Human Reproduction, Vol 13, 1272-1280, Copyright © 1998 by Oxford University Press
JM Emmen, A McLuskey, JA Grootegoed and AO Brinkmann
The cranial suspensory ligament is located on the border of the cranial
(mesonephric) mesentery in adult female mammals, which runs between the
cranial pole of the internal genitalia and the dorsal abdominal wall.
Absence of the cranial suspensory ligament in male mammals depends upon
exposure of its primordium to fetal testicular androgens and is a
prerequisite for testis descent. Female rats were exposed to 5alpha-
dihydrotestosterone propionate at different stages of genital development,
and cranial suspensory ligament development was studied in neonatal and in
adult animals. Androgens suppressed cranial suspensory ligament development
when exposure started during the early stages of genital development, until
day 19 postconception (pc). Androgen receptor expression was
immunohistochemically detected in the cranial mesentery of both sexes from
day 16 pc onwards. A decrease of androgen receptor expression in female
fetuses from day 18 pc onwards coincided with the appearance of a
differentiated cranial suspensory ligament, as evidenced by the expression
of two cell differentiation markers: alpha- smooth muscle (alpha-SM) actin
and desmin. alpha-SM actin was located on the outer border of the cranial
mesentery of both sexes at day 17 pc, and expression increased only in
female fetuses. On day 19 pc, desmin expression was also detectable in the
a-SM actin-positive cells. Proliferation and apoptosis indices of cells in
the cranial mesentery, as analysed by 5'-bromodeoxyuridine incorporation
and by detection of DNA strand breaks (TUNEL method) respectively, did not
show any difference between the sexes, neither on day 17 nor on day 18 pc.
Since primordial cells of the cranial suspensory ligament highly express
the androgen receptor during the period of gestation when androgens can
suppress cranial suspensory development, altered morphogenesis of these
cells may be a direct consequence of androgen action.
ARTICLES
Androgen action during male sex differentiation includes suppression of cranial suspensory ligament development
Department of Endocrinology and Reproduction, Faculty of Medicine and Health Sciences, Erasmus University Rotterdam, The Netherlands.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  C. Staub, M. Rauch, F. Ferriere, M. Trepos, I. Dorval-Coiffec, P. T. Saunders, G. Cobellis, G. Flouriot, C. Saligaut, and B. Jegou Expression of Estrogen Receptor ESR1 and Its 46-kDa Variant in the Gubernaculum Testis Biol Reprod, October 1, 2005; 73(4): 703 - 712. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. M. Adham, G. Steding, T. Thamm, E. E. Bullesbach, C. Schwabe, I. Paprotta, and W. Engel The Overexpression of the Insl3 in Female Mice Causes Descent of the Ovaries Mol. Endocrinol., February 1, 2002; 16(2): 244 - 252. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. A. Hughes Minireview: Sex Differentiation Endocrinology, August 1, 2001; 142(8): 3281 - 3287. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. A. Emmen, A. McLuskey, I. M. Adham, W. Engel, J. A. Grootegoed, and A. O. Brinkmann Hormonal Control of Gubernaculum Development during Testis Descent: Gubernaculum Outgrowth in Vitro Requires Both Insulin-Like Factor and Androgen Endocrinology, December 1, 2000; 141(12): 4720 - 4727. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Zimmermann, G. Steding, J. M. A. Emmen, A. O. Brinkmann, K. Nayernia, A. F. Holstein, W. Engel, and I. M. Adham Targeted Disruption of the Insl3 Gene Causes Bilateral Cryptorchidism Mol. Endocrinol., May 1, 1999; 13(5): 681 - 691. [Abstract] [Full Text]
|
|