Molecular mechanisms by which hormones and cytokines regulate cell junction dynamics in the testis
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Figure 1
A schematic drawing illustrates the regulation of apical ES by testosterone. In the presence of testosterone, intact apical ES are established and constituted by cadherin/cadherin (Zhang et al. 2005b) and integrin/laminin interlocks (Wong et al. 2005). Cadherin and integrin are closely associated with their cytoplasmic interacting partners to form stable ES (Wong et al. 2008). In the absence of testosterone, a significant increase in phosphorylation of β-catenin (Zhang et al. 2005b) and FAK (Wong et al. 2005) are observed. The change of phosphorylated state of the cytoplasmic partners destabilizes the protein interlocks, resulting in the disassembly of the apical ES. α-cat, α-catenin; β-cat, β-catenin; MTMR2, myotubularin-related protein 2; FAK, focal adhesion kinase; ES, ectoplasmic specializations.
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Figure 2
A schematic drawing illustrates the effect of TNF-α on junction restructuring in the seminiferous epithelium. Intact ES and BTB are maintained in the absence of TNF-α. At stage VIII of the epithelial cycle, a surge of TNF-α triggers different MAPK pathways and regulates the opening of the BTB (Li et al. 2006, Sze et al. 2008) as well as the apical ES (Mealy et al. 1990) by controlling the junction protein levels and altering the transcription of junction proteins to allow the migration of preleptotene/leptotene spermatocytes across the BTB and the release of mature spermatids to the tubular lumen. It is also noted that at stage VIII, testosterone enhances transcytosis of occludin in Sertoli cells, possibly from the cell surface at the apical end of the migrating spermatocytes to cell surface at the basal end to reassemble the BTB (Yan et al. 2008a). TNF-α, tumor necrosis factor-α; TNFRI, tumor necrosis factor receptor I; ZO-1, zonula occludens-1, BTB, blood–testis barrier; ES, ectoplasmic specializations.
- © 2009 Society for Endocrinology
