Expression Regulation (expression + regulation)

Distribution by Scientific Domains

Selected Abstracts

Molecular cloning and expression regulation of PRG-3, a new member of the plasticity-related gene family

Nicolai E. Savaskan
Abstract Phospholipid-mediated signalling on neurons provokes diverse responses such as neurogenesis, pattern formation and neurite remodelling. We have recently uncovered a novel set of molecules in the mammalian brain, named plasticity-related genes (PRGs), which mediate lipid phosphate phosphatase activity and provide evidence for their involvement in mechanisms of neuronal plasticity. Here, we report on a new member of the vertebrate-specific PRG family, which we have named plasticity-related gene-3 (PRG-3). PRG-3 is heavily expressed in the brain and shows a specific expression pattern during brain development where PRG-3 expression is found predominantly in neuronal cell layers and is already expressed at embryonic day 16. In the mature brain, strongest PRG-3 expression occurs in the hippocampus and cerebellum. Overexcitation of neurons induced by kainic acid leads to a transient down-regulation of PRG-3. Furthermore, PRG-3 is expressed on neurite extensions and promotes neurite growth and a spreading-like cell body in neuronal cells and COS-7 cells. In contrast to previously described members of the PRG family, PRG-3 does not perform its function through enzymatic phospholipid degradation. In summary, our findings feature a new member of the PRG family which shows dynamic expression regulation during brain development and neuronal excitation. [source]

Glutamate activation of Oct-2 in cultured chick Bergmann glia cells: Involvement of NF,B

J. Alfredo Méndez
Abstract Glutamate, the major excitatory neurotransmitter in the central nervous system, is critically involved in gene expression regulation at the transcriptional and translational levels. Its activity through ionotropic as well as metabotropic receptors modifies the protein repertoire in neurons and glial cells. In avian cerebellar Bergmann glia cells, glutamate receptors trigger a diverse array of signaling cascades that include activity-dependent transcription factors such as the activator protein-1, the cAMP response-element binding protein, and Oct-2. We analyze the upstream regulatory elements involved in Oct-2 activation. Our results demonstrate that Ca2+ influx, protein kinase C, phosphatidylinositol-3 kinase, Src, and nuclear factor (NF),B are involved in this signaling pathway. Our findings link ,-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor activation to a negative phase of chkbp gene regulation, controlled by NF,B. © 2005 Wiley-Liss, Inc. [source]

Expression of osteopontin in chronic rhinosinusitis with and without nasal polyps

ALLERGY, Issue 1 2009
X. Lu
Background:, Osteopontin (OPN) is a multifunctional 34-kDa extracellular matrix protein that can influence the inflammatory process. However, the presence of OPN in human sinonasal mucosa and its roles in the inflammatory process of chronic rhinosinusitis (CRS) are not clear. This study investigated the expression of OPN in human sinonasal mucosa, its cytokine-driven expression regulation, and its effect on cytokine production in sinonasal mucosa. Methods:, Surgical samples were investigated by means of quantitative reverse transcriptase polymerase chain reaction for evaluation of OPN messenger RNA (mRNA) expression, and the presence and location of OPN protein expression were analyzed using immunohistochemistry. Furthermore, nasal explant culture was used to investigate the mutual regulatory interactions between interferon (IFN)-,, interleukin (IL)-4, IL-5, IL-13, IL-1,, and tumor necrosis factor (TNF)-, and OPN in sinonasal mucosa. Results:, Osteopontin expression was significantly upregulated in CRS tissues compared with control tissues. There was a further significant increase of OPN expression in patients with nasal polyps (NPs) and asthma. Immunohistochemistry revealed positive staining of OPN in epithelial cells, submucosal glands, infiltrating cells, and extracellular matrix. Osteopontin mRNA was induced by IFN-,, IL-1,, and TNF-,, but inhibited by IL-4 and IL-13. On the contrary, OPN induced IFN-,, IL-4, IL-5, IL-13, IL-1,, and TNF-, production in sinonasal mucosa. Conclusions:, The expression of OPN is upregulated in CRS. The mutual regulatory interactions between OPN and inflammatory cytokines suggest that OPN may play an important role in the pathogenesis of CRS. [source]

Wnt signaling stabilizes the DIXDC1 protein through decreased ubiquitin-dependent degradation

CANCER SCIENCE, Issue 3 2010
Lei Wang
(Cancer Sci 2010; 101: 700,706) Wnt signaling plays key roles in development, cell growth, differentiation, polarity formation, neural development, and carcinogenesis. DIX Domain Containing 1 (DIXDC1), a novel component of the Wnt pathway, was recently cloned. DIXDC1 is the human homolog of Ccd1, a positive regulator of the Wnt signaling pathway during zebrafish neural patterning. Little has been known about DIXDC1 gene expression regulation. In the present study, we showed that the DIXDC1 protein was induced upon Wnt-3a stimulation, whereas the DIXDC1 mRNA level was not significantly increased after Wnt-3a treatment. Positive DIXDC1 staining was detected in colon cancer cells and was colocalized with ,-catenin staining. However, the DIXDC1 mRNA expression decreased in human colon cancer cells compared to the matched normal colon epithelial cells. Our further investigation showed that the DIXDC1 protein was degraded through the proteasome pathway, and the activation of canonical Wnt signaling decreased the ubiquitin-dependent degradation of both the ectopic and endogenous DIXDC1 protein. In order to explore the possible mechanism of the ubiquitination of DIXDC1, we found that the phosphorylation of DIXDC1 was inhibited by Wnt-3a. Collectively, these results indicate that canonical Wnt/,-catenin pathway activation might upregulate DIXDC1 through a post-translational mechanism by inhibiting the ubiquitin-mediated degradation of the DIXDC1 protein. [source]

Chronic rhinosinusitis with and without nasal polyps is associated with decreased expression of glucocorticoid-induced leucine zipper

X-H. Zhang
Summary Background Chronic rhinosinusitis without nasal polyps (CRSsNP) and with nasal polyps (CRSwNP) is characterized by persistent inflammation of sinonasal mucosa. Glucocorticoid-induced leucine zipper (GILZ) is a recently described anti-inflammatory mediator. Objective Here we analysed the expression of GILZ in CRSsNP and CRSwNP, its association with response to surgery, and its cytokine-driven expression regulation in the upper airways. Methods The messenger RNA (mRNA) and protein expression of GILZ in 33 CRSsNP, 32 CRSwNP, and 11 control samples was assessed by means of a quantitative RT-PCR and immunohistochemistry, respectively. Nasal explant culture was used to investigate the effect of IFN-,, IL-4, IL-13, IL-1,, and TNF-, on GILZ mRNA expression in normal sinonasal mucosa. Results The GILZ mRNA and protein expression was significantly suppressed in both CRSsNP and CRSwNP patients compared with controls. No significant difference in GILZ expression was found between CRSsNP and CRSwNP patients. Comparing patients responsive and patients recalcitrant to surgery, a significant further decrease of GILZ expression was found in recalcitrant patients both in the CRSsNP and in the CRSwNP group. IL-1,, TNF-,, IL-4, and IL-13 reduced, whereas IFN-, enhanced GILZ mRNA levels in the sinonasal mucosa. Conclusion Down-regulated expression of GILZ may contribute to the pathogenesis of CRSsNP and CRSwNP and associate with response to surgery. GILZ expression in the upper airways can be regulated differentially by different cytokines. [source]