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Immunology‚ Endocrine & Metabolic Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry - Immunology‚ Endocrine and Metabolic Agents)

Volume 8 Issue 1
ISSN: 1871-5222
eISSN: 1875-5844


   All Titles

  “Unlocking” the Blood-Testis Barrier and the Ectoplasmic Specialization by Cytokines During Spermatogenesis: Emerging Targets for Male Contraception
  pp.20-27 (8) Authors: C. Yan Cheng, Michelle W.M. Li, Dolores D. Mruk

Cytokines are known to regulate an array of physiological functions in the testis, including cell differentiation, apoptosis, steroidogenesis, and cell division. Recent studies have illustrated that cytokines also take a crucial role in the regulation of junction dynamics. These include the regulation of cell-cell adhesion and tight junction permeability barriers in multiple epithelia and endothelia, such as those found in the small intestine, kidney, skin, and testis. In this review, we summarize recent findings in this field with an emphasis on the role of cytokines in junction restructuring events during spermatogenesis in the seminiferous epithelium of testes. This review also identifies several areas of research that functional studies can be designed to unravel the physiological significance of cytokines in junction restructuring at the Sertoli-Sertoli or Sertoli-germ cell interface in the seminiferous epithelium. It is expected that multiple cytokines, such as TGF-β3 and TNFα, are working in concert with other yet-to-be identified molecules to coordinate the intriguing events of junction restructuring during different stages of the seminiferous epithelial cycle in adult testes in mammals.

  Keywords: Cytokines, transforming growth factors, tumor necrosis factor, testis, spermatogenesis, Sertoli cells, blood-testis barrier, tight junction, adherens junction, ectoplasmic specialization
  Affiliation: Population Council, The Mary M. Wohlford Laboratory for Male Contraceptive Research, 1230 York Avenue, New York, New York 10065, USA.
  Key: New Content Free Content Open Access Plus Subscribed Content

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