TY - JOUR
T1 - Interactions between type 1 astrocytes and LHRH-secreting neurons (GT1-1 cells)
T2 - Modification of steroid metabolism and possible role of TGFβ1
AU - Cavarretta, I.
AU - Magnaghi, V.
AU - Ferraboschi, P.
AU - Martini, L.
AU - Melcangi, R. C.
PY - 1999/11
Y1 - 1999/11
N2 - The hypothesis that type 1 astrocytes (A1) might modify the activities of the enzymes 5α-reductase (5α-R) and 3α-hydroxysteroid dehydrogenase (3α-HSD) present in the GT1-1 cells has been tested. The data obtained indicate that, utilizing a co-culture technique, A1 are able to: (1) decrease the formation of dihydrotestosterone (DHT) from testosterone (T); (2) increase the formation of dihydroprogesterone (DHP) from progesterone (P); (3) decrease the conversion of DHP into tetrahydroprogesterone (THP) in GT1-1 cells. Moreover, GT1-1 cells are able to increase the formation of DHP in A1; that of DHT was unchanged. The present data might suggest the possible existence of a third isoform of the enzyme 5α-R; details on this hypothesis are provided in the text. Interestingly, the inhibitory effect exerted by A1 on the formation of DHT in GT1-1 cells can be mimicked by transforming growth factor β1 (TGFβ1). Since TGFβ1 had been previously shown to be directly involved in the stimulatory control of LHRH secretion by GT1-1 cells, acting both on LHRH release [R.C. Melcangi, M. Galbiati, E. Messi, F. Piva, L. Martini, M. Motta, Type 1 astrocytes influence luteinizing hormone-releasing hormone release from the hypothalamic cell line GT1-1: is transforming growth factor-β the principle involved? Endocrinology 136 (1995) 679-686.] and gene expression [M. Galbiati, M. Zanisi, E. Messi, I. Cavarretta, L. Martini, R.C. Melcangi, Transforming growth factor-β and astrocytic conditioned medium influence LHRH gene expression in the hypothalamic cell line GT1, Endocrinology 137 (1996) 5605-5609], the present data also show that TGFβ1 might intervene in modulating feedback signals reaching hypothalamic LHRH producing neurons. The present findings underline once more the importance of the physiological cross-talk between A1 and neurons.
AB - The hypothesis that type 1 astrocytes (A1) might modify the activities of the enzymes 5α-reductase (5α-R) and 3α-hydroxysteroid dehydrogenase (3α-HSD) present in the GT1-1 cells has been tested. The data obtained indicate that, utilizing a co-culture technique, A1 are able to: (1) decrease the formation of dihydrotestosterone (DHT) from testosterone (T); (2) increase the formation of dihydroprogesterone (DHP) from progesterone (P); (3) decrease the conversion of DHP into tetrahydroprogesterone (THP) in GT1-1 cells. Moreover, GT1-1 cells are able to increase the formation of DHP in A1; that of DHT was unchanged. The present data might suggest the possible existence of a third isoform of the enzyme 5α-R; details on this hypothesis are provided in the text. Interestingly, the inhibitory effect exerted by A1 on the formation of DHT in GT1-1 cells can be mimicked by transforming growth factor β1 (TGFβ1). Since TGFβ1 had been previously shown to be directly involved in the stimulatory control of LHRH secretion by GT1-1 cells, acting both on LHRH release [R.C. Melcangi, M. Galbiati, E. Messi, F. Piva, L. Martini, M. Motta, Type 1 astrocytes influence luteinizing hormone-releasing hormone release from the hypothalamic cell line GT1-1: is transforming growth factor-β the principle involved? Endocrinology 136 (1995) 679-686.] and gene expression [M. Galbiati, M. Zanisi, E. Messi, I. Cavarretta, L. Martini, R.C. Melcangi, Transforming growth factor-β and astrocytic conditioned medium influence LHRH gene expression in the hypothalamic cell line GT1, Endocrinology 137 (1996) 5605-5609], the present data also show that TGFβ1 might intervene in modulating feedback signals reaching hypothalamic LHRH producing neurons. The present findings underline once more the importance of the physiological cross-talk between A1 and neurons.
KW - GT1-1 cells
KW - LHRH
KW - Steroids
KW - TGFβ1
KW - Type 1 astrocytes
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U2 - 10.1016/S0960-0760(99)00121-1
DO - 10.1016/S0960-0760(99)00121-1
M3 - Article
C2 - 10619356
AN - SCOPUS:0032739843
VL - 71
SP - 41
EP - 47
JO - Journal of Steroid Biochemistry and Molecular Biology
JF - Journal of Steroid Biochemistry and Molecular Biology
SN - 0960-0760
IS - 1-2
ER -