri 63110, USA.
P M Warlow
S Sheikh
F Furlan
T H Steinberg
R Civitelli
Barnes-Jewish Hospital · USJewish Hospital · US

Funding

INTERCELLULAR COMMUNICATION IN BONE CELL PHYSIOLOGYR01AR041255 · NIAMS · WASHINGTON UNIVERSITY · PI CIVITELLI, ROBERTO · 1997 to 2017
$5.3M
CADHERIN REGULATION OF OSTEOBLAST FUNCTIONR01AR043470 · NIAMS · WASHINGTON UNIVERSITY · PI CIVITELLI, ROBERTO · 1996 to 2004
$1.0M
EXPRESSION AND REGULATION OF GAP JUNCTIONS IN BONE CELLSR01DK046686 · NIDDK · WASHINGTON UNIVERSITY · PI STEINBERG, THOMAS H · 1993 to 2001
$399k
INTERCELLULAR COMMUNICATION IN BONE CELL PHYSIOLOGYR29AR041255 · NIAMS · JEWISH HOSPITAL OF SAINT LOUIS · PI CIVITELLI, ROBERTO · 1992 to 1996
–
NIAMS NIH HHS AR41255NIAMS NIH HHS AR43470NIAMS NIH HHS R01 AR041255NIAMS NIH HHS R01 AR043470NIDDK NIH HHS DK46686NIDDK NIH HHS R01 DK046686
6 · The paper itself

Abstract

Connexin(Cx)43 is the major gap junction protein present in osteoblasts. We have shown that overexpression of Cx45 in osteoblasts expressing endogenous Cx43 leads to decreased cell-cell communication (Koval, M., S.T. Geist, E.M. Westphale, A.E. Kemendy, R. Civitelli, E.C. Beyer, and T.H. Steinberg. 1995. J. Cell Biol. 130:987-995) and transcriptional downregulation of several osteoblastic differentiation markers (Lecanda, F., D.A. Towler, K. Ziambaras, S.-L. Cheng, M. Koval, T.H. Steinberg, and R. Civitelli. 1998. Mol. Biol. Cell 9:2249-2258). Here, using the Cx43-null mouse model, we determined whether genetic deficiency of Cx43 affects skeletal development in vivo. Both intramembranous and endochondral ossification of the cranial vault were delayed in the mutant embryos, and cranial bones originating from migratory neural crest cells were also hypoplastic, leaving an open foramen at birth. Cx43-deficient animals also exhibited retarded ossification of the clavicles, ribs, vertebrae, and limbs, demonstrating that skeletal abnormalities are not restricted to a neural crest defect. However, the axial and appendicular skeleton of Cx43-null animals were essentially normal at birth. Cell to cell diffusion of calcein was poor among Cx43-deficient osteoblasts, whose differentiated phenotypic profile and mineralization potential were greatly impaired, compared with wild-type cells. Therefore, in addition to the reported neural crest cell defect, lack of Cx43 also causes a generalized osteoblast dysfunction, leading to delayed mineralization and skull abnormalities. Cell to cell signaling, mediated by Cx43 gap junctions, was critical for normal osteogenesis, craniofacial development, and osteoblastic function.

Indexed as

AnimalsBone and BonesCell DivisionConnexin 43Craniofacial AbnormalitiesEmbryonic and Fetal DevelopmentGenotypeGestational AgeMiceMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutNeural CrestOsteoblastsOsteogenesisReverse Transcriptase Polymerase Chain ReactionConnexin 43

Identifiers

PMID11076975
PMCPMC2169447
OpenAlexW2105432265

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.