Wn confirmed that fertility was retained in these mice only from 60 weeks of age (Takehashi et al., 2007), but all CYP1 Species occludin knockout mice were infertile by 360 weeks of age using the tubules devoid of spermatocytes and spermatids (Saitou et al., 2000; Takehashi et al., 2007). Collectively, these findings illustrate that when other TJ proteins, such as GLUT4 Gene ID claudins and JAMs, might be able to supersede the loss of occludin at the BTB to retain spermatogenesis; on the other hand, occluding is completely crucial to retain the BTB function and spermatogenesis beyond 10 weeks of age in rodents in the course of adulthood, illustrating the functional partnership among BTB and maintenance of spermatogenesis. Interestingly, the necessity of occludin to spermatogenesis will not apply to humans as occludin was not located in human Sertoli cells in an earlier study (Moroi et al., 1998). Having said that, a recent study by RT-PCR has identified occludin in human Sertoli cells (Xiao and Cheng, unpublished observations), illustrating additional study around the function of occludin in huamn BTB is warranted. The lack of occludin in human seminiferous epithelium also illustrates that the BTB is usually a complex ultrastructure and its constituency is species-specific. Other research have also shown that the part of occludin in blood issue barriers is organand/or tissue-specific. As an illustration, occludin will not be necessary for the formation of TJ strands; and in some cell kinds, it is actually not even required for the maintenance of TJs. It was reported that occludin was not found inside the TJ strands in between porcine aortic endothelial cells (Hirase et al., 1997), revealing that in some tissues, occludin is not a constituent protein of your TJ barrier. Moreover, in occludin knockout mice, the TJ barrier formed in between intestinal epithelial cells was indistinguishable from those of the wild variety ultrastructurally (Saitou et al., 2000), demonstrating that in some epithelia that commonly express occludin, a missing of occludin does not necessarily impact the formation and/or upkeep from the TJ barrier. In addition, even though research have shown that treatment of synthetic occludin peptide disrupted TJ barrier in between Sertoli cells (Chung et al., 2001) as well as that involving intestinal epithelial cells (Nusrat et al., 2005), a study in human intestinal T84 epithelialNIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptInt Rev Cell Mol Biol. Author manuscript; out there in PMC 2014 July 08.Mok et al.Page(T84) cell cultures has shown that the occludin peptide-induced TJ-barrier disruption was mediated by redistribution of other TJ proteins (e.g. claudin-1) and TJ adaptor (e.g. ZO-1) (Nusrat et al., 2005), illustrating occludin may act as a “signaling” regulatory TJ protein. Far more essential, the use of monoclonal antibody against the second extracellular loop of occludin in T84 cells was identified to disrupt epithelial cell polarity but not the TJ barrier (Tokunaga et al., 2007). Collectively, these findings illustrate the complicated functional part of occludin at the TJ barrier, supporting the notion of its species- and/or tissue-specific function regarding its involvement in TJ-barrier formation and upkeep. Nonetheless, these findings illustrate that occludin, in contrast to claudins, may well have other role(s) and serving as a signaling molecule in controlling the permeability in TJs, for instance fine-tuning the barrier function, in addition to serving because the developing block of TJs in some epithelia. This notion is also s.