| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Abstract
We previously reported that gonocytes from 3-day-old rat
testes proliferate in response to estradiol. In the
present study, we found that purified gonocytes contained
the mRNAs of estrogen receptor 
and the chaperones
Hsp90, p23 and Cyp40, but no inducible Hsp70. Immunoblot
analysis showed high levels of ER, Hsp90, p23,
Cyp40, and the constitutive Hsc70 in gonocytes. Prenatal
exposure to the estrogenic compounds diethylstilbestrol,
bisphenol A, genistein and coumestrol increased
significantly Hsp90 mRNA levels in testis, but not p23 and
Cyp40. In situ hybridization analysis indicated that Hsp90
mRNA was prominent in gonocytes, where it was increased
following phytoestrogen exposure, whereas BPA induced a
more generalized increase throughout the testis.
Immunoblot analysis of testicular extracts demonstrated
that Hsp90 protein levels were significantly increased
following estrogen exposure, and immunohistochemical
analysis indicated that this increase occurred
predominantly in gonocytes. By contrast, no change was
observed in the expression of Cyp40, p23, and ER,
while Hsc70 was increased by BPA only. Using an antibody
and RT-PCR probes specific for Hsp90
, we
subsequently confirmed that Hsp90 was primarily
expressed in gonocytes, and that it was increased
following estrogen exposure. Hsp90 immunolocalization in
fetal and prepubertal testes showed an increased
expression in fetal gonocytes upon estrogen exposure, but
no difference in the subsets of Hsp90-positive germ cells
in prepubertal testes. These results demonstrate that
prenatal estrogen exposure specifically affects Hsp90
expression in gonocytes. Considering the interaction of
Hsp90 with several signaling molecules, changes in its
expression levels may lead to subsequent changes in
gonocyte development.
Key words:
Environment •
Gamete Biology •
Testis •
Developmental biology •
Estradiol receptor
This article has been cited by other articles:
|
|
 |
|
  K. Toda, T. Okada, Y. Hayashi, and T. Saibara Preserved tissue structure of efferent ductules in aromatase-deficient mice J. Endocrinol., October 1, 2008; 199(1): 137 - 146. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Culty, R. Thuillier, W. Li, Y. Wang, D. B. Martinez-Arguelles, C. G. Benjamin, K. M. Triantafilou, B. R. Zirkin, and V. Papadopoulos In Utero Exposure to Di-(2-ethylhexyl) Phthalate Exerts Both Short-Term and Long-Lasting Suppressive Effects on Testosterone Production in the Rat Biol Reprod, June 1, 2008; 78(6): 1018 - 1028. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. T. Akingbemi, T. D. Braden, B. W. Kemppainen, K. D. Hancock, J. D. Sherrill, S. J. Cook, X. He, and J. G. Supko Exposure to Phytoestrogens in the Perinatal Period Affects Androgen Secretion by Testicular Leydig Cells in the Adult Rat Endocrinology, September 1, 2007; 148(9): 4475 - 4488. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Wang and M. Culty Identification and Distribution of a Novel Platelet-Derived Growth Factor Receptor {beta} Variant: Effect of Retinoic Acid and Involvement in Cell Differentiation Endocrinology, May 1, 2007; 148(5): 2233 - 2250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Merlet, C. Racine, E. Moreau, S. G. Moreno, and R. Habert Male fetal germ cells are targets for androgens that physiologically inhibit their proliferation PNAS, February 27, 2007; 104(9): 3615 - 3620. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Delbes, C. Levacher, and R. Habert Estrogen effects on fetal and neonatal testicular development. Reproduction, October 1, 2006; 132(4): 527 - 538. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
