Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was designed to explore the interaction of interleukin-13 (IL-13) with vascular endothelial cells (EC). In vitro exposure to IL-13 of human umbilical vein EC induced surface expression of vascular cell adhesion molecule-1 (VCAM-1). At optimal concentrations (10 to 50 ng/mL) and exposure times (24 hours), IL-13 was a twofold to threefold less effective inducer of VCAM-1 than IL-1, which was used as reference EC activator. When IL-13 was combined with IL-1, an almost additive induction of VCAM-1 was observed. Induction of VCAM-1 by IL-13 was selective in that E-selectin and intercellular adhesion molecule-1 (ICAM-1) were unaffected. IL-13 caused a modest reduction of IL-1 induction of E-selectin and ICAM-1. Surface expression of VCAM-1 on IL-13-treated cells was associated with mRNA induction (as assessed by Northern analysis and reverse transcriptase-polymerase chain reaction), with predominance of transcripts encoding the 7 Ig domain form of this molecule. In agreement with previous reports, IL-13 inhibited cytokine production in human monocytes. In contrast, IL-13 was a weak inducer and an amplifier (in concert with IL-1) of IL-6 expression in EC. Mesothelial cells, which share properties with EC and regulate the traffic and function of leukocytes in serosal cavities, were stimulated to express VCAM-1 and IL-6 by IL-13. Thus, IL-13 elicits a spectrum of responses in vascular endothelium remarkably similar to that of IL-4 and IL-10. Interaction of these cytokines with vascular endothelium may play an important role in the induction and expression of Th2-dependent responses.
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PMID:Regulation of endothelial and mesothelial cell function by interleukin-13: selective induction of vascular cell adhesion molecule-1 and amplification of interleukin-6 production. 752 94

The expression of the cytokine and IFN-related genes was studied in mouse embryo using RT-PCR method capable of detecting low levels of mRNA. Total RNA was prepared from the days 7 embryos by acid guanidinium thiocyanate-phenol-chloroform (AGPC) method. cDNA was synthesized by M-MLV reverse transcriptase, and amplified using the specific oligonucleotide primers for IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, TNF-alpha, IFN-alpha, IFN-beta, IFN-gamma, IFN-alpha/beta receptor (IFN-alpha/beta R), IFN-gamma receptor (IFN-gamma R), interferon reguratory factor (IRF)-1, IRF-2 and 2'-5' oligoadenylate synthetase (2-5AS) by PCR method. Although the expressions of IL-1 beta, IL-4, IL-5, IL-6, TNF-alpha and IFN-gamma mRNA were detected in all the embryos tested, the expressions of IL-2, IL-3, IFN-alpha and IFN-beta mRNA were not detected at all. On the other hand, the expressions of IFN-related genes such as IFN-alpha/beta R, IFN-gamma R, IRF-1, IRF-2 and 2-5AS mRNA, were also detected. These results suggest that these cytokine may play an important role in early embryonic development.
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PMID:[Expression of cytokines and interferon-related genes in the mouse embryo]. 754 Jan 2

Acute inflammation is characterized by increased production of acute phase proteins in the liver. The induction of the hepatocytic response is primarily mediated through soluble cytokines such as IL-1, IL-6, TNF-alpha, and transforming growth factor beta, which bind to specific cell surface receptors and regulate gene expression of acute-phase proteins. Hepatoma cell lines, such as HepG2, represent a model system for studying acute-phase protein synthesis. HepG2 is induced to produce a variety of acute-phase proteins, including alpha 1-antitrypsin, alpha 1-antichymotrypsin, fibrinogen, alpha 1-acid glycoprotein, and haptoglobin, upon stimulation with cytokines. Analysis of HepG2 by reverse transcriptase PCR indicated that this cell line synthesized mRNA specific for the human C5a receptor (CD88). Flow cytometric analysis of HepG2 cells indicated that these cells bound anti-CD88 Ab, thus confirming our RT-PCR data by demonstrating that these cells also express the C5a receptor. Because C5a has been shown to be a potent mediator of inflammation and HepG2 cells express CD88, we assessed the possibility that C5a was capable of stimulating acute-phase protein synthesis by HepG2 cells. The results indicate that binding of human C5a to CD88 on HepG2 cells resulted in an increased production of alpha 1-antitrypsin- and alpha 1-antichymotrypsin-specific mRNA as assayed by RT-PCR. Analysis of culture supernatants derived from C5a-stimulated HepG2 cells showed an increased production of alpha 1-antitrypsin as measured by solid-phase ELISA. alpha 1-antitrypsin production by HepG2 cells was a direct result of C5a stimulation as evidenced by the fact that anti-C5a receptor Ab inhibited the response. These results suggest that C5a may be an important mediator of APP production in the regulation of the inflammatory response.
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PMID:Expression of functional receptors for human C5a anaphylatoxin (CD88) on the human hepatocellular carcinoma cell line HepG2. Stimulation of acute-phase protein-specific mRNA and protein synthesis by human C5a anaphylatoxin. 754 17

By reverse transcriptase polymerase chain reaction on messenger RNA from human polymorphonuclear cells, we have isolated a sequence identical to the cDNA coding for intracellular interleukin 1 receptor antagonist (icIL-1ra), but containing an additional in-frame 63-bp sequence located three codons downstream of the translation start of icIL-1ra. This additional sequence is inserted between the first and second exon of the intracellular form, the latter of which is colinear with part of the first exon of the secreted form of IL-1ra. The additional sequence is coded by an extra exon located 2 kb downstream the first icIL-1ra-specific exon. The complementary DNA sequence of the alternatively spliced form of icIL-1ra shows that the predicted protein differs from classical icIL-1ra in the NH2 terminus by insertion of a leaderless sequence of 21 amino acids rich in glycine and glutamic acid residues. Transcripts coding for this new form of icIL-1ra were detected in activated fibroblasts, keratinocytes, and at low levels in myelomonocytic cells. The recombinant protein expressed in COS cells had an apparent molecular mass in sodium dodecyl sulfate polyacrylamide gel electrophoresis of 25 kD compared to 22 kD of classical icIL-1ra, and was mostly intracellular. The ability of this new form of icIL-1ra to inhibit IL-1 activity, in terms of induction of E-selectin and human immunodeficiency virus replication, was comparable to that of classical icIL-1ra. We propose to refer to this new form of icIL-1ra as icIL-1ra type II.
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PMID:Cloning and characterization of a new isoform of the interleukin 1 receptor antagonist. 762 20

Studies in murine models of osteoporosis have suggested the hypothesis that ovarian steroids may control osteoclastic bone remodeling by limiting the production of interleukin-6 (IL-6) from osteoblasts and bone marrow stromal cells. To investigate this hypothesis in a human model, we have examined 12 separate strains of normal human osteoblasts (HOB) and 11 separate strains of human bone marrow stromal cells (HBMSC) and determined whether ovarian steroids regulate the induction of IL-6 by interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha) or IL-1 + TNF. Treatment with IL-1, TNF or IL-1 + TNF resulted in the induction of IL-6 from both cell types with IL-1 + TNF inducing a synergistic induction of IL-6 in HOB (24- to 324-fold) and HBMSC (35-288 fold). Addition of 17 beta-estradiol or progesterone did not significantly alter IL-6 messenger RNA or protein levels in either HOB or HBMSC cultures stimulated with IL-1, TNF or IL-1 + TNF. Cultures incubated up to 96 h with the steroids did not affect IL-6 expression. Furthermore ovarian steroids did not affect IL-6 production in either HBMSC cultures representative of preosteoblasts or HOB cultures representative of highly differentiated osteoblasts. Specific chloramphenicol acetyl transferase assays and reverse transcriptase-polymerase chain reaction studies also demonstrated that the lack of an estrogen effect was not due to the failure of HOB to express functional estrogen receptors. Therefore, we conclude that the regulation of human osteoclastic bone remodeling by ovarian steroids does not occur through the direct regulation of IL-6 gene transcription or protein secretion in either early stages of osteoblast differentiation or the differentiated osteoblast.
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PMID:Production of interleukin-6 in human osteoblasts and human bone marrow stromal cells: evidence that induction by interleukin-1 and tumor necrosis factor-alpha is not regulated by ovarian steroids. 764 14

Human nasal mucosal samples exposed in vitro to substance P or allergenic Ag were tested for the mRNA of IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, TNF-alpha, and IFN-gamma using specific reverse transcriptase-polymerase chain reaction assays. After the administration of substance P, at dosages ranging from 10(-6) to 10(-9) M, an enhanced expression of the mRNA for IL-1 beta, -3, -5, -6, TNF-alpha, and IFN-gamma was observed in all mucosal samples of allergic subjects and in half of the nonallergic subjects. The expression of IL-2 and IL-4 was low. Mucosal samples of allergic subjects showed an increased expression of mRNA for cytokines after administration of specific Ag, whereas no enhancement was observed in samples from nonallergic subjects. Our data suggest that substance P may regulate allergic reactions via enhanced production of certain regulatory cytokines.
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PMID:Cytokine expression after the topical administration of substance P to human nasal mucosa. The role of substance P in nasal allergy. 769 47

The pro-inflammatory molecules, tumor necrosis factor alpha (TNF alpha), interleukin 1 (IL-1), interleukin 6 (IL-6), and prostaglandin E2 (PGE2), are postulated to have a role in human pregnancy and parturition. The ability of interleukin 4 (IL-4) to suppress the production of TNF alpha, IL-1, IL-6, and PGE2 by activated monocytes prompted us to investigate a possible regulatory role for IL-4 in human gestation. Immunohistochemical techniques were used to show that human amnion epithelium stained positively for IL-4. Tissue from both the first (n = 5) and third (n = 46) trimester expressed immunoreactive IL-4, which was detected by the use of four antihuman IL-4 monoclonal antibodies. Analysis of mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR) on RNA extracts of amnion epithelial cells indicated that they were the source of IL-4. One of the anti-IL-4 antibodies used stained IL-4 protein associated with the basement membrane of the amnion epithelium. The mechanism of this association was investigated. IL-4 was shown to be a heparin-binding cytokine, which would enable it to bind to components of the extracellular matrix. Thus, this study identified a previously undescribed cellular source of IL-4, implicating a role for IL-4 in human gestation. Additionally, glycosaminoglycan binding may regulate IL-4 activity in vivo.
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PMID:Interleukin 4 production by human amnion epithelial cells and regulation of its activity by glycosaminoglycan binding. 778 6

The aim of this study was to examine the expression of interleukin-1 receptor antagonist (IL-1ra) in human polymorphonuclear cells (PMN) treated with transforming growth factor-beta 1 (TGF beta 1). TGF beta 1 induced IL-1ra transcripts in human circulating PMN and the induction was not blocked by protein synthesis inhibitors. Actinomycin D blocked induction by TGF beta 1 of IL-1ra transcripts, suggesting the involvement of gene transcription. The half life of IL-1ra transcripts was prolonged by TGF beta 1. By reverse transcriptase-polymerase chain reaction, TGF beta 1 was found to augment the transcripts coding for both the intracellular (keratinocyte type) and the secreted form of IL-1ra. TGF beta 1 induced the production of IL-1ra in PMN. Induction of IL-1ra by TGF beta 1 in PMN may represent a further mechanism by which this molecule can counteract the potent pro-inflammatory properties of IL-1.
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PMID:Induction by transforming growth factor-beta 1 of the interleukin-1 receptor antagonist and of its intracellular form in human polymorphonuclear cells. 780 48

The expression of the cytokine genes in normal placenta was studied using RT-PCR method capable of detecting low levels of mRNA. Total RNA was prepared from placenta of specific pathogen-free BALB/c mice at the 16th day of gestation by acid guanidinium thiocyanate-phenol-chloroform (AGPC) method. cDNA was synthesized by M-MLV reverse transcriptase, and amplified using the specific oligonucleotide primers for IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, TNF-alpha, IFN-alpha, IFN-beta and IFN-gamma by PCR method. IL-1 beta, IL-6, TNF-alpha, IFN-alpha, IFN-beta and IFN-gamma mRNA were detected in all the placentas tested. On the other hand, the expressions of IL-2, IL-3, IL-4, and IL-5 mRNA were not detected at all. These results suggest that these cytokines may play a role in the evolution of pregnancy.
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PMID:[Expression of cytokine messenger RNA in murine placenta]. 783 98

Chemotactic cytokines, or chemokines, are likely mediators of inflammatory cell recruitment in renal allograft rejection. A recent addition to the C-X-C super gene family branch of chemokines is epithelial-derived neutrophil-activating factor-78 (ENA-78). ENA-78 is a 78-amino acid peptide with neutrophil-activating and chemotactic properties. This chemokine is unique in that it was originally isolated and cloned from an IL-1-stimulated human pulmonary epithelial cell line, A549. In this article, we investigated whether ENA-78 could be produced by human renal epithelial cells. We found that primary cultures of human renal cortical epithelial cells with tubular cell attributes could express significantly increased steady state levels of ENA-78 mRNA when stimulated with IL-1 beta (2.0 ng/ml). In addition, these cells also secreted significantly increased ENA-78 antigen compared with controls when stimulated with IL-1 beta (2.0 ng/ml). Other proinflammatory agonists, including TNF alpha, IFN gamma, and LPS failed to stimulate ENA-78 steady state mRNA or antigenic peptide production by renal cortical epithelial cells. In addition, biopsy tissue from acutely rejecting human renal allografts had higher copy number of ENA-78 mRNA compared with nonrejecting renal allograft controls using a quantitative reverse transcriptase polymerase chain reaction method with a mutant ENA-78 transcript. In the proinflammatory milieu of the rejecting renal allograft, IL-1 beta produced by host and donor mononuclear cells may drive ENA-78 production by allograft tubule cells, thus effecting leukocyte recruitment into the tubulointerstitial compartment.
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PMID:Epithelial-derived neutrophil-activating factor-78 production in human renal tubule epithelial cells and in renal allograft rejection. 783 12


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