Osteocytic connexin 43 channels affect fracture healing

Yunhe Chen, Meng Chen, Tong Xue, Guobin Li, Dongen Wang, Peng Shang, Jean X Jiang, Huiyun Xu

Research output: Contribution to journalArticle

Abstract

The cross-talk between cells is very critical for moving forward fracture healing in an orderly manner. Connexin (Cx) 43-formed gap junctions and hemichannels mediate the communication between adjacent cells and cells and extracellular environment. Loss of Cx43 in osteoblasts/osteocytes results in delayed fracture healing. For investigating the role of two channels in osteocytes in bone repair, two transgenic mouse models with Cx43 dominant negative mutants driven by a 10 kb-DMP1 promoter were generated: R76W (gap junctions are blocked, whereas hemichannels are promoted) and Δ130–136 (both gap junctions and hemichannels are blocked). R76W mice (promotion of hemichannels) showed a significant increase of new bone formation, whereas delayed osteoclastogenesis and healing was observed in Δ130–136 (impairment of gap junctions), but not in R76W mice (hemichannel promotion may recover the delay). These results suggest that gap junctions and hemichannels play some similar and cooperative roles in bone repair.

Original languageEnglish (US)
Pages (from-to)19824-19832
Number of pages9
JournalJournal of Cellular Physiology
Volume234
Issue number11
DOIs
StatePublished - Nov 1 2019

Fingerprint

Connexin 43
Fracture Healing
Gap Junctions
Bone
Repair
Osteocytes
Osteogenesis
Osteoblasts
Bone and Bones
Communication
Transgenic Mice

Keywords

  • Cx43
  • fracture healing
  • gap junction
  • hemichannel
  • transgenic mouse model

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Chen, Y., Chen, M., Xue, T., Li, G., Wang, D., Shang, P., ... Xu, H. (2019). Osteocytic connexin 43 channels affect fracture healing. Journal of Cellular Physiology, 234(11), 19824-19832. https://doi.org/10.1002/jcp.28581

Osteocytic connexin 43 channels affect fracture healing. / Chen, Yunhe; Chen, Meng; Xue, Tong; Li, Guobin; Wang, Dongen; Shang, Peng; Jiang, Jean X; Xu, Huiyun.

In: Journal of Cellular Physiology, Vol. 234, No. 11, 01.11.2019, p. 19824-19832.

Research output: Contribution to journalArticle

Chen, Y, Chen, M, Xue, T, Li, G, Wang, D, Shang, P, Jiang, JX & Xu, H 2019, 'Osteocytic connexin 43 channels affect fracture healing', Journal of Cellular Physiology, vol. 234, no. 11, pp. 19824-19832. https://doi.org/10.1002/jcp.28581
Chen Y, Chen M, Xue T, Li G, Wang D, Shang P et al. Osteocytic connexin 43 channels affect fracture healing. Journal of Cellular Physiology. 2019 Nov 1;234(11):19824-19832. https://doi.org/10.1002/jcp.28581
Chen, Yunhe ; Chen, Meng ; Xue, Tong ; Li, Guobin ; Wang, Dongen ; Shang, Peng ; Jiang, Jean X ; Xu, Huiyun. / Osteocytic connexin 43 channels affect fracture healing. In: Journal of Cellular Physiology. 2019 ; Vol. 234, No. 11. pp. 19824-19832.
@article{8f00e8a9ba884e3cb7649662cf290ac6,
title = "Osteocytic connexin 43 channels affect fracture healing",
abstract = "The cross-talk between cells is very critical for moving forward fracture healing in an orderly manner. Connexin (Cx) 43-formed gap junctions and hemichannels mediate the communication between adjacent cells and cells and extracellular environment. Loss of Cx43 in osteoblasts/osteocytes results in delayed fracture healing. For investigating the role of two channels in osteocytes in bone repair, two transgenic mouse models with Cx43 dominant negative mutants driven by a 10 kb-DMP1 promoter were generated: R76W (gap junctions are blocked, whereas hemichannels are promoted) and Δ130–136 (both gap junctions and hemichannels are blocked). R76W mice (promotion of hemichannels) showed a significant increase of new bone formation, whereas delayed osteoclastogenesis and healing was observed in Δ130–136 (impairment of gap junctions), but not in R76W mice (hemichannel promotion may recover the delay). These results suggest that gap junctions and hemichannels play some similar and cooperative roles in bone repair.",
keywords = "Cx43, fracture healing, gap junction, hemichannel, transgenic mouse model",
author = "Yunhe Chen and Meng Chen and Tong Xue and Guobin Li and Dongen Wang and Peng Shang and Jiang, {Jean X} and Huiyun Xu",
year = "2019",
month = "11",
day = "1",
doi = "10.1002/jcp.28581",
language = "English (US)",
volume = "234",
pages = "19824--19832",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley-Liss Inc.",
number = "11",

}

TY - JOUR

T1 - Osteocytic connexin 43 channels affect fracture healing

AU - Chen, Yunhe

AU - Chen, Meng

AU - Xue, Tong

AU - Li, Guobin

AU - Wang, Dongen

AU - Shang, Peng

AU - Jiang, Jean X

AU - Xu, Huiyun

PY - 2019/11/1

Y1 - 2019/11/1

N2 - The cross-talk between cells is very critical for moving forward fracture healing in an orderly manner. Connexin (Cx) 43-formed gap junctions and hemichannels mediate the communication between adjacent cells and cells and extracellular environment. Loss of Cx43 in osteoblasts/osteocytes results in delayed fracture healing. For investigating the role of two channels in osteocytes in bone repair, two transgenic mouse models with Cx43 dominant negative mutants driven by a 10 kb-DMP1 promoter were generated: R76W (gap junctions are blocked, whereas hemichannels are promoted) and Δ130–136 (both gap junctions and hemichannels are blocked). R76W mice (promotion of hemichannels) showed a significant increase of new bone formation, whereas delayed osteoclastogenesis and healing was observed in Δ130–136 (impairment of gap junctions), but not in R76W mice (hemichannel promotion may recover the delay). These results suggest that gap junctions and hemichannels play some similar and cooperative roles in bone repair.

AB - The cross-talk between cells is very critical for moving forward fracture healing in an orderly manner. Connexin (Cx) 43-formed gap junctions and hemichannels mediate the communication between adjacent cells and cells and extracellular environment. Loss of Cx43 in osteoblasts/osteocytes results in delayed fracture healing. For investigating the role of two channels in osteocytes in bone repair, two transgenic mouse models with Cx43 dominant negative mutants driven by a 10 kb-DMP1 promoter were generated: R76W (gap junctions are blocked, whereas hemichannels are promoted) and Δ130–136 (both gap junctions and hemichannels are blocked). R76W mice (promotion of hemichannels) showed a significant increase of new bone formation, whereas delayed osteoclastogenesis and healing was observed in Δ130–136 (impairment of gap junctions), but not in R76W mice (hemichannel promotion may recover the delay). These results suggest that gap junctions and hemichannels play some similar and cooperative roles in bone repair.

KW - Cx43

KW - fracture healing

KW - gap junction

KW - hemichannel

KW - transgenic mouse model

UR - http://www.scopus.com/inward/record.url?scp=85069744380&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85069744380&partnerID=8YFLogxK

U2 - 10.1002/jcp.28581

DO - 10.1002/jcp.28581

M3 - Article

C2 - 30980397

AN - SCOPUS:85069744380

VL - 234

SP - 19824

EP - 19832

JO - Journal of Cellular Physiology

JF - Journal of Cellular Physiology

SN - 0021-9541

IS - 11

ER -