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Role for endogenous estrogen in prepubertal Sertoli cell maturation.
Anim Reprod Sci. 2012 Nov; 135(1-4):106-12.AR

Abstract

Reducing prepubertal endogenous estrogens led to increased numbers of Sertoli cells and the associated increased testicular size and testicular sperm production capacity in boars. The increased number of Sertoli cells might be due to a longer time for proliferation; delayed differentiation of Sertoli cells during suppressed endogenous estrogens would be consistent with this hypothesized, prolonged proliferation interval. This study used immunohistochemical detection of anti-Müllerian hormone (AMH), a marker of immature Sertoli cells, and of CDKN1B, a cell cycle inhibitor associated with more mature Sertoli cells, to determine if suppressing endogenous estrogens detectably delayed "differentiation" of porcine Sertoli cells. Testes were from littermate pairs of boars previously treated with Letrozole, an aromatase inhibitor, or vehicle, from the first week of age until tissue collection at 2, 3, 4, 5 or 6 months of age. Four animals were examined at each age following Letrozole treatment and their corresponding littermates evaluated following treatment with vehicle. Amount of AMH protein in Sertoli cells decreased with age of boar and could not be detected at 6 months of age. The AMH labeling was greater in the Letrozole-treated boars compared with littermate vehicle controls at 4 months of age (P=0.03). The percentage of CDKN1B-labeled Sertoli cells apparently increased with age through 5 months of age. At 4 and 5 months of age, the mean percentage of CDKN1B-labeled Sertoli cells was less in the Letrozole-treated animals than in the vehicle control animals (P = 0.03 and 0.04, respectively). These results are consistent with the hypothesis that continual inhibition of aromatase (and concomitatant reduced estrogen synthesis) causes a delay in Sertoli cell maturation in boars.

Authors+Show Affiliations

University of California, Davis, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

23041111

Citation

Kao, Eddy, et al. "Role for Endogenous Estrogen in Prepubertal Sertoli Cell Maturation." Animal Reproduction Science, vol. 135, no. 1-4, 2012, pp. 106-12.
Kao E, Villalon R, Ribeiro S, et al. Role for endogenous estrogen in prepubertal Sertoli cell maturation. Anim Reprod Sci. 2012;135(1-4):106-12.
Kao, E., Villalon, R., Ribeiro, S., & Berger, T. (2012). Role for endogenous estrogen in prepubertal Sertoli cell maturation. Animal Reproduction Science, 135(1-4), 106-12. https://doi.org/10.1016/j.anireprosci.2012.09.003
Kao E, et al. Role for Endogenous Estrogen in Prepubertal Sertoli Cell Maturation. Anim Reprod Sci. 2012;135(1-4):106-12. PubMed PMID: 23041111.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role for endogenous estrogen in prepubertal Sertoli cell maturation. AU - Kao,Eddy, AU - Villalon,Rosalina, AU - Ribeiro,Salustiano, AU - Berger,Trish, Y1 - 2012/09/20/ PY - 2011/11/04/received PY - 2012/08/30/revised PY - 2012/09/06/accepted PY - 2012/10/9/entrez PY - 2012/10/9/pubmed PY - 2013/6/5/medline SP - 106 EP - 12 JF - Animal reproduction science JO - Anim Reprod Sci VL - 135 IS - 1-4 N2 - Reducing prepubertal endogenous estrogens led to increased numbers of Sertoli cells and the associated increased testicular size and testicular sperm production capacity in boars. The increased number of Sertoli cells might be due to a longer time for proliferation; delayed differentiation of Sertoli cells during suppressed endogenous estrogens would be consistent with this hypothesized, prolonged proliferation interval. This study used immunohistochemical detection of anti-Müllerian hormone (AMH), a marker of immature Sertoli cells, and of CDKN1B, a cell cycle inhibitor associated with more mature Sertoli cells, to determine if suppressing endogenous estrogens detectably delayed "differentiation" of porcine Sertoli cells. Testes were from littermate pairs of boars previously treated with Letrozole, an aromatase inhibitor, or vehicle, from the first week of age until tissue collection at 2, 3, 4, 5 or 6 months of age. Four animals were examined at each age following Letrozole treatment and their corresponding littermates evaluated following treatment with vehicle. Amount of AMH protein in Sertoli cells decreased with age of boar and could not be detected at 6 months of age. The AMH labeling was greater in the Letrozole-treated boars compared with littermate vehicle controls at 4 months of age (P=0.03). The percentage of CDKN1B-labeled Sertoli cells apparently increased with age through 5 months of age. At 4 and 5 months of age, the mean percentage of CDKN1B-labeled Sertoli cells was less in the Letrozole-treated animals than in the vehicle control animals (P = 0.03 and 0.04, respectively). These results are consistent with the hypothesis that continual inhibition of aromatase (and concomitatant reduced estrogen synthesis) causes a delay in Sertoli cell maturation in boars. SN - 1873-2232 UR - https://www.unboundmedicine.com/medline/citation/23041111/Role_for_endogenous_estrogen_in_prepubertal_Sertoli_cell_maturation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-4320(12)00286-2 DB - PRIME DP - Unbound Medicine ER -