D Sertoli cells, led to infertility in mice as a consequence of the lack of BTB with out TJ strands formed involving Sertoli cells (Gow et al., 1999). Besides being the important developing block of TJs, claudins also ascertain the properties of TJ barriers by assembling TJs with different claudin members. For instance, TJ strands formed by claudin-1 are highly branched network although claudin-11-based TJ strands, as these located in Sertoli cells, are mainly parallel strands with small branching (Gow et al., 1999; Morita et al., 1999b). Furthermore, the selectivity of ions and solutes of a permeCXC Chemokines Proteins Species ability barrier is also dependent around the composition of claudins as illustrated by gain-or-loss function research in animals, humans or cell lines involving certain claudins. For instance, overexpression of claudin-2, but not claudin-3, in MDCK I cells which express only claudin-1 and -4, results in a “leaky” TJ barrier, as shown by a lower in transepithelial electrical resistance (TER) across the cell epithelium. This as a result reflects the differential ability amongst distinctive claudins in conferring the TJ-barrier function (Furuse et al., 2001). Furthermore, in claudin-15 knockout mice, the tiny intestine displayed malabsorption of glucose as a consequence of a disruption of paracellular transport of Na+ ions across the TJ barrier (Tamura et al., 2011). Claudin-16,NIH-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.Pagehowever, was shown to be vital to paracellular transport of Mg2+ across the TJ barrier (Simon et al., 1999).NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptClaudins also play an important part in sustaining the BTB function through spermatogenesis. In reality, TJ strands at the BTB is contributed significantly by claudin-11 considering the fact that deletion of claudin-11 leads to a loss of the BTB ultrastructure, resulting inside the lack of TJ strands between Sertoli cells (Gow et al., 1999). Interestingly, Sertoli cells, which typically cease to divide after postnatal day 15, are found to become proliferating in adult claudin-11 knockout mice (Gow et al., 1999). That is most likely as a result of the loss of make contact with inhibition following the disappearance of TJs. This hence suggests that the permeability barrier imposed by claudin-11 also has a part in regulating cell cycle function in Sertoli cells. Furthermore, a recent report has shown that claudin-3 may be a crucial protein involving inside the intermediate compartment throughout translocation of spermatocytes across the BTB (Komljenovic et al., 2009). Immunofluorescence staining illustrated that during the transit of preleptotene spermatocytes across the BTB at stage VII X in mice, localization of claudin-3 in the BTB was discovered apically to preleptotene spermatocytes (“old” BTB) at stage VII; even so, at stage VIII arly IX, claudin-3 was detected at each apically (“old” BTB) and basally (“new” BTB) on the translocating spermatocytes; and ultimately claudin-3 was detected only at the basal side (“new” BTB) of leptotene spermatocytes FGF Family Proteins Accession transformed from preleptotene spermatocytes (Komljenovic et al., 2009). Despite this stage-specific localization of claudin-3 coinciding with all the intermediate compartment, this observation needs additional verification by functional studies, which include if its knockdown would indeed impede the migration of spermatocytes in the BTB. In addition, the function of claudin-3 can be species-specific considering the fact that claudin-3 is just not.
