| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
RESEARCH |
1 Prince Henrys Institute of Medical Research, Monash Medical Centre, PO Box 5152, Clayton 3168, Victoria, Australia and 2 Departments of Anatomy and 3 Cell Biology and Biochemistry and Molecular Biology, Monash University, Clayton 3168, Victoria, Australia
Correspondence should be addressed to P G Stanton; Email: peter.stanton{at}princehenrys.org
Claudin-11 and occludin are protein components in tight junctions (TJs) between Sertoli cells which are important for the maintenance of the bloodtestis barrier. Barrier formation occurs during puberty, with evidence suggesting hormonal regulation of both claudin-11 and occludin. This study aimed to investigate the regulation of claudin-11 and occludin mRNA expression by testosterone (T) and FSH and their immunolocalisation at rat Sertoli cell TJs in vitro, and to correlate any steroid regulation with the functional capacity of TJs. Sertoli cells formed functional TJs within 3 days as assessed by transepithelial electrical resistance (TER). Both T and dihydrotestosterone significantly (P < 0.01) increased TER twofold and claudin-11 mRNA two- to threefold within 3 days. FSH partially stimulated TER and claudin-11 mRNA, but estradiol had no effect. T also promoted claudin-11 localisation into extensive intercellular contacts. In contrast to claudin-11, Tand FSH did not change occludin mRNA expression, however, T promoted localisation of occludin at cell contacts in a similar manner to claudin-11. Addition of flutamide to T-stimulated cells caused a twofold decrease in both TER and claudin-11 mRNA expression, and resulted in the loss of both proteins from cell contacts. This effect was reversible following flutamide removal. It is concluded that androgens i) co-regulate claudin-11 mRNA expression and TER, implicating claudin-11 in TJ formation and ii) promote the localisation of claudin-11 and occludin at Sertoli cell contacts. Hence, the ability of androgens to maintain spermatogenesis in vivo is partly via their effects on TJ proteins and regulation of the bloodtestis barrier.
This article has been cited by other articles:
![]() |
S. Mazaud-Guittot, E. Meugnier, S. Pesenti, X. Wu, H. Vidal, A. Gow, and B. Le Magueresse-Battistoni Claudin 11 Deficiency in Mice Results in Loss of the Sertoli Cell Epithelial Phenotype in the Testis Biol Reprod, January 1, 2010; 82(1): 202 - 213. [Abstract] [Full Text] [PDF] |
||||
![]() |
W.-Y. Lui and W. M Lee Molecular mechanisms by which hormones and cytokines regulate cell junction dynamics in the testis J. Mol. Endocrinol., August 1, 2009; 43(2): 43 - 51. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. K. Nicholls, C. A. Harrison, R. B. Gilchrist, P. G. Farnworth, and P. G. Stanton Growth Differentiation Factor 9 Is a Germ Cell Regulator of Sertoli Cell Function Endocrinology, May 1, 2009; 150(5): 2481 - 2490. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Sa, R. Neves, S. Fernandes, C. Alves, F. Carvalho, J. Silva, N. Cremades, I. Malheiro, A. Barros, and M. Sousa Cytological and Expression Studies and Quantitative Analysis of the Temporal and Stage-Specific Effects of Follicle-Stimulating Hormone and Testosterone During Cocultures of the Normal Human Seminiferous Epithelium Biol Reprod, November 1, 2008; 79(5): 962 - 975. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. A Tarulli, S. J Meachem, S. Schlatt, and P. G Stanton Regulation of testicular tight junctions by gonadotrophins in the adult Djungarian hamster in vivo Reproduction, June 1, 2008; 135(6): 867 - 877. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |