A disrupted TJ barrier induced by therapy of epithelial cells with synthetic peptides corresponding to the extracellular domain of JAMs (Liang et al., 2000). In addition, a leaky TJ-permeability barrier was located within the intestinal epithelial cells of JAM-A knockout mice, indicating the significance of JAM proteins in barrier function (Laukoetter et al., 2007). Interestingly, such leaky TJ barrier could possibly be the outcome of an SARS-CoV-2 Proteins site induction of claudin-10 and -15 detected within the intestinal epithelial cells obtained from JAM-A knockout mice versus the wild-type. It was shown that an induction of specific claudins would result in an increase in permeability of certain ions across the TJ barrier (Laukoetter et al., 2007). An induction of claudins following knockout of JAM-A plus a down-regulation of occludin just after JAM-A antibody treatment thus illustrate that JAMs might regulate the TJ barrier by altering the localization and/or expression of other TJ proteins (Severson and Parkos, 2009). Irrespective of the significance of JAMs in modulating the barrier function in cell lines or intestinal epithelia, the significance of JAMs to the BTB remains unknown. Although JAM-A and JAM-B are located in the BTB (Morrow et al., 2010), deletion of JAM-A or homozygous mutation of JAM-B had no impact on the BTB integrity (Sakaguchi et al., 2006; Shao et al., 2008). It’s identified that mice with JAM-A deleted or JAM-B mutated remained fertile and their seminiferous epithelium was histologically normal (Sakaguchi et al., 2006; Shao et al., 2008). Even though deletion of JAM-A in mice led to reduced litter size, this is possibly resulted from impaired motility of spermatozoa as JAM-A was also shown to become involved in sperm tail formation (Shao et al., 2008). As opposed to claudins and occludin whose functions are mainly associated towards the TJ-permeability barrier as they are structural components of the blood-tissue barriers, JAMs are involved in various cellular functions and pathological circumstances, for instance leukocyte migration, angiogenesis, hypertension and tumorigenesis (Bazzoni, 2011). Amongst them, the participation of JAMs in the transmigration of leukocyte across the endothelial TJ barrier through inflammation is of terrific interest given that preleptotene spermatocytes may perhaps be using JAMs to traverse the BTB with similar mechanism (Wang and Cheng, 2007). It’s noted that apart from Sertoli cells, germ cells also expressed JAM proteins including JAM-A and JAM-C (Wang and Cheng, 2007), hence it was Carbonic Anhydrase Proteins Biological Activity proposed that aside from playing the role for anchoring germ cells to Sertoli cells, JAMs might also be accountable for the spermatocyte transit at the BTB. In reality, the loss of JAM-C, an integrated component on the apical ES in the Sertolispermatid interface, led to failure of spermiogenesis and infertility (Gliki et al., 2004). In brief, a great deal work is necessary to define the role of JAMs through spermatogenesis, in certain, its function at the BTB. 2.1.4. ZO Adaptor Proteins–Underneath the TJs, cytoplasmic plaques are formed by way of the cytoplasmic tails of TJ proteins straight linked with adaptor proteins, like ZO proteins, at a 1:1 stoichiometric ratio (e.g. occludin-ZO-1, claudin-ZO-1, JAM-ZO-1), which in turn bind towards the underlying actin filaments. As such, TJ proteins are linked to actinNIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptInt Rev Cell Mol Biol. Author manuscript; obtainable in PMC 2014 July 08.Mok et al.Pagecytoskeleton for the assistance of barrier integrity. 3.
