Publication: Detection of anti-mullerian hormone receptor II protein in the postnatal rat testis from birth to sexual maturity
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Date
2006
Authors
Mendis-Handagama, S.M.L.C. ; Di Clementi, N. ; Ariyaratne,H.B.S. ; Mrkonjich, L.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Anti-Mullerian hormone (AMH) produced
by the immature Sertoli cells negatively regulates the
postnatal Leydig cell (i.e. adult Leydig cells/ALC)
differentiation, however, the mechanism is sparsely
understood. AMH negatively regulates the steroidogenic
function of fetal Leydig cells (FLC) and ALC. However,
when this function is established in the ALC lineage and
whether AMH has a function in FLC in the postnatal
testis are not known. Therefore, the objectives of this
study were to examine the presence of AMH receptor
type II (AMHR-II) in FLC and cells in the ALC lineage
in the postnatal mammalian testis using the rat model
Male Sprague Dawley rats of days 1, 5, 7-21, 28, 40, 60
and 90 were used. AMHR-II in testicular interstitial cells
was detected in testis tissue using immunocytochemistry.
Findings showed that the mesenchymal and the
progenitor cells of the ALC lineage, were negative for
AMHR-II. The newly formed ALC were the first cell
type of the ALC lineage to show positive labeling for
AMHR-II, and the first detection was on postnatal day
13, although they were present in the testis from day 10.
From days 13-28, labeling intensity for AMHR-II in the
ALC was much weaker than those at days 40-90. FLC
were also positive. The time lag between the first
detection of the newly formed ALC in the testis and the
first detection of AMHR-II in them suggests that the
establishment of the negative regulatory role of AMH on
ALC steroidogenesis does not take place immediately
upon their differentiation; no change in cell size occurs
during this period. The absence of AMHR-II in
mesenchymal cells suggests that it is unlikely that the
negative regulatory effect of AMH on ALC
differentiation in the postnatal testis is achieved via a
direct action of AMH on mesenchymal cells. The
presence of AMHR-II in postnatal FLC suggests a possible role by AMH on FLC, which warrants future
investigations.
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