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Department of Experimental Medicine (S.U., N.R., D.P., E.C., F.M.G., A.P., P.C., P.M., L.C., E.A.J.), University of L’Aquila, 67100 L’Aquila, Italy; and Departments of Medical Physiopathology (M.A., L.G.), and Experimental Medicine and Pathology (M.D’A.) University of Rome "La Sapienza," 00161 Rome, Italy
Address all correspondence and requests for reprints to: Prof. Massimino D’Armiento, Department of Experimental Medicine, Section of Endocrinology, University of L’Aquila, Coppito, Building 2, Room A2/54, 67100 L’Aquila, Italy. E-mail: darmiento{at}axscaq.aquila.infn.it
The present study reports the modulation of basement membrane (BM)
components, laminin, entactin, and type IV collagen, expression in
prepubertal rat Sertoli cell by the thyroid hormone T3.
Immunocytochemical studies of permeabilized Sertoli cells in culture
showed that T3 treatment (10-7 M
for 24 h) increased the number of cells staining positive for
laminin and/or entactin (from 58 ± 5.3% to 86.4 ± 6.5%,
P < 0.01). In contrast, a strong inhibition of
type IV collagen immunopositivity was observed. Western blot analysis
of Sertoli cell-conditioned media indicated that T3
treatment significantly (P < 0.01) increased the
level of secreted entactin by 60–65% without affecting the levels of
laminin A and B1/B2 chains. Moreover, thyroid
hormone treatment of Sertoli cells significantly reduced type IV
collagen secretion by 62% (P < 0.05). Slot blot
analysis of poly-A RNA demonstrated a significant
(P < 0.01) increase in the level of entactin
messenger RNA (mRNA) by 140% (P < 0.01) and a
50% reduction of type IV collagen 
1 chain mRNA after thyroid
hormone treatment. No effect of the hormone was observed on the
accumulation of the laminin B1 and B2 chain mRNAs in Sertoli cell
cultures. These effects cannot be ascribed to changes in the
degradation of BM components, because no effect of thyroid hormone was
observed on plasminogen activators or metalloproteinase secretion by
Sertoli cells.
These observations indicate the Sertoli cell as a source of entactin within the testis, demonstrate the ability of T3 to differentially regulate the expression of BM components, and can be regarded as a part of the integrated mechanism by which thyroid hormone affects testicular development and differentiation.
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