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Journal of Neuroscience, Vol 14, 5644-5651, Copyright © 1994 by Society for Neuroscience
Region-specific regulation of transforming growth factor alpha (TGF alpha) gene expression in astrocytes of the neuroendocrine brain
YJ Ma, K Berg-von der Emde, M Moholt-Siebert, DF Hill and SR Ojeda
Division of Neuroscience, Oregon Regional Primate Research Center, Beaverton 97006.
Certain glial cells of the hypothalamus have been implicated in the
neuroendocrine control of reproductive development. Hypothalamic astrocytes
appear to exert this function via a cell-cell interactive mechanism that
involves the production of transforming growth factor alpha (TGF alpha), a
polypeptide able to affect both glial and neuronal functions in the CNS. In
the hypothalamus, TGF alpha stimulates neuronal secretion of luteinizing
hormone-releasing hormone (LHRH), the neuropeptide controlling sexual
development, via activation of epidermal growth factor receptors (EGFR).
Since astrocytes but not LHRH neurons express EGFR, it has been postulated
that the stimulatory effect of TGF alpha on LHRH release is not exerted
directly on LHRH neurons, but rather via glial intermediacy. The present
experiments were undertaken to define whether TGF alpha is able to exert
paracrine/autocrine effects on isolated hypothalamic astrocytes, and to
determine if estradiol-previously shown to increase TGF alpha mRNA levels
in the hypothalamus of immature animals--can act directly on hypothalamic
astrocytes to upregulate TGF alpha gene expression. Treatment with either
TGF alpha or its structural homolog, epidermal growth factor (EGF),
increased TGF alpha mRNA levels within 8 hr of exposure; the phorbol ester
12-O-tetradecanoyl-phorbol-13-acetate (TPA) was similarly effective.
Blockade of EGFR with either tyrphostin RG- 50864, an inhibitor of tyrosine
kinase activity, or a monoclonal antibody that prevents ligand binding
abolished the upregulatory effect of TGF alpha on TGF alpha mRNA levels. In
contrast to hypothalamic astrocytes, cerebellar astrocytes did not respond
to either TGF alpha or EGF with changes in TGF alpha mRNA
abundance.(ABSTRACT TRUNCATED AT 250 WORDS)
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