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Axon‐Schwann cell interactions regulate the expression of c‐ jun in Schwann cells
Author(s) -
Shy M.E.,
Shi Y.,
Wrabetz L.,
Kamholz J.,
Scherer S.S.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19960301)43:5<511::aid-jnr1>3.0.co;2-l
Subject(s) - schwann cell , axon , axotomy , myelin , biology , microbiology and biotechnology , neuroglia , neuroscience , central nervous system , regeneration (biology)
The transcription factor c‐ jun is selectively expressed by non‐myelinating Schwann cells in normal peripheral nerve, and by “denervated,” previously myelinating Schwann cells, after axotomy. When axons regenerate into the distal nerve‐stump, the expression of c‐ jun declines as Schwann cells remyelinate axons. Treating cultured Schwann cells with forskolin, a drug that mimics many of the effects of axon‐Schwann cell interactions, decreases the expression of c‐ jun but increases the expression of myelin‐specific genes. Overexpressing c‐ jun in cultured Schwann cells, however, does not decrease the expression of a myelin basic protein promoter‐reporter construct, indicating that c‐ jun expression may not directly regulate myelin‐specific gene expression. These data suggest that c‐ jun is involved in regulating the phenotype of non‐myelinating and denervated Schwann cells. © 1996 Wiley‐Liss, Inc.