Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood-epididymal barrier creates a unique microenvironment critical for sperm maturation. There is little information on proteins comprising epididymal tight and adhering junctions or on factors regulating their expression. Claudins are a family of transmembrane proteins reported to be exclusively localized to tight junctions. In the present study the expression of claudin-l (Cl-1) was examined with respect to the different cell types of the epididymis and its various regions as well as its expression during postnatal development and regulation by testicular factors, using both immunocytochemistry and Northern blot analysis. RT-PCR of adult epididymal and testicular RNA (positive control) indicated that Cl-1 messenger RNA (mRNA) transcripts were present in all regions of the epididymis. In the adult, Cl-1 was localized immunocytochemically along the entire length of the lateral plasma membranes between adjacent principal cells, including apical areas containing tight junctions, as well as at the interface between principal and basal cells and along the basal plasma membrane of the epithelium in relation to the basement membrane. Northern blot analysis of adult epididymis with a rat Cl-1 complementary DNA indicated the presence of two hybridizing bands of 4.0 and 1.5 kb. Postnatally, in the caput-corpus and cauda epididymidis, mRNA levels for both transcripts were lowest on day 7. In the caput-corpus epididymidis, mRNA levels for the 1.5-kb transcript increased significantly between 7 and 14 days, whereas the levels of the 4.0-kb transcript were significantly higher by day 21. Postnatal studies revealed that in the initial segment and caput epididymidis, Cl-1 immunostaining was present along the entire length of the lateral plasma membranes of undifferentiated epididymal epithelial cells as early as day 7, including apical areas containing tight junctions. By day 21, staining was identical to that of adult animals, but as this is an age when androgen levels are not at their peak, the data would suggest that they are not a prominent factor regulating Cl-1 expression. Orchidectomy and orchidectomy plus testosterone replacement experiments revealed differences in Cl-1 immunostaining in the initial segment, suggesting that localization of Cl-1 in epididymal tight junctions is androgen dependant. Thus, Cl-1 expression in the initial segment appears to be only partially under the control of androgens. However, in all other epididymal regions, orchidectomy with or without testosterone replacement, revealed no changes to the normal staining pattern, suggesting that androgens do not regulate Cl-1 expression in these regions. Taken together, these studies demonstrate that Cl-1 expression in the epididymis is not localized exclusively to tight junctions, but appears along the entire interfaces of adjacent epithelial cells as well as along the basal plasma membrane, suggesting a role for Cl-1 as an adhesion molecule. The data also suggest that the regulation of Cl-1 in the epididymis is complex and multifactorial.
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PMID:Claudin-1 is not restricted to tight junctions in the rat epididymis. 1115 59

Several studies have implicated fatty-acids as inflammatory regulators, suggesting that there may be a direct role for common dietary fatty-acids in regulating innate immune cells. In humans, a single high-fat meal increases systemic cytokines and leukocytes. In mice, short term high-fat feeding increases adipose tissue (AT) leukocytes and alters the inflammatory profile of AT macrophages. We have seen that short term high fat feeding to C57BL/6J male mice increases palmitic and oleic acid within AT depots, but oleic acid increase is highest in the mesenteric AT (MAT). In vitro, oleic acid increases M2 macrophage markers (CD206, MGL1, and ARG1) in a murine macrophage cell line, while addition of palmitic acid is able to inhibit that increase. Three day supplementation of a chow diet, with oleic acid, induced an increase in M2 macrophage markers in the MAT, but not in the epididymal AT. We tested whether increases in M2 macrophages occur during short term ad lib feeding of a high fat diet, containing oleic acid. Experiments revealed two distinct populations of macrophages were altered by a three day high milk-fat diet. One population, phenotypically intermediate for F4/80, showed diet-induced increases in CD206, an anti-inflammatory marker characteristic of M2 macrophages intrinsic to the AT. Evidence for a second population, phenotypically F4/80(HI)CD11b(HI) macrophages, showed increased association with the MAT following short term feeding that is dependent on the adhesion molecule, ICAM-1. Collectively, we have shown that short term feeding of a high-fat diet changes two population of macrophages, and that dietary oleic acid is responsible for increases in M2 macrophage polarization.
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PMID:Dietary oleic acid increases m2 macrophages in the mesenteric adipose tissue. 2409 82

Adipose tissue is considered to be an endocrine organ, and adipocyte size correlates with insulin resistance and metabolic parameters in obesity. There is little data on the effects of angiopoietin-1 in adipose tissue and kidney in streptozotocin (STZ)-induced diabetes. In this study, we investigated the protective effect of COMP-angiopoietin-1 (COMP-Ang1), a potent variant of angiopoietin-1, on vascular endothelial cells in epididymal adipose tissue and its regulatory effect on other metabolic parameters, such as lipid droplet diameter, macrophage infiltration, and renal inflammation in STZ-treated mice. Our data showed that COMP-Ang1 increased the density of platelet endothelial cell adhesion molecule-1 (PECAM-1)-1-positive vascular endothelial cells in adipose tissue, which were significantly decreased by treatment with STZ. COMP-Ang1 ameliorated the STZ-induced decrease in lipid droplet diameter and increase in macrophage infiltration in adipose tissue. Serum free fatty acid and triglyceride levels were decreased after administration of COMP-Ang1. There was a beneficial effect on serum insulin levels after treatment with COMP-Ang1 in STZ-induced diabetic mice. Fasting blood glucose levels in COMP-Ang1-treated mice were significantly lower than those of LacZ-treated mice. Cotreatment with COMP-Ang1 and STZ also had similar effects on the above parameters. Administration of soluble Tie2, an inhibitor of angiopoietin-1, reversed the effects of COMP-Ang1. COMP-Ang1 was found to ameliorate the up-regulation of proinflammatory molecules and F4/80-positive macrophage infiltration in the kidneys of STZ-treated mice. COMP-Ang1 increased the phosphorylation of Akt in epididymal adipose tissue and kidneys of STZ-induced diabetic mice. These data indicate that COMP-Ang1 regulates lipogenic effects in adipose tissue and renal inflammation in STZ-induced diabetic mice.
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PMID:COMP-angiopoietin-1 mitigates changes in lipid droplet size, macrophage infiltration of adipose tissue and renal inflammation in streptozotocin-induced diabetic mice. 2921 68