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Endocrinology, Vol 137, 5605-5609, Copyright © 1996 by Endocrine Society
ARTICLES |
M Galbiati, M Zanisi, E Messi, I Cavarretta, L Martini and RC Melcangi
Department of Endocrinology, University of Milan, Italy.
On the basis of our previous observations indicating that a principle [possibly transforming growth factor-beta1 (TGFbeta1)] secreted by type 1 astrocytes may increase the release of LHRH in the GT1 cell line, it was deemed of interest to analyze whether TGFbeta1 might influence LHRH gene expression in addition to LHRH release in GT1-1 neurons. The effects of TGFbeta1 on the levels of LHRH messenger RNA (mRNA) present in GT1-1 cells have been compared to those found after either coculture of these cells with type 1 astrocytes or exposure of GT1-1 cells to the conditioned medium in which type 1 astrocytes were grown for 24 h. The data obtained indicate that 1) TGFbeta1 increases LHRH mRNA levels 1 and 6 h after the beginning of treatment; longer exposures (24 h) bring about a decrease in LHRH gene expression; 2) a significant stimulatory effect of TGFbeta1 (1 and 6 h of exposure) is also evident on LHRH release; 3) the exposure to the conditioned medium of type 1 astrocytes is able to increase LHRH gene expression in GT1-1 cells at 1 h; LHRH mRNA levels show a small decrease after 6 h of exposure, which becomes more evident at 24 h; and 4) the coculture of GT1-1 cells with type 1 astrocytes is not able to modify LHRH mRNA levels at any time considered. The present data support the concept that glial cells are able to control, possibly through the release of TGFbeta, the gene expression of LHRH in hypothalamic neurons.
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