The relative importance of physiological inputs that
ultimately determine the size of Sertoli cell populations in
the testis likely differs among species. Our previous data
demonstrate the particular significance of estrogen signaling as
a limiting factor in pigs, which contrasts with the lack of
evidence for regulation by thyroid hormone, a well-known
determinant of Sertoli cell proliferation in rodents.
Species differences in Sertoli cell response to altered hormone
levels might partially reflect the separation of two distinct
waves of proliferation or the presence of a single wave or
overlapping waves. Hence, differences in the relative importance
of androgen signaling in the establishment of Sertoli cell
populations among species should not be surprising. Sertoli
cell numbers are reduced in global androgen receptor knockout
mice perinatally, suggesting that reduced androgen signaling
during fetal development decreases Sertoli cell numbers in
rodents. In addition, postnatal treatment of rats
with flutamide also decreased Sertoli cell numbers, even
though this treatment increased FSH, which typically
stimulates Sertoli cell proliferation in rodents. The
androgenic effect on rodent Sertoli cells is unlikely to be
mediated directly by Sertoli cell androgen receptor function
since neonatal rodent Sertoli cells apparently do not express the
androgen receptor and specific loss of androgen
receptor expression in Sertoli cells does not influence the size
of the Sertoli cell population . Involvement of peritubular myoid cells has been suggested.
In contrast, the presence
of androgen receptors in Sertoli cells of neonatal pigs
suggests that restrictive androgen-mediated signaling directly
at the Sertoli cell might exist in these young pigs, consistent
with apparent differences in how testicular growth and
differentiation are regulated in pigs and rodents, as supported
by our current and previously published observations.
The relative importance of physiological inputs thatultimately determine the size of Sertoli cell populations inthe testis likely differs among species. Our previous datademonstrate the particular significance of estrogen signaling asa limiting factor in pigs, which contrasts with the lack ofevidence for regulation by thyroid hormone, a well-knowndeterminant of Sertoli cell proliferation in rodents.Species differences in Sertoli cell response to altered hormonelevels might partially reflect the separation of two distinctwaves of proliferation or the presence of a single wave oroverlapping waves. Hence, differences in the relative importanceof androgen signaling in the establishment of Sertoli cellpopulations among species should not be surprising. Sertolicell numbers are reduced in global androgen receptor knockoutmice perinatally, suggesting that reduced androgen signalingduring fetal development decreases Sertoli cell numbers inrodents. In addition, postnatal treatment of ratswith flutamide also decreased Sertoli cell numbers, eventhough this treatment increased FSH, which typicallystimulates Sertoli cell proliferation in rodents. Theandrogenic effect on rodent Sertoli cells is unlikely to bemediated directly by Sertoli cell androgen receptor functionsince neonatal rodent Sertoli cells apparently do not express theandrogen receptor and specific loss of androgenreceptor expression in Sertoli cells does not influence the sizeของประชากรเซลล์ Sertoli มีส่วนร่วมของ peritubular myoid เซลล์ได้รับการแนะนำในความคมชัด การปรากฏตัวของตัวรับแอนโดรเจนในเซลล์ Sertoli สุกรทารกแรกเกิดแนะนำที่เข้มงวดแอนโดรเจนสื่อส่งสัญญาณโดยตรงเซลล์ที่ Sertoli อาจมีอยู่ในเหล่านี้สุกรหนุ่ม สอดคล้องกันมีความแตกต่างชัดเจนในวิธีการที่ลูกอัณฑะเจริญเติบโต และความแตกต่างถูกควบคุมในสุกรและหนู ตามที่ได้รับการสนับสนุนโดยข้อสังเกตของเราปัจจุบัน และเผยแพร่ก่อนหน้านี้
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