PMID- 7823132
OWN - NLM
STAT- MEDLINE
DCOM- 19950214
LR  - 20191101
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 15
IP  - 1 Pt 1
DP  - 1995 Jan
TI  - Transforming growth factor-beta 1 and forskolin modulate gap junctional 
      communication and cellular phenotype of cultured Schwann cells.
PG  - 262-73
AB  - Following peripheral nerve injury, Schwann cells undergo a series of cellular 
      alterations that are thought to assist the regenerative process. Some of these 
      changes are stimulated by the local release of cytokines and mitogenic factors. 
      To test the hypothesis that cytokine regulation of gap junctional communication 
      between cells helps to coordinate Schwann cell responses, cultured rat Schwann 
      cells, from sciatic nerve, were utilized to study phasic changes induced by 
      transforming growth factor-beta 1 (TGF beta 1), a cytokine released after nerve 
      injury, or forskolin in combination with bovine pituitary extract (F-BPE), known 
      for its mitogenic effects in vitro. In mitotically quiescent cultures, TGF beta 1 
      significantly decreased both electrical and dye coupling mediated by gap 
      junctions. Single-channel analysis revealed that cultured Schwann cells expressed 
      gap junctions with two distinct channel sizes of about 26 pS and 44 pS. TGF beta 
      1 treatment reduced coupling due to both populations of channels. Exposure to TGF 
      beta 1 had a minimal effect on proliferation but significantly altered cellular 
      morphology; cell bodies became flattened with multipolar processes within 72 hr. 
      Additionally, immunolabeling for both low-affinity nerve growth factor receptor 
      (L-NGFR) and glial fibrillary acidic protein (GFAP) were reduced, suggesting 
      increased differentiation. In contrast, treatment with F-BPE significantly 
      enhanced both electrical and dye coupling and stimulated Schwann cell 
      proliferation. Additionally, cell bodies became more rounded with polarized, 
      cytoplasmic processes contiguously aligned with adjacent cells. F-BPE reduced 
      immunolabeling for L-NGFR but increased expression of both GFAP and the major 
      peripheral myelin protein, P0. These data indicate that TGF beta 1 and/or F-BPE 
      induce phenotypic changes in Schwann cells, including the coordinated regulation 
      of proliferation and modulation of intercellular communication via gap junctions. 
      Such mechanisms may underlie phasic responses that orchestrate recovery from 
      nerve injury, indicating that Schwann cell gap junctions may be critical for 
      peripheral nerve function.
FAU - Chandross, K J
AU  - Chandross KJ
AD  - Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 
      10461.
FAU - Chanson, M
AU  - Chanson M
FAU - Spray, D C
AU  - Spray DC
FAU - Kessler, J A
AU  - Kessler JA
LA  - eng
GR  - NS20013/NS/NINDS NIH HHS/United States
GR  - NS20778/NS/NINDS NIH HHS/United States
GR  - NS22956/NS/NINDS NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Drug Combinations)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Proteins)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 0 (Tissue Extracts)
RN  - 0 (Transforming Growth Factor beta)
RN  - 1F7A44V6OU (Colforsin)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Animals
MH  - Cattle
MH  - Cell Communication/*drug effects
MH  - Cells, Cultured
MH  - Colforsin/*pharmacology
MH  - DNA/biosynthesis
MH  - Drug Combinations
MH  - Gap Junctions/*drug effects/physiology
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Phenotype
MH  - Pituitary Gland/chemistry
MH  - Proteins/metabolism
MH  - Rats
MH  - Receptors, Nerve Growth Factor/metabolism
MH  - Schwann Cells/cytology/drug effects/*physiology
MH  - Tissue Extracts/pharmacology
MH  - Transforming Growth Factor beta/*pharmacology
PMC - PMC6578323
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
PMCR- 1995/07/01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PHST- 1995/07/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.15-01-00262.1995 [doi]
PST - ppublish
SO  - J Neurosci. 1995 Jan;15(1 Pt 1):262-73. doi: 10.1523/JNEUROSCI.15-01-00262.1995.