Wn confirmed that fertility was retained in these mice only from 60 weeks of age (Takehashi et al., 2007), but all GNE-371 In Vivo occludin knockout mice have been infertile by 360 weeks of age with the tubules devoid of spermatocytes and spermatids (Saitou et al., 2000; Takehashi et al., 2007). Collectively, these findings illustrate that while other TJ proteins, including claudins and JAMs, might be capable to supersede the loss of occludin at the BTB to keep spermatogenesis; nonetheless, occluding is totally vital to retain the BTB function and spermatogenesis beyond 10 weeks of age in rodents for the duration of adulthood, illustrating the functional partnership among BTB and Leptin Proteins Storage & Stability maintenance of spermatogenesis. Interestingly, the necessity of occludin to spermatogenesis will not apply to humans as occludin was not identified in human Sertoli cells in an earlier study (Moroi et al., 1998). Even so, a recent study by RT-PCR has identified occludin in human Sertoli cells (Xiao and Cheng, unpublished observations), illustrating additional study around the function of occludin in huamn BTB is warranted.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 often a complicated ultrastructure and its constituency is species-specific. Other studies have also shown that the function of occludin in blood concern barriers is organand/or tissue-specific. For example, occludin just isn’t critical for the formation of TJ strands; and in some cell types, it’s not even necessary for the maintenance of TJs. It was reported that occludin was not found in the TJ strands in between porcine aortic endothelial cells (Hirase et al., 1997), revealing that in some tissues, occludin just isn’t a constituent protein from the TJ barrier. Additionally, in occludin knockout mice, the TJ barrier formed between intestinal epithelial cells was indistinguishable from these on the wild kind ultrastructurally (Saitou et al., 2000), demonstrating that in some epithelia that usually express occludin, a missing of occludin will not necessarily impact the formation and/or maintenance on the TJ barrier. In addition, even though studies have shown that remedy of synthetic occludin peptide disrupted TJ barrier involving Sertoli cells (Chung et al., 2001) also as that amongst 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 well act as a “signaling” regulatory TJ protein. A lot more vital, 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 complex functional function of occludin at the TJ barrier, supporting the notion of its species- and/or tissue-specific function relating to its involvement in TJ-barrier formation and maintenance. Nonetheless, these findings illustrate that occludin, as opposed to claudins, could have other part(s) and serving as a signaling molecule in controlling the permeability in TJs, for instance fine-tuning the barrier function, apart from serving because the developing block of TJs in some epithelia. This notion can also be s.
