La transplantation heterotopique

Un modele pour l'etude de la regulation de la spermatogenese. Quelques considerations histomorphologiques a propos du declin de la spermatogenese chez l'homme

Translated title of the contribution: Heterotopic transplantation as a model to study the regulation of spermatogenesis: Some histomorphological considerations about sperm decline in man

L. Johnson, G. U. Falk, L. C. Suggs, D. J. Henderson, G. E. Spoede, S. W. Brown, T. A. McGowen, H. Meguerditchian, J. J. Barnard

Research output: Contribution to journalArticle

Abstract

A novel animal model (syngeneic neonatal testicular graft transplanted under the skin of the outer ear in adult inbred Fischer rats that had been castrated, hypophysectomised, and/or subjected to hormonal replacement therapy) was developed to study regulation of spermatogenesis and Sertoli cell number. Given that Sertoli Cell number and testicular size are important in determining spermatozoan production rates, this model was first used to study Sertoli cell proliferation, testicular size, and establishment of germ cells. The specific objectives were to determine the developmental pattern of Sertoli cell numbers in transplanted testes and the effect of number of testes transplanted, sex of hosts, pituitary hormonal removal, and replacement on Sertoli cell number, hormonal status of the host, and establishment of germ cells. A few tubules had complete spermatogenesis at 90 days posttransplantation, indicating that Sertoli cells in some of these tubules were functional. Leydig cell structure appeared to be normal, but the density of these interstitial cells was greater than that in testes of intact rats. Although the weight of the seminal vesicles and prostate were maintained in the castrated host with transplants, both serum FSH and LH concentrations were higher than intact control rats. Leukocytic infiltration of testes was not observed in intact rats or in rats receiving neonatal testes. Although transplanted testes showed a delay in reaching the plateau value for Sertoli cell number per testis and although the value reached was lower than in intact testes, the developmental pattern of Sertoli cell proliferation (early division of cells followed by stabilized number of cells) in transplanted testes was similar to that in intact rats. Hypophysectomy reduced the growth of testicular grafts, and hormonal replacement via retransplantation to pituitary intact hosts enhances Sertoli cell proliferation and testicular growth. When two on four testes were transplanted into castrated males or ovariectomized female hosts for 65 days, there was no difference in the graft weights or Sertoli cell numbers between sexes of hosts. Four transplanted testes per rat produced more total testicular parenchyma and a greater number of Sertoli cells per testis than did two testes regardless of sex of the host. Transplantation of six or eight testes produced more total Sertoli cells/host than that found in testes of intact rats. Using hormonal therapy in hypophysectomized hosts, the testicular parenchymal weight was greater for pituitary-intact hosts and FSH- LH combination than the control media. There was no statistically significant difference among the media control, LH, FSH, and GH. This testicular transplant model has shown that the period of Sertoli cell proliferation can be delayed by hypophysectomy, that Sertoli cell number can be influenced by endogenous and exogenous hormones, and that a major component in regulation of testicular size is at the level of the testis. Hence, this model should facilitate study of experimental endocrine manipulation control and potential experimental intervention to increase Sertoli cell number, testicular size, and spermatogenesis. Regarding human sperm count decline in recent years, there appears to be no significant decline in Sertoli cell number or spermatogenic potential in a group of North American men. However, there was a significant decline in volume/man of Leydig cells and volume/man of Leydig cell cytoplasm.

Original languageFrench
Pages (from-to)549-555
Number of pages7
JournalContraception Fertilite Sexualite
Volume25
Issue number7-8
StatePublished - 1997

Fingerprint

Heterotopic Transplantation
Sertoli Cells
Spermatogenesis
Spermatozoa
Testis
Cell Count
Leydig Cells
Transplants
Cell Proliferation
Hypophysectomy
Weights and Measures
Germ Cells
External Ear
Sperm Count
Seminal Vesicles

Keywords

  • Endocrine
  • In vivo
  • Neonatal
  • Rat
  • Regulation
  • Sertoli
  • Spermatogenesis
  • Testis
  • Transplantation

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

La transplantation heterotopique : Un modele pour l'etude de la regulation de la spermatogenese. Quelques considerations histomorphologiques a propos du declin de la spermatogenese chez l'homme. / Johnson, L.; Falk, G. U.; Suggs, L. C.; Henderson, D. J.; Spoede, G. E.; Brown, S. W.; McGowen, T. A.; Meguerditchian, H.; Barnard, J. J.

In: Contraception Fertilite Sexualite, Vol. 25, No. 7-8, 1997, p. 549-555.

Research output: Contribution to journalArticle

Johnson, L. ; Falk, G. U. ; Suggs, L. C. ; Henderson, D. J. ; Spoede, G. E. ; Brown, S. W. ; McGowen, T. A. ; Meguerditchian, H. ; Barnard, J. J. / La transplantation heterotopique : Un modele pour l'etude de la regulation de la spermatogenese. Quelques considerations histomorphologiques a propos du declin de la spermatogenese chez l'homme. In: Contraception Fertilite Sexualite. 1997 ; Vol. 25, No. 7-8. pp. 549-555.
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abstract = "A novel animal model (syngeneic neonatal testicular graft transplanted under the skin of the outer ear in adult inbred Fischer rats that had been castrated, hypophysectomised, and/or subjected to hormonal replacement therapy) was developed to study regulation of spermatogenesis and Sertoli cell number. Given that Sertoli Cell number and testicular size are important in determining spermatozoan production rates, this model was first used to study Sertoli cell proliferation, testicular size, and establishment of germ cells. The specific objectives were to determine the developmental pattern of Sertoli cell numbers in transplanted testes and the effect of number of testes transplanted, sex of hosts, pituitary hormonal removal, and replacement on Sertoli cell number, hormonal status of the host, and establishment of germ cells. A few tubules had complete spermatogenesis at 90 days posttransplantation, indicating that Sertoli cells in some of these tubules were functional. Leydig cell structure appeared to be normal, but the density of these interstitial cells was greater than that in testes of intact rats. Although the weight of the seminal vesicles and prostate were maintained in the castrated host with transplants, both serum FSH and LH concentrations were higher than intact control rats. Leukocytic infiltration of testes was not observed in intact rats or in rats receiving neonatal testes. Although transplanted testes showed a delay in reaching the plateau value for Sertoli cell number per testis and although the value reached was lower than in intact testes, the developmental pattern of Sertoli cell proliferation (early division of cells followed by stabilized number of cells) in transplanted testes was similar to that in intact rats. Hypophysectomy reduced the growth of testicular grafts, and hormonal replacement via retransplantation to pituitary intact hosts enhances Sertoli cell proliferation and testicular growth. When two on four testes were transplanted into castrated males or ovariectomized female hosts for 65 days, there was no difference in the graft weights or Sertoli cell numbers between sexes of hosts. Four transplanted testes per rat produced more total testicular parenchyma and a greater number of Sertoli cells per testis than did two testes regardless of sex of the host. Transplantation of six or eight testes produced more total Sertoli cells/host than that found in testes of intact rats. Using hormonal therapy in hypophysectomized hosts, the testicular parenchymal weight was greater for pituitary-intact hosts and FSH- LH combination than the control media. There was no statistically significant difference among the media control, LH, FSH, and GH. This testicular transplant model has shown that the period of Sertoli cell proliferation can be delayed by hypophysectomy, that Sertoli cell number can be influenced by endogenous and exogenous hormones, and that a major component in regulation of testicular size is at the level of the testis. Hence, this model should facilitate study of experimental endocrine manipulation control and potential experimental intervention to increase Sertoli cell number, testicular size, and spermatogenesis. Regarding human sperm count decline in recent years, there appears to be no significant decline in Sertoli cell number or spermatogenic potential in a group of North American men. However, there was a significant decline in volume/man of Leydig cells and volume/man of Leydig cell cytoplasm.",
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author = "L. Johnson and Falk, {G. U.} and Suggs, {L. C.} and Henderson, {D. J.} and Spoede, {G. E.} and Brown, {S. W.} and McGowen, {T. A.} and H. Meguerditchian and Barnard, {J. J.}",
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T1 - La transplantation heterotopique

T2 - Un modele pour l'etude de la regulation de la spermatogenese. Quelques considerations histomorphologiques a propos du declin de la spermatogenese chez l'homme

AU - Johnson, L.

AU - Falk, G. U.

AU - Suggs, L. C.

AU - Henderson, D. J.

AU - Spoede, G. E.

AU - Brown, S. W.

AU - McGowen, T. A.

AU - Meguerditchian, H.

AU - Barnard, J. J.

PY - 1997

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N2 - A novel animal model (syngeneic neonatal testicular graft transplanted under the skin of the outer ear in adult inbred Fischer rats that had been castrated, hypophysectomised, and/or subjected to hormonal replacement therapy) was developed to study regulation of spermatogenesis and Sertoli cell number. Given that Sertoli Cell number and testicular size are important in determining spermatozoan production rates, this model was first used to study Sertoli cell proliferation, testicular size, and establishment of germ cells. The specific objectives were to determine the developmental pattern of Sertoli cell numbers in transplanted testes and the effect of number of testes transplanted, sex of hosts, pituitary hormonal removal, and replacement on Sertoli cell number, hormonal status of the host, and establishment of germ cells. A few tubules had complete spermatogenesis at 90 days posttransplantation, indicating that Sertoli cells in some of these tubules were functional. Leydig cell structure appeared to be normal, but the density of these interstitial cells was greater than that in testes of intact rats. Although the weight of the seminal vesicles and prostate were maintained in the castrated host with transplants, both serum FSH and LH concentrations were higher than intact control rats. Leukocytic infiltration of testes was not observed in intact rats or in rats receiving neonatal testes. Although transplanted testes showed a delay in reaching the plateau value for Sertoli cell number per testis and although the value reached was lower than in intact testes, the developmental pattern of Sertoli cell proliferation (early division of cells followed by stabilized number of cells) in transplanted testes was similar to that in intact rats. Hypophysectomy reduced the growth of testicular grafts, and hormonal replacement via retransplantation to pituitary intact hosts enhances Sertoli cell proliferation and testicular growth. When two on four testes were transplanted into castrated males or ovariectomized female hosts for 65 days, there was no difference in the graft weights or Sertoli cell numbers between sexes of hosts. Four transplanted testes per rat produced more total testicular parenchyma and a greater number of Sertoli cells per testis than did two testes regardless of sex of the host. Transplantation of six or eight testes produced more total Sertoli cells/host than that found in testes of intact rats. Using hormonal therapy in hypophysectomized hosts, the testicular parenchymal weight was greater for pituitary-intact hosts and FSH- LH combination than the control media. There was no statistically significant difference among the media control, LH, FSH, and GH. This testicular transplant model has shown that the period of Sertoli cell proliferation can be delayed by hypophysectomy, that Sertoli cell number can be influenced by endogenous and exogenous hormones, and that a major component in regulation of testicular size is at the level of the testis. Hence, this model should facilitate study of experimental endocrine manipulation control and potential experimental intervention to increase Sertoli cell number, testicular size, and spermatogenesis. Regarding human sperm count decline in recent years, there appears to be no significant decline in Sertoli cell number or spermatogenic potential in a group of North American men. However, there was a significant decline in volume/man of Leydig cells and volume/man of Leydig cell cytoplasm.

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KW - Endocrine

KW - In vivo

KW - Neonatal

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KW - Regulation

KW - Sertoli

KW - Spermatogenesis

KW - Testis

KW - Transplantation

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