Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have established a cell line, RENTts3.1, by infection of primary rat endometrial cells with a retrovirus carrying a temperature-sensitive mutant of SV40 large T-antigen. These cells show a temperature-dependent phenotype with respect to morphology, growth and expression of macrophage colony-stimulating factor 1 (CSF-1) mRNA. At the permissive temperature, the cells grow with a doubling time of 24 h and exhibit an elongated, fibroblast-like morphology. They express vimentin and type III collagen mRNA. At the non-permissive temperature, the cells stop growing and exhibit an epitheloid morphology with flat enlarged cytoplasm. At the higher temperature, the cells continue to express type III collagen, but also express CSF-1 mRNA, and the cellular content of this transcript is influenced by glucocorticoid treatment. No expression of the epithelial markers cytokeratin, uteroglobin, beta-endorphin or preproenkephalin was detected, suggesting a stromal origin of the cell line. Electron microscopic data of cells cultivated on different substrates also support this conclusion. This cell line may be useful for the study of the molecular processes involved in decidual transformation of the endometrial mucosa.
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PMID:Establishment of a temperature-dependent cell line from rat endometrium by retroviral infection. 166 43

We have developed a dissociated primary cell culture of noradrenergic neurons from the locus ceruleus of postnatal (1- to 5-d-old) mice or rats. Slices of the brain stem were made on a Vibratome. Then the region of locus ceruleus, which was identified by observing the slices under a dissecting microscope, was dissected out from the slices. The removed fragments of brain slices were dissociated and cultured up to 3 weeks on a non-neuronal feeder layer, which consisted predominantly of astroglial cells, or on a fibronectin-treated collagen substratum. After 2 weeks of culture, about 70% of total neuronlike cells revealed positive catecholamine histofluorescence, indicating that they were probably noradrenergic neurons. About 98% of large- and medium-sized cultured neurons (soma diameter greater than or equal to 20 microns) was histofluorescence positive. The fluorescence-positive cells had long processes rich in varicosities, and the shape of their soma was either multipolar or fusiform. Electron microscopy using permanganate fixation revealed that the varicosities along their processes had small granular vesicles, which may contain norepinephrine. Physiological properties of these noradrenergic neurons were investigated with intracellular microelectrodes or with the whole-cell version of the patch clamp. We observed that many cells were producing spontaneous firing. Many of these spontaneously firing cells had no obvious contact with neighboring cells. The neurons were depolarized when glutamate was applied by pressure ejection. They also responded to GABA and glycine with either hyperpolarization or depolarization, and these responses were antagonized by picrotoxin and strychnine. Application of substance P generally produced depolarization with an increase in input resistance. The neurons responded with hyperpolarization to somatostatin, beta-endorphin, and enkephalin. This culture system will become a useful tool for elucidating the cellular and molecular properties of the central noradrenergic neurons.
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PMID:Noradrenergic neurons from the locus ceruleus in dissociated cell culture: culture methods, morphology, and electrophysiology. 243 74

The blood catecholamine, 11-hydroxycorticosteroid and free hydroxyproline content and collagen metabolism in the rabbit aortic wall were studied under conditions of chronic electrostimulation and bilateral amygdaloid electrocoagulation. It was found that electrostimulation of the amygdaloid lateral nucleus causes changes in the adrenocorticotropin content, activating collagen metabolism and accumulation in the aortic wall. A fall of the noradrenaline, 11-hydroxycorticosteroid concentration and activation of collagen metabolism, accompanied by its accumulation in the aortic wall, are seen during the 1st month after electrocoagulation.
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PMID:[Adrenal hormone level and collagen metabolism in the aortic wall under the effect of changes in the amygdaloid complex]. 712 48

Fibronectin is a ubiquitous extracellular matrix (ECM) protein known to play a critical role in cell adhesion. In the present study we dissected the effects of glucocorticoids and cyclic adenosine 3',5'-monophosphate (cAMP) on FN expression in cultures of cytotrophoblasts isolated from human term placentas to identify compounds which may influence uterine-placental adherence. Based on immunoassay data, relative to controls, glucocorticoid treatment (1-1000 nM) of cytotrophoblasts specifically inhibited media levels of oncofetal FN (i.e., FNs bearing an oncofetal epitope) 65-92%. Treatment of cytotrophoblasts with androgens, estrogens, and progestins (1-1000 nM) did not markedly affect onfFN expression. Corticotropin-releasing hormone (CRH) treatment (200 nM) alone had no effect on levels on onfFN. In combination experiments using 100 nM dexamethasone (DEX), 1000 nM medroxyprogesterone acetate (MPA), 10 nM estradiol (E2) and 200 nM corticotropin-releasing hormone CRH, we observed that DEX treatment also promoted approximately an 85% reduction in media levels of onfFN. This indicated that glucocorticoids profoundly suppress FN expression in the presence of high concentrations of other steroids and pregnancy-associated paracrine effectors. To examine the influence of ECM protein composition on glucocorticoid-mediated suppression of onfFN expression, cells were inoculated on untreated culture wells or on wells coated with FN, laminin, or collagen I. We observed that DEX treatment downregulated onfFN levels 70-85% under each of these conditions, suggesting that glucocorticoid effects on FN expression were not dependent on the presence of an exogenous ECM. Treatment of cytotrophoblasts with 8-bromo-cAMP resulted in a dose-dependent reduction in onfFN expression to 3% of control levels with an EC50 of 150 nM. Based on Northern blotting, treatment of cytotrophoblasts with 100 nM DEX, 1 mM 8-bromo-cAMP, or 2 nM relaxin inhibited steady state levels of FN mRNA approximately 90% relative to controls. Our results suggest that during pregnancy glucocorticoids and compounds that alter intracellular concentrations of cAMP may profoundly suppress FN expression and therefore may have dramatic effects on uterine-placental adherence.
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PMID:Negative regulation of placental fibronectin expression by glucocorticoids and cyclic adenosine 3',5'-monophosphate. 797 10

Group B streptococci were recently reported to possess a cell-associated collagenase. Although the enzyme hydrolyzed the synthetic collagen-like substrate N-(3-[2-furyl]acryloyl)-Leu-Gly-Pro-Ala, we found that neither the highly purified enzyme nor crude group B streptococcal cell lysate solubilized a film of reconstituted rat tail collagen, an activity regarded as obligatory for a true collagenase. We cloned and sequenced the gene for the enzyme (pepB). The deduced amino acid sequence showed 66.4% identity to the PepF oligopeptidase from Lactococcus lactis, a member of the M3 or thimet family of zinc metallopeptidases. The group B streptococcal enzyme also showed oligopeptidase activity and degraded a variety of small bioactive peptides, including bradykinin, neurotensin, and peptide fragments of substance P and adrenocorticotropin.
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PMID:Characterization of PepB, a group B streptococcal oligopeptidase. 875 83

Glomerular accumulation of the extracellular matrix (ECM) with subsequent sclerosis is a common finding in most progressive renal diseases. Recently MSW (Mouse South Western) protein was cloned by its ability to bind the bidirectional promoter of the collagen IV genes. This protein was also reported as the large subunit of the DNA replication complex A1, as well as the promoter binding protein of corticotropin-releasing hormone and the angiotensinogen gene. To investigate the mechanism of accumulation of the ECM as it relates to glomerular cellular events, the expression of MSW protein was studied in the remnant kidney model. Progressive expression of MSW protein was found in the glomerular sclerotic lesion at week 4 and at later time points after renal ablation. The expression of proliferating cell nuclear antigen (PCNA) and type IV collagen was also correlated with the expression of MSW protein by immunofluorescence. RNA dot blot analysis also showed that the expression of MSW mRNA was increased at week 7 in association with the augmented expression of type IV collagen. These results, taken together, suggest that MSW protein plays an important role in the regulation of type IV collagen gene expression in vivo and may contribute to glomerular cell proliferation and the development of glomerulosclerosis.
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PMID:A novel transcription factor is correlated with both glomerular proliferation and sclerosis in the rat renal ablation model. 937 Sep 42

Vitronectin is a multifunctional plasma glycoprotein which may regulate the systems related to protease cascades such as the coagulation, fibrinolysis, and complement systems as well as cell adhesion. Solid-phase assays and affinity chromatography on immobilized glycolipids indicated that vitronectin purified under denaturing conditions bound to sulfatide (Gal(3-SO4)beta1-1ceramide), cholesterol 3-sulfate, and various phospholipids, but not gangliosides. Only the unfolded or multimeric form of vitronectin bound to sulfatide, suggesting a conformational dependency of the binding activity, while vitronectin bound to cholesterol 3-sulfate regardless of its conformational state. The recombinant domains of human vitronectin and mutants with certain domains deleted were separately expressed in E. coli as fusion proteins. Using the recombinants, sulfatide-, phosphatidylserine-, cholesterol 3-sulfate-, Type I collagen-, heparin-, and beta-endorphin-binding activities were found to be attributable to hemopexin domain 2 and hemopexin domain 1. The possibility was suggested that the presence of a somatomedin domain and/or connecting region flanking hemopexin domain 1 inactivated its heparin binding. De-N-glycosylation of plasma vitronectin significantly affected the cholesterol sulfate- and collagen-binding activities, although its effects were opposite. These findings suggest that diverse ligand-binding activities could be attributed to pexin family motifs but that the interdomain interactions and glycosylations modulate the ligand binding activities of vitronectin.
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PMID:Characterization of the ligand binding activities of vitronectin: interaction of vitronectin with lipids and identification of the binding domains for various ligands using recombinant domains. 957 50

Osteoporosis is a chronic disorder characterized by low bone mass and fragility fractures. It affects more than 25 million men and women in the United States alone. Although several candidate genes, such as the vitamin-D-receptor gene or the estrogen-receptor gene, have been suggested in the pathogenesis of osteoporosis, the genetic dissection of this disorder remains a daunting task. To search systematically for chromosomal regions containing genes that regulate bone mineral density (BMD), we scanned the entire autosomal genome by using 367 polymorphic markers among 218 individuals (153 sibpairs) from 96 nuclear families collected from three townships of Anqing, China. In these 96 families, DNA samples from both parents were available for 82 (85.4%) families. By using age- and gender-adjusted forearm BMD measurements, a peak on chromosome 2 near D2S2141, D2S1400, and D2S405, a region previously linked to spinal BMD, showed evidence of linkage to both proximal and distal forearm BMD (multipoint LOD=2.15 and 2.14 for proximal and distal forearm BMD, respectively). One region on chromosome 13 (multipoint LOD=1.67) in the proximity of D13S788 and D13S800 showed evidence of linkage to distal forearm BMD only. Possible candidate genes included CALM2 (calmodulin 2) at 2p21.3-p21.1, a putative STK (serine/threonine kinase) at 2p23-24, POMC (pro-opiomelanocortin) at 2p23.3, and COL4A1 and COL4A2 (collagen IV alpha-1 and alpha-2 subunits) at 13q34. Because of the limited sample size, the suggestive evidence of linkage of this study should be considered as tentative and needs to be replicated in other larger populations.
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PMID:A genome-wide scan for loci linked to forearm bone mineral density. 1032 46

Peptides related to melanotropin (alphaMSH) and corticotropin (ACTH), collectively termed melanocortins, are known to improve the postlesion repair of injured peripheral nerves. In addition, melanocortins exert trophic effects on the outgrowth of neurites from central nervous system neurons in vitro. Here we report, for the first time, the stimulation by alpha-MSH of spinal neurite outgrowth in vivo after injury. In the in vivo model, spinal cord trauma was produced at lower thoracic spinal levels of adult rats. Under a surgical microscope a laminectomy was performed exposing the dorsum of the spinal cord. Then the dura was cut longitudinally and the dorsal columns were identified. Iridectomy scissors were used to transect the dorsal half of the spinal cord bilaterally, thereby completely lesioning the main corticospinal tract component. Then the lesion gap was immediately filled with a solid collagen matrix. Ingrowth of fibers was quantified using an advanced image analyser using a video image of sections transmitted by a camera. In the control situation virtually no ingrowth of sprouting injured fibers into the collagen implant in the lesion gap was seen. However, when the collagen matrix contained 10(-8) M alpha-MSH, a profound and significant stimulation of fiber ingrowth into the implant was observed (alpha-MSH, 21.5 +/- 2.9%; control, 1.4 +/- 0.6% p < 0.01). A small percentage of these ingrowing fibers was CGRP-immunoreactive (17.0 +/- 4%), whereas no serotonergic ingrowth was observed. Furthermore, we found that local application of alpha-MSH directs a substantial amount of lesioned anterogradely labelled corticospinal tract axons to regrow into the collagen implant (alpha-MSH, 15.2 +/- 5.2%; control, 0.5 +/- 0.3%, p < 0.01). The observed fiber ingrowth is not accompanied by an invasion of astroglial or reactive microglial cells into the implant. In conclusion, inclusion of alpha-MSH in the collagen implant stimulates the regrowth of injured axons in the adult rat spinal cord.
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PMID:Alpha-melanocyte stimulating hormone promotes regrowth of injured axons in the adult rat spinal cord. 1039 70

Prolactinomas were induced by chronic estrone acetate treatment in female Wistar rats in vivo. After enzymatic dissociation of the tumor tissue, monolayer cell cultures were obtained. In vitro tumor induction was performed by treatment of normal monolayer anterior pituitary cell cultures with a 1:1 mixture of 7,9-dimethylbenz[c]acridine: 8-methylbenz[c]acridine. For immunohistochemistry, the cell cultures were stained by the peroxidase-antiperoxidase method for standardization; the nonspecific hormone release was induced with 30 mM K+. The prolactin, alpha-melanotropin, and adrenocorticotropin levels in the supernatant were measured by specific, sensitive radioimmunoassays. The results indicated surface differences between the in vivo induced prolactinoma cells and normal pituitary cells: the attachment of the prolactinoma cells required 15% collagen treatment, whereas normal cells required only 3-4% collagen. Tumor cells induced in vitro by methylbenz[c]acridine treatment were able to attach only after ammonia activation of the collagen surface. These findings strongly suggest that the mode of tumor induction can result in differences in membrane fluidity; this phenomenon is possibly connected with the levels of prolactin, adrenocorticotropin and alpha-melanotropin hormone production of these endocrine tumor cells.
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PMID:Surface changes and hormone production in pituitary cells during tumorigenesis. 1074 84


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