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Localization and developmental expression of the activin signal transduction proteins Smads 2, 3, and 4 in the baboon fetal ovary.
Biol Reprod. 2004 Mar; 70(3):586-92.BR

Abstract

We recently demonstrated that the reduction in the number of primordial follicles in ovaries of near-term baboon fetuses deprived of estrogen in utero was associated with increased expression of alpha-inhibin, but not activin betaA and betaB or the activin receptors. Therefore, we proposed that estrogen regulates fetal ovarian follicular development by controlling the intraovarian inhibin:activin ratio. As a prelude to conducting experiments to test this hypothesis, in the current study we determined whether the primate fetal ovary expressed Smads 2/3 and 4 and whether expression of these activin-signaling proteins was altered in fetal ovaries of baboons in which estrogen production was suppressed. Western blot analyses demonstrated that the 59 kDa Smad 2, 54 kDa Smad 3, and 64 kDa Smad 4 proteins were expressed in fetal ovaries of untreated baboons at both mid and late gestation and that the level of expression was not significantly altered in late gestation by in vivo treatment with CGS 20267 or CGS 20267 and estrogen. Immunocytochemistry localized Smads 2/3 and 4 to cytoplasm of oocytes and pregranulosa cells at midgestation and oocytes and granulosa cells of primordial follicles in late gestation. Smad 4 was also detected in granulosa cell nuclei in late gestation, and nuclear expression appeared to be decreased in fetal ovaries of baboons deprived of estrogen. The site of localization of Smads correlated with localization of the activin receptors IA and IIB, which we previously showed were abundantly expressed in oocytes and (pre)granulosa cells at both mid and late gestation and unaltered by estrogen deprivation. In summary, the results of the current study are the first to show that the intracellular signaling molecules required to transduce an activin signal are expressed in the baboon fetal ovary and that expression was not altered by estrogen deprivation in utero. These findings, coupled with our previous observations showing that estrogen deprivation reduced follicle numbers and upregulated/induced expression of inhibin but not activin or the activin receptors, lend further support to the hypothesis that estrogen regulates fetal ovarian folliculogenesis by controlling the intraovarian activin:inhibin ratio.

Authors+Show Affiliations

Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Virginia 23501, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

14585818

Citation

Billiar, Reinhart B., et al. "Localization and Developmental Expression of the Activin Signal Transduction Proteins Smads 2, 3, and 4 in the Baboon Fetal Ovary." Biology of Reproduction, vol. 70, no. 3, 2004, pp. 586-92.
Billiar RB, St Clair JB, Zachos NC, et al. Localization and developmental expression of the activin signal transduction proteins Smads 2, 3, and 4 in the baboon fetal ovary. Biol Reprod. 2004;70(3):586-92.
Billiar, R. B., St Clair, J. B., Zachos, N. C., Burch, M. G., Albrecht, E. D., & Pepe, G. J. (2004). Localization and developmental expression of the activin signal transduction proteins Smads 2, 3, and 4 in the baboon fetal ovary. Biology of Reproduction, 70(3), 586-92.
Billiar RB, et al. Localization and Developmental Expression of the Activin Signal Transduction Proteins Smads 2, 3, and 4 in the Baboon Fetal Ovary. Biol Reprod. 2004;70(3):586-92. PubMed PMID: 14585818.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Localization and developmental expression of the activin signal transduction proteins Smads 2, 3, and 4 in the baboon fetal ovary. AU - Billiar,Reinhart B, AU - St Clair,J Benjamin, AU - Zachos,Nicholas C, AU - Burch,Marcia G, AU - Albrecht,Eugene D, AU - Pepe,Gerald J, Y1 - 2003/10/29/ PY - 2003/10/31/pubmed PY - 2004/12/16/medline PY - 2003/10/31/entrez SP - 586 EP - 92 JF - Biology of reproduction JO - Biol Reprod VL - 70 IS - 3 N2 - We recently demonstrated that the reduction in the number of primordial follicles in ovaries of near-term baboon fetuses deprived of estrogen in utero was associated with increased expression of alpha-inhibin, but not activin betaA and betaB or the activin receptors. Therefore, we proposed that estrogen regulates fetal ovarian follicular development by controlling the intraovarian inhibin:activin ratio. As a prelude to conducting experiments to test this hypothesis, in the current study we determined whether the primate fetal ovary expressed Smads 2/3 and 4 and whether expression of these activin-signaling proteins was altered in fetal ovaries of baboons in which estrogen production was suppressed. Western blot analyses demonstrated that the 59 kDa Smad 2, 54 kDa Smad 3, and 64 kDa Smad 4 proteins were expressed in fetal ovaries of untreated baboons at both mid and late gestation and that the level of expression was not significantly altered in late gestation by in vivo treatment with CGS 20267 or CGS 20267 and estrogen. Immunocytochemistry localized Smads 2/3 and 4 to cytoplasm of oocytes and pregranulosa cells at midgestation and oocytes and granulosa cells of primordial follicles in late gestation. Smad 4 was also detected in granulosa cell nuclei in late gestation, and nuclear expression appeared to be decreased in fetal ovaries of baboons deprived of estrogen. The site of localization of Smads correlated with localization of the activin receptors IA and IIB, which we previously showed were abundantly expressed in oocytes and (pre)granulosa cells at both mid and late gestation and unaltered by estrogen deprivation. In summary, the results of the current study are the first to show that the intracellular signaling molecules required to transduce an activin signal are expressed in the baboon fetal ovary and that expression was not altered by estrogen deprivation in utero. These findings, coupled with our previous observations showing that estrogen deprivation reduced follicle numbers and upregulated/induced expression of inhibin but not activin or the activin receptors, lend further support to the hypothesis that estrogen regulates fetal ovarian folliculogenesis by controlling the intraovarian activin:inhibin ratio. SN - 0006-3363 UR - https://www.unboundmedicine.com/medline/citation/14585818/Localization_and_developmental_expression_of_the_activin_signal_transduction_proteins_Smads_2_3_and_4_in_the_baboon_fetal_ovary_ L2 - https://academic.oup.com/biolreprod/article-lookup/doi/10.1095/biolreprod.103.018598 DB - PRIME DP - Unbound Medicine ER -