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 vascular cell responses to the type 1, 2, and 3 isoforms of transforming growth factor-beta (TGF-beta 1, TGF-beta 2, TGF-beta 3) were studied using bovine aortic endothelial (BAECs) and smooth muscle cells (BASMC3) as well as rat epididymal fat pad microvascular endothelia (RFCs). Three distinct bioassays indicated that TGF-beta elicits results that do not differ significantly from those of the TGF-beta 1 isoform in all three cell populations. These assays are: inhibition of proliferation, cell migration, and neovascularization. By contrast the cellular responses to TGF-beta 1 and TGF-beta 3 differed from those to TGF-beta 2. Three distinct receptor assays revealed the presence of type I and type II TGF-beta 1 cell surface binding proteins on BAECs, BASMCs, and RFCs. Experimentation to decipher cell surface binding by the different isoforms revealed that iodinated TGF-beta 1 bound to the surface of all three vascular cell types can be competed off in similar fashion by either TGF-beta 1 or TGF-beta 3; however, competition with TGF-beta 2 produced unique binding profiles dependent on the cell type examined. The ratios of type I to type II TGF-beta receptors in these three vascular cell types vary from 1:1 in BAECs to 1.5:1 in RFCs to 3:1 in BASMCs and can be correlated with the differences noted in cellular responses to TGF-beta 1 and TGF-beta 2 in proliferation, migration, and in vitro angiogenic assays.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of vascular cell behavior by transforming growth factors beta. 163 50

The vascular cell responses to the type 3 isoform of transforming growth factor-beta (TGF-beta 3) were studied using bovine aortic endothelial (BAECs) and smooth muscle cells (BASMCs) as well as rat epididymal fat pad microvascular endothelia (RFCs). Four distinct bioassays indicated that TGF-beta 3 elicits results that do not differ significantly from those of the TGF-beta 1 isoform in all three cell populations. Inhibition of proliferation by TGF-beta 3 at a 5-day time point ranged from 85% on BAECs, to 55% and 53% on RFCs and BASMCs, respectively. The effects of TGF-beta 3 and TGF-beta 1 on cell migration were also found to be similar; migration of large vessel endothelial cells was inhibited 35%, while migration of smooth muscle cells was enhanced 30%. TGF-beta 1 and TGF-beta 3 also had equivalent effects on neovascularization while a 10-fold higher concentration of TGF-beta 2 was required to elicit a similar response. Experimentation to decipher cell surface binding by the different isoforms revealed that iodinated TGF-beta 1 bound to the surface of all three vascular cell types can be competed off in similar fashion by either TGF-beta 1 or TGF-beta 3; however, competition with TGF-beta 2 produced unique binding profiles dependent upon the cell type examined. In summary, both the TGF-beta 1 and TGF-beta 3 isoforms of the transforming growth factor-beta family evoke comparable responses in proliferation, migration, angiogenic and cell surface binding assays using three distinct vascular cell types, while the biofunctions of TGF-beta 2 on these cells are distinct.
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PMID:Vascular cell responses to TGF-beta 3 mimic those of TGF-beta 1 in vitro. 176 38

Clusterin, also known as sulphated glycoprotein-2 or testosterone-repressed prostate message-2, is a ubiquitous protein found in a variety of tissues and species. In the reproductive tract of the male rat, clusterin is regulated in a complex age-dependent and cell-specific manner. It is expressed at high levels in the epididymis and testis and at very low levels in the prostate under basal conditions. The expression of this gene in the prostate and seminal vesicles is associated with androgen withdrawal, while in the testis clusterin mRNA is repressed by cyclic AMP (cAMP). To understand the mechanisms that control the expression of the clusterin gene better, we isolated and characterized the gene encoding rat clusterin, and analysed its cytosine methylation pattern in various tissues. Several putative regulatory DNA elements were identified, including a consensus AP-1 site in the 5' flanking region. Two AP-1 sites and two transforming growth factor-beta inhibitory elements, one AP-2 site and eight half-sites for glucocorticoid/androgen response elements were found within the first intron, and one cAMP response element was found in the first exon. The cytosine methylation pattern indicated that testicular or epididymal DNA in the rat is hypomethylated in the region between positions -534 and -99 of the clusterin gene, when compared with tissues with lower levels of expression such as prostate as well as liver, lung, kidney and spleen.
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PMID:Regulators for the rat clusterin gene: DNA methylation and cis-acting regulatory elements. 799 55

The transforming growth factor-beta1 (TGF-beta1) and the transforming growth factor-beta receptor type II (TGF-betaRII) were studied in the epididymis of sexually mature marmoset monkeys (Callithrix jacchus) by immunohistochemical localization of the protein and by polymerase chain reaction (PCR) analysis of the mRNA level. In order to specify reactive cell types, the morphology of all three segments (caput, corpus, and cauda epididymidis) was evaluated by light microscopy. Six different cell types could be distinguished: principal, basal, apical, and clear cells, as well as intraepithelial lymphocytes and macrophages. Using immunohistochemistry, specific staining for TGF-beta1 in the caput was found in 47% of the apical cells, whereas the TGF-betaRII was located in the apical portion of 91% of all principal cells. In the corpus epididymidis, 20% of the apical cells were immunopositive for TGF-beta, and binding of the receptor antibody occurred in 17% of the principal cells (all numbers based on counts of counterstained nuclei). All differences between percentages in the caput and corpus were significant as determined by chi-square test. PCR analysis revealed detectable levels of TGF-beta1 mRNA in the marmoset epididymis. Our results indicate for the first time that TGF-beta1 is synthesized in the marmoset epididymis, possibly in a different subpopulation of epididymal cells than the TGF-beta receptor type II. Thus, TGF-beta might be of functional relevance in the primate epididymis.
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PMID:TGF-beta could be involved in paracrine actions in the epididymis of the marmoset monkey (Callithrix jacchus). 1038 17