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Receptor Beta (receptor + beta)
Kinds of Receptor Beta Selected AbstractsPerinatal exposure to bisphenol-A changes N -methyl- D -aspartate receptor expression in the hippocampus of male rat offspringENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2010Xiao-Hong Xu Abstract Bisphenol-A (BPA) is one of the most common environmental endocrine disrupters with mixed estrogen agonist/antagonist properties. The toxicity of BPA has been extensively evaluated in a variety of tests in rodents, including developmental and reproductive toxicity, and carcinogenicity. The objective of the present study is to evaluate whether or not perinatal maternal exposure to BPA at 0.05, 0.5, 5, 50, and 200 mg/kg/d affects N -methyl- D -aspartate (NMDA) receptor (NMDAR) subunits NR1, NR2A, 2B, estrogen receptor beta (ER,), and aromatase cytochrome P450 (P450arom) protein expressions of hippocampus in male rat offspring during postnatal development. Western-blotting analyses showed that perinatal exposure to BPA significantly affected the expression of NMDAR subunits. At the lower doses of 0.05 to 50 mg/kg/d, BPA concentration dependently inhibited the expression of NMDAR subunits. However, at the higher dose (200 mg/kg/d), the effects of BPA on these subunits were different, with a stronger inhibition of NR1 expression and a slighter inhibition of NR2A, 2B expression when compared with those at the lower dosage of BPA. In addition, perinatal exposure to BPA inhibited the expression of ER, protein, but increased P450arom protein expression in a concentration-dependent manner, especially during the early postnatal period (the first 1,3 postnatal weeks). No significant influence of BPA on P450arom was observed at postnatal week 8. These data suggest that environmental BPA exposure may affect the development of the brain, enhancing the local biosynthesis of estrogen in the brain, inhibiting ER, and NMDAR expressions. Environ. Toxicol. Chem. 2010;29:176,181. © 2009 SETAC [source] Role of ceramide kinase in peroxisome proliferator-activated receptor beta-induced cell survival of mouse keratinocytesFEBS JOURNAL, Issue 15 2008Kiyomi Tsuji Ceramide (Cer) is known to be a lipid mediator in apoptosis and to have an important role in cell fate, via control of intracellular Cer levels. Recently, ceramide kinase (CerK) was identified as an enzyme that converts Cer to ceramide 1-phosphate (C1P). We examined potential functions of CerK in the regulation of keratinocyte survival, and the possible involvement of peroxisome proliferator-activated receptor beta (PPAR,). PPAR, is known to be a nuclear receptor acting as a ligand-inducible transcription factor and has been implicated in the control of keratinocyte survival. In the mouse keratinocyte cell line SP1, serum starvation induced cell death and the accumulation of intracellular Cer, an apoptotic event. However, apoptosis was inhibited by activation of PPAR,. Interestingly, activation of PPAR, enhanced the mRNA expression of CerK and CerK activity. Furthermore, the cell survival effect of PPAR, was greatly diminished in keratinocytes isolated from CerK-null mice. Chromatin immunoprecipitation revealed that, in vivo, PPAR, binds to the CerK gene via a sequence located in the first intron. Electrophoretic mobility-shift assays confirmed that PPAR, associates with this sequence in vitro. These findings indicated that CerK gene expression was directly regulated by PPAR,. In conclusion, our results demonstrate that PPAR,-mediated upregulation of CerK gene expression is necessary for keratinocyte survival against serum starvation-induced apoptosis. [source] Simultaneous activation of JAK1 and JAK2 confers IL-3 independent growth on Ba/F3 pro-B cellsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2005Huei-Mei Huang Abstract JAK1 and JAK2 are tyrosine kinases involved in the regulation of cell proliferation, differentiation, and survival. These proteins may play a key role in mediating the effects of the cytokine IL-3 on hematopoietic cells. IL-3 induces tyrosine phosphorylation of both JAK1 and JAK2. However, it is not clear whether the activation of JAK1, JAK2, or both is sufficient to confer factor-independent growth in IL-3 dependent cells. To address this issue, fusion proteins CD16/CD7/JAK (CDJAK), comprised of a CD16 extracellular domain, a CD7 transmembrane domain, and a JAK cytoplasmic region (either a wild-type JAK or a dominant negative mutant of JAK) were constructed. We established several Ba/F3 derivatives that stably overexpress the conditionally active forms of either CDJAK1, CDJAK2, or both these fusion proteins. In this study, the autophosphorylation of CDJAK1 or CDJAK2 was induced by crosslinking with anti-CD16 antibody. We demonstrated that, like their wild-type counterparts, CDJAK1 and CDJAK2 were preassociated with the IL-3 receptor beta and alpha subunits, respectively. Furthermore, the simultaneous activation of both CDJAK1 and CDJAK2 fusion proteins, but not either one alone, led to the tyrosine phosphorylation of the IL-3 receptor beta subunit, the activation of downstream signaling molecules, including STAT5, Akt, and MAPK, and the conferring of factor-independent growth to IL-3-dependent Ba/F3 cells. Coexpression of dominant negative mutants CDJAK1KE or CDJAK2KE with wild type CDJAK2 or CDJAK1, respectively, inhibited these activation activities. These results suggest that JAK1 and JAK2 must work cooperatively and not independently and that their actions are dependent on having normal kinase activity to trigger downstream signals leading to IL-3 independent proliferation and survival of Ba/F3 cells. © 2005 Wiley-Liss, Inc. [source] IL-2 gene C/T polymorphism is associated with prostate cancerJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 6 2006Hsi-Chin Wu Abstract Cytokines are reported to be associated with the formation of prostate cancer. Our aim was to investigate whether C/T polymorphisms of the interleukin-2 (IL-2) gene and IL-2 receptor beta (IL-2RB) gene are associated with prostate cancer. We compared the frequency of the polymorphisms of the IL-2 gene and the IL-2RB gene between 96 patients with prostate cancer and 105 healthy male volunteers from the same area (age >60 years). They were followed for at least 5 years. There was a significant difference in distribution of the genotype of the IL-2 gene polymorphism between the prostate cancer group and the control group (P = 0.017). The distribution of the TT homozygote of the IL-2 gene was significantly higher in the cancer group (32.3%) than in the control group (16.2%). However, no significant statistical difference was found between the polymorphism of the IL-2 gene and prostate cancer in survival analysis during a 5-year follow up period (log rank test; P = 0.19). There was no significant difference in the distribution of the genotype of the IL-2RB gene polymorphism between controls and cancer patients (P = 0.388). This study suggests that the IL-2 gene may be associated with susceptibility to prostate cancer in the Taiwan population. J. Clin. Lab. Anal. 20:245,249, 2006. © 2006 Wiley-Liss, Inc. [source] Initial steroid bolus injection promotes vigorous CD8+ alloreactive responses toward early graft acceptance immediately after liver transplantation in humansLIVER TRANSPLANTATION, Issue 9 2007Hiroto Egawa We have found that steroid bolus withdrawal prior to graft reperfusion increased the incidence of acute cellular rejection (ACR). This study aims to clarify how initial steroid bolus (ISB) injection at reperfusion influences the kinetics of CD8+ alloreactive immune responses immediately after living donor liver transplantation (LDLT). A total of 49 hepatitis C virus (HCV)-infected recipients were classified into 3 groups according to hierarchical clustering by preoperative CD8+CD45 isoforms. The naive T cell proportion was considerably higher in Group I than in Groups II and III, whereas Group II recipients had the highest effector memory (EM) T cells and Group III the highest effector T cells. The frequency of ACR was significantly higher in recipients without ISB than in those with ISB. In particular, the ACR rates were the highest in Group II without ISB. Following ISB, the proportion of effector T cells was promptly upregulated within 6 hours after graft reperfusion, simultaneously with the upregulation of CD27,CD28, subsets, interferon-gamma (IFN-,), tumor necrosis factor-alpha and perforin expression, which significantly correlated with increasing interleukin (IL)-12 receptor beta 1 cells. These were then downregulated to below preoperative levels by tacrolimus (Tac) administered at 24 hours. These changes did not occur in the absence of ISB. In Group II without ISB, the downregulation of IL-12R,1+ cells was the greatest, consistent with the highest rates of ACR and mortality (60%). In conclusion, ISB must be done in place, especially in Group II with preexisting high EM T cells, to enable the development of early allograft acceptance. Liver Transpl 13:1262,1271, 2007, © 2007 AASLD. [source] Distribution of sex steroid hormone receptors in the brain of an African cichlid fish, Astatotilapia burtoniTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 16 2010Lauren A. Munchrath Abstract Sex steroid hormones released from the gonads play an important role in mediating social behavior across all vertebrates. Many effects of these gonadal hormones are mediated by nuclear steroid hormone receptors, which are crucial for integration in the brain of external (e.g., social) signals with internal physiological cues to produce an appropriate behavioral output. The African cichlid fish Astatotilapia burtoni presents an attractive model system for the study of how internal cues and external social signals are integrated in the brain as males display robust plasticity in the form of two distinct, yet reversible, behavioral and physiological phenotypes depending on the social environment. In order to better understand where sex steroid hormones act to regulate social behavior in this species, we have determined the distribution of the androgen receptor, estrogen receptor alpha, estrogen receptor beta, and progesterone receptor mRNA and protein throughout the telencephalon and diencephalon and some mesencephalic structures of A. burtoni. All steroid hormone receptors were found in key brain regions known to modulate social behavior in other vertebrates including the proposed teleost homologs of the mammalian amygdalar complex, hippocampus, striatum, preoptic area, anterior hypothalamus, ventromedial hypothalamus, and ventral tegmental area. Overall, there is high concordance of mRNA and protein labeling. Our results significantly extend our understanding of sex steroid pathways in the cichlid brain and support the important role of nuclear sex steroid hormone receptors in modulating social behaviors in teleosts and across vertebrates. J. Comp. Neurol. 518:3302,3326, 2010. © 2010 Wiley-Liss, Inc. [source] Detection and localization of an estrogen receptor beta splice variant protein (ER,2) in the adult female rat forebrain and midbrain regionsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 3 2007Wilson C.J. Chung Abstract Estrogens regulate neural processes such as neuronal development, reproductive behavior, and hormone secretion, and signal through estrogen receptor (ER) , and ER, (here called ER,1). Recent studies have found variations in ER, and ER,1 mRNA splicing in rodents and humans. Functional reporter gene assays suggest that these splicing variations alter ER-mediated transcriptional regulation. Estrogen receptor beta 2 (ER,2), an ER,1 splice variant containing an 18 amino acid (AA) insert in the ligand binding domain, binds estradiol with ,10-fold lower affinity than ER,1, suggesting that it may serve as a low-affinity ER. Moreover, ER,2 reportedly acts in a dominant-negative fashion when heterodimerized with ER,1 or ER,. To explore the function of ER,2 in brain, an antiserum (Two,ER.1) targeting the 18 AA insert was developed and characterized. Western blot analysis and transient expression of ER,2 in cell lines demonstrated that Two,ER.1 recognizes ER,2. In the adult female rat brain, ER,2 immunoreactivity is localized in the cell nucleus and is expressed with a distribution similar to that of ER,1 mRNA. ER,2 immunoreactive cell numbers were high in, for example, piriform cortex, paraventricular nucleus, supraoptic nucleus, arcuate nucleus, and hippocampal CA regions, whereas it was low in the dentate gyrus. Moreover, ER,2 is coexpressed in gonadotropin-releasing hormone and oxytocin neurons. These studies demonstrate ER, splice variant proteins in brain and support the hypothesis that ER signaling diversity depends not only on ligand or coregulatory proteins, but also on regional and phenotypic selectivity of ER splice variant proteins. J. Comp. Neurol. 505:249,267, 2007. © 2007 Wiley-Liss, Inc. [source] Control of Cell Number in the Bed Nucleus of the Stria Terminalis of Mice: Role of Testosterone Metabolites and Estrogen Receptor SubtypesTHE JOURNAL OF SEXUAL MEDICINE, Issue 4pt1 2010Shin-ichi Hisasue MD ABSTRACT Introduction., The bed nucleus of the stria terminalis (BNST) exhibits several sex differences that may be related to male sexual behavior and gender identity. In mice and rats, sex differences in the principal nucleus of the BNST (BNSTp) are due to sexually dimorphic cell death during perinatal life. Although testosterone treatment of newborn female rats increases BNSTp cell number, the relevant hormone metabolite(s) are not known, and the effect of testosterone on the development of BNSTp cell number in mice has not been examined. Aim., To identify the sex hormone metabolites and receptors controlling cell number, volume, and cell size in the BNSTp of mice. Methods., In the first experiment, C57BL/6J male mice were injected on the day of birth with peanut oil; females were injected with testosterone propionate (TP), estradiol benzoate (EB), dihydrotestosterone propionate (DHTP), or oil alone, and the BNSTp of all animals was examined in adulthood. In the second experiment, to compare effects of EB to the effects of estrogen receptor subtype specific agonists, newborn female mice were injected with EB, propyl-pyrazole-triol (PPT, a selective estrogen receptor alpha [ER,] agonist), or diarylpropionitrile (DPN, a selective estrogen receptor beta [ER,] agonist). Main Outcome Measures., Nuclear volume measurements and stereological cell counts in the BNSTp in adulthood. Results., TP treatment of newborn females completely masculinized both BNSTp volume and cell number. EB masculinized neuron number, whereas DHTP had no effect on volume or cell number. In the second experiment, EB again fully masculinized neuron number in the BNSTp and in this study also masculinized BNSTp volume. PPT and DPN each significantly increased cell number, but neither completely mimicked the effects of EB. Conclusions., We conclude that estrogenic metabolites of testosterone control sexually dimorphic cell survival in the BNSTp and that activation of both ER, and ER, may be required for complete masculinization of this brain region. Hisasue S, Seney ML, Immerman E, and Forger NG. Control of cell number in the bed nucleus of the stria terminalis of mice: Role of testosterone metabolites and estrogen receptor subtypes. J Sex Med 2010;7:1401,1409. [source] The etiology of otosclerosis: A combination of genes and environment,THE LARYNGOSCOPE, Issue 6 2010Isabelle Schrauwen MSc Abstract Otosclerosis is a common form of hearing loss characterized by abnormal bone remodeling in the otic capsule. It is a complex genetic disease, caused by a combination of genetic and environmental factors. During the past decade, several attempts have been made to identify factors for otosclerosis. This review provides an overview of the current understanding of the etiology of otosclerosis and describes the genetic and environmental factors that have been implicated in the disease. Environmental factors include fluoride and viral factors, particularly measles. Genetic association studies for otosclerosis have reported several associations of genetic variants that influence the risk of disease, mainly involving bone remodeling pathways, although their individual risk contributions are small. Rare monogenic forms of otosclerosis also exist, which are caused by a mutation in a single gene leading to a clear familial segregation of the disease. Linkage analysis of large otosclerosis families has led to the identification of seven loci, and recently evidence was found that T cell receptor beta is a gene responsible for familial otosclerosis, suggesting an underlying immunological pathway. However, this might also represent an autoimmune process, a hypothesis that is supported by other data as well. In conclusion, a variety of pathways have been identified to be involved in the development of otosclerosis, showing that distinct mechanisms involving both genetic and environmental risk factors can influence and contribute to a similar disease outcome. [source] Quantitative RT-PCR analysis of estrogen receptor gene expression in laser microdissected prostate cancer tissueTHE PROSTATE, Issue 8 2009Thomas J. Walton Abstract BACKGROUND Real-time quantitative RT-PCR analysis of laser microdissected tissue is considered the most accurate technique for determining tissue gene expression. The discovery of estrogen receptor beta (ER,) has focussed renewed interest on the role of estrogen receptors in prostate cancer, yet few studies have utilized the technique to analyze estrogen receptor gene expression in prostate cancer. METHODS Fresh tissue was obtained from 11 radical prostatectomy specimens and from 6 patients with benign prostate hyperplasia. Pure populations of benign and malignant prostate epithelium were laser microdissected, followed by RNA isolation and electrophoresis. Quantitative RT-PCR was performed using primers for androgen receptor (AR), estrogen receptor beta (ER,), estrogen receptor alpha (ER,), progesterone receptor (PGR) and prostate specific antigen (PSA), with normalization to two housekeeping genes. Differences in gene expression were analyzed using the Mann,Whitney U -test. Correlation coefficients were analyzed using Spearman's test. RESULTS Significant positive correlations were seen when AR and AR-dependent PSA, and ER, and ER,-dependent PGR were compared, indicating a representative population of RNA transcripts. ER, gene expression was significantly over-expressed in the cancer group compared with benign controls (P,<,0.01). In contrast, PGR expression was significantly down-regulated in the cancer group (P,<,0.05). There were no significant differences in AR, ER, or PSA expression between the groups. This study represents the first to show an upregulation of ER, gene expression in laser microdissected prostate cancer specimens. CONCLUSIONS In concert with recent studies the findings suggest differential production of ER, splice variants, which may play important roles in the genesis of prostate cancer. Prostate 69: 810,819, 2009. © 2009 Wiley-Liss, Inc. [source] Expression of the porcine adrenergic receptor beta 2 gene in longissimus dorsi muscle is affected by cis -regulatory DNA variationANIMAL GENETICS, Issue 1 2009E. Muráni Summary The beta-2 adrenergic receptor (AR) mediates metabolic actions of catecholamines, including glycogenolysis, lipolysis and proteolysis, in muscle and adipose tissue. Factors influencing the density of beta-2 ARs thus might affect carcass composition and meat quality. One such factor might represent cis -regulatory DNA variation affecting mRNA expression of the adrenergic receptor beta 2 (ADRB2) gene in relevant tissues. To identify potential cis -regulatory DNA variation of porcine ADRB2, we comparatively sequenced part of the 5, flanking region and identified 10 single nucleotide polymorphisms (SNPs). The SNP at position g.673C>T (AF000134) resides in an evolutionarily conserved region (ECR) in an in silico predicted androgen response element. Quantification of total transcript levels and allelic expression imbalance (AEI) revealed significant variability in mRNA expression of ADRB2 in longissimus dorsi muscle of slaughter pigs, partly attributable to cis -regulatory DNA variation. However, the g.673C>T SNP has, in the given temporo-spatial context, no significant effect but is apparently in linkage disequilibrium with the causal cis -regulatory DNA variant. We used the g.673C>T SNP as a marker to study the association of ADRB2 variation with carcass and meat quality in four commercial lines. We found association with the pH of loin at 45 min and 24 h postmortem (p.m.) and with the pH of ham at 24 h p.m. Supporting evidence for ADRB2 as a candidate gene for pork quality is provided by our assignment of the gene to the telomeric end of the q arm of porcine chromosome 2, where several quantitative trait loci for meat quality were reported. [source] Expression of LIF and LIF receptor beta in Alzheimer's and Parkinson's diseasesACTA NEUROLOGICA SCANDINAVICA, Issue 1 2010M. Soilu-Hänninen Background,,, Signaling through the leukemia inhibitory factor (LIF) receptor (LIFR) is crucial for nervous system development. There are few studies concerning the expression of LIF and LIFR in normal and degenerating adult human brain. Objectives,,, To study the expression of LIF and LIFR in Alzheimer's disease (AD), Parkinson's disease (PD), and control brains. Patients and methods,,, LIF and LIFR mRNA copy numbers were determined by quantitative real-time RT-PCR from four brain regions of 34 patients with AD, 40 patients with PD, and 40 controls. Immunohistochemistry was performed in seven PD and in four AD patients and in seven normal controls. Results,,, In general, the LIF copy numbers were 1 log higher than the LIFR copy numbers. In the AD brains, LIF expression was higher than in the controls in the hippocampus and in the temporal cortex, and in the PD brains in the hippocampus and in the anterior cingulated cortex. Expressions of LIF and LIFR in different brain regions were opposite except for the AD hippocampus and PD anterior cingulated cortex, where the expression patterns were parallel. Conclusions,,, Co-operative expression of LIF and LIFR in AD hippocampus and PD anterior cingulated cortex may indicate a role for LIF in neuronal damage or repair in these sites. [source] Hypermethylation of FHIT as a prognostic marker in nonsmall cell lung carcinomaCANCER, Issue 7 2004Riichiroh Maruyama M.D. Abstract BACKGROUND Methylation of CpG islands in the promoter and upstream coding regions has been identified as a mechanism for transcriptional inactivation of tumor suppressor genes. The purpose of the current study was to determine the correlation between the aberrant promoter methylation of multiple genes and survival in patients with nonsmall cell lung carcinoma (NSCLC). METHODS The methylation status of nine genes was determined in 124 surgically resected NSCLC cases using methylation-specific polymerase chain reaction. RESULTS The methylation frequencies of the genes tested in NSCLC specimens were 52% for E-cadherin (CDH1), 41% for RAS association domain family protein (RASSF1A), 38% for fragile histidine triad (FHIT) and adenomatous polyposis coli (APC), 27% for retinoic acid receptor beta (RAR,) and H-cadherin (CDH13), 20% for p16INK4A, 0.8% for O6 -methylguanine-DNA-methyltransferase (MGMT), and 0% for glutathione S-transferase P1 (GSTP1). The survival of the patients with FHIT methylation-positive tumors was found to be significantly shorter than that for those patients with methylation-negative tumors (P = 0.03), even in those patients with International Union Against Cancer TNM Stage I or Stage II disease (P = 0.007). In contrast, there were no significant survival differences noted between the methylation-positive and methylation-negative tumors for the other genes tested. In addition, based on multivariate analyses, FHIT methylation-positive status was found to be independently associated with poor survival (P = 0.046) and disease stage (P < 0.0001). CONCLUSIONS The results of the current study suggest that methylation of FHIT is a useful biomarker of biologically aggressive disease in patients with NSCLC. Cancer 2004;100:1472,7. © 2004 American Cancer Society. [source] | |||||||||||||