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INSERM, U-407, Communications Cellulaires en Biologie de la Reproduction, Faculté de Médecine Lyon-Sud, F-69921 Oullins, France
Address all correspondence and requests for reprints to: Dr. Mohamed Benahmed, INSERM, U-407, Faculté de Médecine Lyon-Sud, BP 12, F-69921 Oullins Cedex, France. E-mail: benahmed{at}lsgrisn1.univ-lyon1.fr
The proliferation and differentiation of testicular progenitor stem
cells into highly specialized germ cells (spermatozoa) are largely
controlled by the hormonally (FSH and testosterone) regulated adjacent
supporting Sertoli cells. However, the factors involved in this control
remain largely unknown. In the present study, the technique of
differential display PCR was used to identify target transcripts to FSH
action in cultured murine Sertoli cells. Among these target
transcripts, we identified the oligodendrocyte-specific protein (OSP),
also known as claudin 11, which had recently been shown to play a key
role in the formation of the hematotesticular barrier. Our data show
that the testicular expression of OSP is dependent upon male gonad
development and systemic and local signaling molecules. Indeed, OSP is
expressed early in fetal development in Sertoli cells, immediately
after the peak of SRY (sex-determining region, Y gene) expression, but
just before that of the anti-Mullerian hormone. Postnatally, OSP
expression starts to increase from day 3 to reach a plateau between
days 6 and 16 postnatally. In the prepubertal and adult testes, an
apparent decline in OSP messenger RNA (mRNA) levels was found, probably
because of the increasing number of germ cells (which do not express
OSP). Among the signaling molecules that control testicular OSP
expression, we have identified FSH and tumor necrosis factor-
(TNF). Indeed, using a model of purified cultured mouse Sertoli
cells, we demonstrate that FSH inhibits, in a dose
(ED50 = 4 ng/ml)- and time (maximal effect after
24 h)-dependent manner, the levels of OSP mRNA. Such an inhibitory
effect was mimicked by 8-bromo-cAMP, suggesting that FSH may use the
cAMP/protein kinase A pathway to inhibit OSP mRNA levels. TNF was
also shown to inhibit OSP expression in cultured Sertoli cells. The
maximal effect was observed after 48 h of TNF treatment with an
ED50 of 4.5 ng/ml. Together, our results indicate that OSP
expression 1) starts during fetal life at a critical period, probably
under SRY control and during testicular formation; and 2) is regulated
by hormones (FSH) and cytokines (TNF) in the adult testis,
suggesting a critical role for these molecules in the (re)modeling
process of the hematotesticular barrier during spermatogenesis.
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