PMID- 9700486
OWN - NLM
STAT- MEDLINE
DCOM- 19981030
LR  - 20191102
IS  - 0894-1491 (Print)
IS  - 0894-1491 (Linking)
VI  - 24
IP  - 1
DP  - 1998 Sep
TI  - Nerve injury and inflammatory cytokines modulate gap junctions in the peripheral 
      nervous system.
PG  - 21-31
AB  - In the peripheral nervous system (PNS), myelinating Schwann cells express the gap 
      junction protein connexin32 (Cx32) and lower levels of connexin43 (Cx43). 
      Although the function of Cx43 in Schwann cells is not yet known, in adult mammals 
      Cx32 is thought to form reflexive contacts within individual myelinating glial 
      cells and provide direct pathways for intracellular ionic and metabolic exchange 
      from the cell body to the innermost periaxonal cytoplasmic regions. In response 
      to nerve injury, Schwann cells in the degenerating region down-regulate 
      expression of Cx32 and there is increased expression of connexin46 (Cx46) mRNA 
      and protein. The cascade of Schwann cell responses seen after the injury-induced 
      decrease in Cx32, and the observation that dividing Schwann cells express Cx46, 
      and possibly other connexins, and are coupled through gap junction channels, 
      raise the intriguing possibility that there are coordinated changes in Schwann 
      cell proliferation and connexin expression. Moreover, intercellular junctional 
      coupling among cells in general may be important during injury responses. 
      Consistent with this hypothesis, dividing Schwann cells are preferentially 
      coupled through junctional channels as compared to non-dividing cells, which are 
      generally uncoupled. Moreover, the strength of junctional coupling among cultured 
      Schwann cells is modulated by a number of cytokines to which Schwann cells are 
      exposed to in vivo after nerve injury, and Cx46 mRNA and protein levels correlate 
      with the degree of coupling. Other injury-induced cellular changes in connexin 
      expression that may be functionally important during injury responses include a 
      transient increase in Cx43 in endoneurial fibroblasts. This paper reviews what is 
      known about connexin expression and function in the adult mammalian PNS, and 
      focuses on some of the changes that occur following nerve injury. Moreover, 
      evidence that inflammatory cytokines released after injury modulate connexin 
      expression and junctional coupling strength is presented.
FAU - Chandross, K J
AU  - Chandross KJ
AD  - National Institutes of Health, National Institute of Neurological Disorders and 
      Stroke, Laboratory of Developmental Neurogenetics, Bethesda, Maryland 20892-4160, 
      USA. chandros@codon.nih.gov
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Glia
JT  - Glia
JID - 8806785
RN  - 0 (Connexins)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Animals
MH  - Connexins/metabolism
MH  - Cytokines/*physiology
MH  - Gap Junctions/*physiology
MH  - Humans
MH  - Inflammation Mediators/*physiology
MH  - *Peripheral Nerve Injuries
MH  - Peripheral Nerves/*metabolism
MH  - Schwann Cells/physiology
RF  - 172
EDAT- 1998/08/13 00:00
MHDA- 1998/08/13 00:01
CRDT- 1998/08/13 00:00
PHST- 1998/08/13 00:00 [pubmed]
PHST- 1998/08/13 00:01 [medline]
PHST- 1998/08/13 00:00 [entrez]
AID - 10.1002/(SICI)1098-1136(199809)24:1<21::AID-GLIA3>3.0.CO;2-3 [pii]
AID - 10.1002/(sici)1098-1136(199809)24:1<21::aid-glia3>3.0.co;2-3 [doi]
PST - ppublish
SO  - Glia. 1998 Sep;24(1):21-31. doi: 
      10.1002/(sici)1098-1136(199809)24:1<21::aid-glia3>3.0.co;2-3.