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

The presence of albumin binding sites on the abluminal front of vascular endothelium was examined on the capillaries of the adipose tissue. The experimental procedure consisted in injecting interstitially within the rat epididymal fat and epicardial fat, albumin (alone or bearing oleic acid) either conjugated with gold particles (Alb-Au or Alb-OA-Au) or radioiodinated [( 125I]-Alb). In controls, polyethyleneglycol-gold complex (PEG-Au) and [125I]-IgG were used as tracers. The results revealed that: a) albumin binding sites are expressed on the abluminal front of endothelium especially concentrated on plasmalemmal vesicles; b) the retrotranscytosis of albumin conjugates from the interstitium to the capillary lumen is a poorly represented process; c) the binding of the tracers used appears to be time and concentration dependent; d) albumin conjugates do not bind significantly to plasmalemmal vesicles of adipocytes, pericytes and smooth muscle cells; e) PEG-Au and [125I]-IgG do not show a binding pattern similar to that of albumin conjugates.
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PMID:Albumin binding sites are expressed on the abluminal plasma membrane of capillary endothelium. 164 24

Albumin is the major carrier of long chain free fatty acids, that are known to be heavily utilized by fat cells. To investigate the cellular structures involved in the interaction of albumin with preadipocytes, precursor fat cells isolated from rat epididymal fat pads were cultured in Dulbecco's modified Eagle's medium supplemented with 5% fetal calf serum and antibiotics. Cell differentiation was induced by 1.7 nM insulin added to the culture medium. The ensuing cells in various stages of differentiation were incubated with albumin, alone or bearing oleic acid, adsorbed to 5 nm gold particles (Alb-Au or Alb-OA-Au) for 10 min at 37 degrees C. As control, polyethyleneglycol-gold and IgG-gold complexes were used in same conditions. After extensive washing, the cell monolayer was fixed in 2.5% glutaraldehyde, and processed for electron microscopy. Examination of thin sections and morphometric analysis showed that: a) in the process of adipogenesis induced in vitro four cell types were simultaneously present: fibroblast-like cells (F), early adipocytes (EA), adipocytes (A) and aged adipocytes (AA); b) upon incubation with Alb-Au, the probe labelled preferentially coated pits and coated vesicles and only some uncoated vesicles; in time the tracer was found in endosomes, occasionally, multivesicular bodies and lysosome-like structures. The binding and uptake was dependent on the stage of cell differentiation, being less pronounced in fibroblast-like cells and increased in later stages (A and AA); c) Alb-OA-Au labelled the same structural features like the Alb-Au (i.e. coated pits and vesicles); however, the binding to the cell membrane was fourfold higher than that of Alb-Au in F and EA stages and was maintained at the same level in A and AA stages; d) control probes were taken up only by adipocytes and aged adipocytes, cells that express a strong phagocytic function for all tracers used. These results indicated that albumin bound to gold and especially albumin-bearing fatty acids-gold, bind preferentially to coated pits and vesicles of preadipocytes. Further internalization of albumin-gold particles seems to be non-specific, since both the probes and the controls adsorbed to gold were delivered to the same endosomal-lysosomal compartment.
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PMID:Cellular structures involved in albumin interaction with preadipocytes in various stages of adipogenesis, in vitro. 801 43

Hepatic expression profiling has revealed miRNA changes in liver diseases, while hepatic miR-155 expression was increased in murine non-alcoholic fatty liver disease, suggesting that miR-155 might regulate the biological process of lipid metabolism. To illustrate the effects of miR-155 gain of function in transgenic mouse liver on lipid metabolism, transgenic mice (i.e., Rm155LG mice) for the conditional overexpression of mouse miR-155 transgene mediated by Cre/lox P system were firstly generated around the world in this study. Rm155LG mice were further crossed to Alb-Cre mice to realize the liver-specific overexpression of miR-155 transgene in Rm155LG/Alb-Cre double transgenic mice which showed the unaltered body weight, liver weight, epididymal fat pad weight and gross morphology and appearance of liver. Furthermore, liver-specific overexpression of miR-155 transgene resulted in significantly reduced levels of serum total cholesterol, triglycerides (TG) and high-density lipoprotein (HDL), as well as remarkably decreased contents of hepatic lipid, TG, HDL and free fatty acid in Rm155LG/Alb-Cre transgenic mice. More importantly, microarray data revealed a general downward trend in the expression profile of hepatic genes with functions typically associated with fatty acid, cholesterol and triglyceride metabolism, which is likely at least partially responsible for serum cholesterol and triglyceride lowering observed in Rm155LG/Alb-Cre mice. In this study, we demonstrated that hepatic overexpression of miR-155 alleviated nonalcoholic fatty liver induced by a high-fat diet. Additionally, carboxylesterase 3/triacylglycerol hydrolase (Ces3/TGH) was identified as a direct miR-155 target gene that is potentially responsible for the partial liver phenotypes observed in Rm155LG/Alb-Cre mice. Taken together, these data from miR-155 gain of function study suggest, for what we believe is the first time, the altered lipid metabolism and provide new insights into the metabolic state of the liver in Rm155LG/Alb-Cre mice.
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PMID:Overexpression of miR-155 in the liver of transgenic mice alters the expression profiling of hepatic genes associated with lipid metabolism. 2579 9