Tight junctions (TJs) form continuous intercellular contacts in intercellular junctions. TJs involve integral proteins such as occludin (OCLN) and claudins (CLDNs) as well as peripheral proteins such as zona occludens-1 (ZO-1) and junctional adhesion molecules (JAMs). TJs control paracellular transportation across cell-to-cell junctions. Although TJs have been studied for several decades, comparison of the transcriptional-translational levels of these molecules in canine organs has not yet been performed. In this study, we examined uterine expression of CLDNs, OCLN, junction adhesion molecule-A, and ZO-1 in canine. Expression levels of canine uterine TJ proteins, including CLDN1, 2, 4, 5, JAM-A, ZO-1, and OCLN, were measured using reverse transcription PCR, real-time PCR, and Western blotting, whereas TJs distribution was determined by immunohistochemistry. The mRNA and protein expression levels of OCLN, CLDN-1, 4, JAM-1, and ZO-1 were identified in the uterus. Immunohistochemistry demonstrated that TJs were localized to the endometrium and/or myometrium of the uterus. Our results show that canine TJ proteins, including CLDNs, OCLN, JAM-A, and ZO-1, were expressed in the canine uterus. Taken together, these proteins may perform unique physiological roles in the uterus. Therefore, these findings may serve as a basis for further studies on TJ proteins and their roles in the physiological or pathological condition of the canine uterus.

Worldwide there is concern about the continuing release of a broad range of environmental endocrine disrupting chemicals, including polychlorinated biphenyls, dioxins, phthalates, polybrominated diphenyl ethers (PBDEs), and other halogenated organochlorines persistent organic pollutants (POPs) into the environment. They are condemned for health adverse effects such as cancer, reproductive defects, neurobehavioral abnormalities, endocrine and immunological toxicity. These effects can be elicited via a number of mechanisms among others include disruption of endocrine system, oxidation stress and epigenetic. However, most of the mechanisms are not clear, thus several number of studies are ongoing trying to elucidate them in order to protect the public by reducing these adverse effects. In this review, we briefly limited review the process, the impacts, and the potential mechanisms of dioxin/dioxin like compound, particularly, their possible roles in adverse developmental and reproductive processes, diseases, and gene expression and associated molecular pathways in cells.

Active calcium transport is carried out by calcium channel proteins, cytosolic buffering or transfer proteins, and pump proteins. Several components of this transport system have recently been determined using gene knockout (KO) models. The calbindin‐ D9k/28k and calbindin‐D9k/TRPV6 double KO mice were generated and reported that induction of expression of some duodenal calcium transport proteins can compensate for the CaBP‐9k gene deficiency. In CaBP‐9k KO mice, the levels of these hormones differ between the KO and wild‐type (WT) mice. The induction of TRPV6 in the duodenum was observed in adult KO male mice but induction was not modified by physiologic doses of 1,25(OH)2D3 and compensatory gene induction was not affected by PTH. Duodenal TRPV6 transcription in WT and female KO mice were modulated by 1,25(OH)2D3 in a dose‐dependent manner. Under calcium‐deficient dietary conditions, in DKO mice, serum calcium levels and bone length were decreased. The intestinal and renal expression of TRPV6 mRNA was significantly decreased in DKO mice fed a calcium‐deficient diet as compared to CaBP‐28k KO or WT mice, and DKO mice died after 4 weeks on a calcium‐deficient diet. Body weight, bone mineral density (BMD) and bone length were significantly reduced in all mice fed a calcium and 1,25‐(OH) D3‐ eficient diet, as compared to a normal diet, and none of the mice survived more than 4 weeks. Using microarray analysis, NCKX3 was identified as a gene that was differentially expressed in the kidneys of female and male mice. Although any hormones did not alter NCKX3 expression, however, aldosterone and hydrocortisone did down‐regulate renal NCKX3 expression in female mice. Taken together, these results indicate that deletions of CaBP‐9k and 28k has a significant effect on calcium processing under calcium‐deficient conditions, confirming the importance of dietary calcium and 1,25‐(OH)2D3 during growth and development