Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Type 2 cytokines, such as interleukin-4 (IL-4) and IL-13, are associated with immunoglobulin E (IgE) production. This association has also been observed in CD8+ T cells from patients infected with leprosy and human immunodeficiency virus (HIV). Using intracellular cytokine staining and flow cytometry, the cytokine profile [IL-2, IL-4, IL-10, IL-13, and interferon (IFN)-gamma] of both CD4+ and CD8+ memory/effector T cells circulating in atopic dermatitis (AD) patients was investigated at the single cell level. The levels of type 2 cytokines in CD4+ T cells or CD8+ T cells in AD patients with high levels of serum IgE (AD-H), low levels of serum IgE (AD-L), and healthy controls were compared. Increased production of IL-4 and IL-13 in both CD4+ CD45RO+ T cells and CD8+ CD45RO+ T cells after 4 h in vitro stimulation with phorbol 12-myristate 13-acetate and ionomycin, was more prominent in AD-H patients than in AD-L patients or healthy controls, whereas IFN-gamma-producing CD4+ CD45RO+ T cells and CD8+ CD45RO+ T cells were relatively diminished in AD-H patients. CD4+ T cells and CD8 + T cells from AD-H patients, cultured for 48 h with phorbol 12-myristate 13-acetate and ionomycin, released larger amounts of IL-4 and IL-13 but smaller amounts of IFN-gamma than both types of cells from AD-L patients or healthy controls. In addition, when stimulated with immobilized anti-CD3 monoclonal antibody (MoAb) and anti-CD28 MoAb, CD4+ CD45RO+ T cells and CD8+ CD45RO+ T cells from AD-H patients contained more IL-4-producing cells but fewer IFN-gamma-producing cells compared with healthy controls. Finally, spontaneous mRNA expression of IL-4 in blood CD8+ CD45RO+ T cells isolated from AD-H patients was increased, as determined by reverse transcriptase-polymerase chain reaction. Therefore, in AD patients with high IgE levels, type 2 cytokine (IL-4 and IL-13) expression is associated with IgE production, in both CD4+ CD45RO+ T cell and CD8+ CD45RO+ T cell subsets.
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PMID:Increased type 2 cytokine expression by both CD4+ CD45RO+ T cells and CD8+ CD45RO+ T cells in blood circulation is associated with high serum IgE but not with atopic dermatitis. 985 20

Objectives: We investigated modulation of cell growth and prostate-specific antigen (PSA) gene expression in prostatic cancer cells by the luteinizing hormone-releasing hormone analog (LH-RHa), leuprorelin acetate, alone or combined with other agents. Methods: The effect of the analog on proliferation of both androgen-sensitive and -insensitive prostate cancer cells, maintained in different culture conditions, was evaluated by cell counts at various intervals of time. Basal expression of PSA gene and its variations were determined by a reverse transcriptase-polymerase chain reaction assay. Results: LH-RHa is ineffective in regulating cell growth, when used alone in both hormone-sensitive and -insensitive cell lines. Nevertheless, it counteracts the stimulatory action of androgens on proliferation of LNCaP cells, which respond to low concentrations of dihydrotestosterone. Moreover, LH-RHa has an inhibitory effect on the mitogenic action of epidermal growth factor (EGF) in androgen-unresponsive PC-3 cells. The analog reduces PSA gene expression in both hormone-sensitive and -insensitive cells. Interestingly, it counteracts the gene expression induced by androgens in LNCaP cells and by EGF in PC-3 cells. Conclusions: These data show that LH-RHa may behave like a negative growth factor, which directly regulates cell growth and PSA gene expression. Moreover, our findings support the idea that growth factors may interfere with the androgen signalling pathway.
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PMID:Effect of Leuprorelin Acetate on Cell Growth and Prostate-Specific Antigen Gene Expression in Human Prostatic Cancer Cells. 985 46

We describe the frist reported case in Switzerland of HIV-associated nephropathy (HIVAN). HIVAN shows a typical combination of clinical findings: black race, proteinuria, large hyper-echogenic kidneys, normal blood pressure, positive HIV serology and no autoantibodies. The histologic findings are typical: focal segmental glomerulosclerosis of the collapsing variant, often with marked interstitial nephritis. The disease normally appears before AIDS symptoms develop and follows a very aggressive course to end-stage renal disease. Therapy consists of a combination of nucleoside reverse transcriptase and proteinase inhibitors, ACE inhibitors, and possibly steroids. In end-stage renal disease patients can be managed by haemodialysis, continuous ambulatory peritoneal dialysis (CAPD) or kidney transplantation.
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PMID:[A patient with rapidly progressing renal failure, florid syphilis and positive HIV serology]. 986 91

The 1,839-base pair complementary DNA (cDNA) for rat lung carboxylesterase was cloned by reverse transcriptase polymerase chain reaction from total rat lung RNA using specific primers derived from the 5' and 3' untranslated regions of rat hepatic cholesteryl ester hydrolase (CEH). The unique cDNA was sequenced and found to be similar to hepatic CEH, pI 6.1 esterase, and hydrolase A. In Northern blot analysis, the cDNA hybridized with a single band from lung messenger RNA (mRNA). The 1.7-kb coding sequence, predicting a 62-kD protein, was transfected into COS-7 cells and Chinese hamster ovary (CHO) cells. Expression in COS-7 and CHO cells was accompanied by 4- and 3.2-fold increases in carboxylesterase activity (hydrolysis of p-nitrophenyl acetate), respectively. Unlike the hepatic CEH, the expressed lung carboxylesterase described here did not hydrolyze cholesterol esters. In situ hybridization experiments localized the lung carboxylesterase mRNA to the airway epithelium. The organophosphorus compound phosphoric acid diethyl 4-nitrophenyl ester, paraoxon, completely inhibited this lung carboxylesterase, placing it in the family of B esterases by this criterion.
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PMID:Molecular cloning and expression of rat lung carboxylesterase and its potential role in the detoxification of organophosphorus compounds. 1034 Sep 39

Parathyroid hormone (PTH)-related protein (PTHrP) acts as a local regulator of osteoblast function via mechanisms that involve PTH/PTHrP receptors linked to protein kinase A (PKA) and C (PKC). However, the regulation of PTHrP production and mRNA expression in human osteoblasts is poorly understood. Here we have characterized alternative PTHrP mRNA 3' splicing variants, encoding PTHrP isoforms of 139, 141, and 173 amino acids, and studied the regulation of PTHrP and its mRNAs by activated PKA and PKC in two human osteoblast-like cell lines (KPDXM and TPXM). Using exon-specific Northern analysis and reverse transcriptase-coupled polymerase chain reaction, we identified mRNAs encoding PTHrP(1-139) and PTHrP(1-141) in both cell lines. PTHrP(1-139) mRNAs predominated in TPXM cells and PTHrP(1-173) mRNAs were only detected in TPXM cells. Activation of PKA or PKC resulted in different effects on PTHrP and its mRNAs in the two cell lines. In TPXM cells, peptide-specific immunoassays detected high basal levels of PTHrP, increasing by 2-fold in cell extracts and 4-fold in culture media at 7 h and 24 h after exposure to forskolin, respectively, paralleling changes in PTHrP mRNA expression. Phorbol ester 12-O-tetradecanoyl-phorbol 13-acetate (TPA), a PKC activator, had no effect. In KPDXM cells, PTHrP was not detected in culture media under basal experimental conditions, and barely detectable amounts were present in cell extracts of TPA-treated cells, although the mRNA levels increased substantially in response to TPA. In the responsive cell lines, the effects on mRNA levels were dose dependent, and increased by 6.9- to 10.5-fold and 2.0- to 4.1-fold at 4 h in TPXM and KPDXM cells after exposure to 10 microM forskolin and 150 nM TPA, respectively. PTHrP mRNA levels then declined but were sustained above controls also at 12 h in both cell lines, albeit at considerably higher levels in TPXM cells. The different responsiveness to agents activating PKA- and PKC-dependent pathways may depend on the cellular state of differentiation, or alternatively, cancer cell line-specific defects. Our data demonstrating distinct differences in mRNA species and the amounts of PTHrP produced by the two cell lines as compared with roughly equivalent overall mRNA levels may suggest that post-transcriptional mechanisms play an important role in limiting the production of intracellular and secreted PTHrPs in human osteoblastic cells.
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PMID:Two human osteoblast-like osteosarcoma cell lines show distinct expression and differential regulation of parathyroid hormone-related protein. 1035 98

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a naturally occurring compound shown to inhibit carcinogen-induced preneoplastic lesion formation in mouse mammary organ culture and tumorigenesis in the two-stage mouse skin model. Cancer chemopreventive potential was also suggested in various assays reflective of the three major stages of carcinogenesis. Anti-initiation activity was indicated by its antioxidant and antimutagenic effects, inhibition of the hydroperoxidase function of cyclooxygenase (COX), and induction of phase II drug-metabolizing enzymes. Antipromotion activity was indicated by antiinflammatory effects, inhibition of production of arachidonic acid metabolites catalyzed by either COX-1 or COX-2, and chemical carcinogen-induced neoplastic transformation of mouse embryo fibroblasts. Antiprogression activity was demonstrated by its ability to induce human promyelocytic leukemia (HL-60) cell differentiation. Moreover, pretreatment of mouse skin with resveratrol significantly counteracted 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative stress, as evidenced by numerous biochemical responses. Resveratrol reduced the generation of hydrogen peroxide, and normalized levels of myeloperoxidase and oxidized-glutathione reductase activities. It also restored glutathione levels and superoxide dismutase activity. As judged by the reverse transcriptase-polymerase chain reaction, resveratrol selectively inhibited TPA-induced expression of c-fos and transforming growth factor-beta 1 (TGF-beta 1), but did not affect other TPA-induced gene products including COX-1, COX-2, c-myc, c-jun, and tumor necrosis factor-alpha. These data indicate that resveratrol may interfere with reactive oxidant pathways and/or modulate the expression of c-fos and TGF-beta 1 to inhibit tumorigenesis in mouse skin. As reported herein, in addition to the activities described above, resveratrol inhibited the de novo formation of inducible nitric oxide synthase (iNOS) in mouse macrophages stimulated with lipopolysaccharide. This finding suggests an additional mechanism by which resveratrol may function as a cancer chemopreventive agent.
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PMID:Cancer chemopreventive activity of resveratrol. 1037 Aug 67

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a natural product shown to inhibit carcinogen-induced pre-neoplastic lesions in mouse mammary organ culture and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted mouse skin tumors. Application of TPA to mouse skin induces oxidative stress, as evidenced by numerous biochemical responses, including significant generation of H2O2 and enhanced levels of myeloperoxidase and oxidized glutathione reductase activities and decreases in glutathione levels and superoxide dismutase activity. TPA treatment also elevates the expression of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), c-myc, c-fos, c-jun, transforming growth factor-beta1 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha). As currently reported, pre-treatment of mouse skin with resveratrol negated several of these TPA-induced effects in a dose-dependent manner. H2O2 and glutathione levels were restored to control levels, as were myeloperoxidase, oxidized glutathione reductase and superoxide dismutase activities. As judged by reverse transcriptase-polymerase chain reaction (RT-PCR), TPA-induced increases in the expression of c-fos and TGF-beta1 were selectively inhibited. These data suggest that resveratrol inhibits tumorigenesis in mouse skin through interference with pathways of reactive oxidants and possibly by modulating the expression of c-fos and TGF-beta1.
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PMID:Effects of resveratrol on 12-O-tetradecanoylphorbol-13-acetate-induced oxidative events and gene expression in mouse skin. 1038 Nov 33

Genes induced or suppressed by oxidized low-density lipoproteins (oxLDL) in human monocytic THP-1 cells were searched using differential display reverse transcriptase polymerase chain reactions (DDRT-PCR). Among the many differentially expressed cDNA fragments, one was dramatically stimulated by the oxLDL in a steady state level, which was later found to contain sequences corresponding to ferritin light chain (L-ferritin) in a sequence homology search. The stimulatory effect of the oxLDL on the level of L-ferritin mRNA in the THP-1 cells was both time- and dose-dependent. When the cells were allowed to differentiate in the presence of phorbol 12-myristate 13-acetate (PMA), the differentiated cells were generally less responsive to the oxLDL than the undifferentiated ones. An increase of L-ferritin mRNA was observed when the cells were treated with the lipid components in the oxLDL such as 9-HODE, 13-HODE, and 25-hydroxycholesterol. In addition, a stimulation of the L-ferritin gene expression was also observed when the cells were treated with an endogenous peroxisome proliferator-activated receptor gamma (PPARgamma) ligand, 15d-PGJ2, in a time- and dose-dependent manner. These results suggest that oxLDL or its constituents are related to the stimulation of L-ferritin expression via PPARgamma.
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PMID:Regulation of ferritin light chain gene expression by oxidized low-density lipoproteins in human monocytic THP-1 cells. 1055 12

The functions of Thy-1, a 35-kDa cell-surface glycoprotein, and its natural ligand are still unknown. Anchoring to the membrane via linkage to phosphatidyl-inositol (PI) raises the possibility of cleavage off the membrane by PI-specific phospholipases. Soluble Thy-1 (sThy-1) could interfere with the binding of the unknown natural ligand followed by regulation of different cell functions. In this study we established an enzyme-linked immunosorbent assay (ELISA) to measure and quantify sThy-1 in serum and wound fluid. Recombinant human Thy-1 (rhThy-1) was expressed in Drosophila S2 cells, purified from culture supernatant and used as standard for quantitation of sThy- by the ELISA technique. There were no differences in sThy-1 levels in serum of healthy donors and patients with systemic sclerosis, leg ulcers, or rheumatoid arthritis, respectively, detected by ELISA. In contrast, at the local site of inflammation, in wound fluid of venous leg ulcers and in synovial fluid from joint puncture, we found strongly elevated levels of sThy-1 compared with sThy-1 in the serum of the same patient. Thy-1 is expressed in humans on brain cells, fibroblasts, a subpopulation of CD34+ blood stem cells, and possibly activated human dermal microvascular endothelial cells. In this study, we never found Thy-1 mRNA or protein expression in resting endothelial cells as shown by reverse transcriptase polymerase chain reaction (RT-PCR) and flow-cytometry. Thy- expression could be induced on endothelial cells by phorbol myristate acetate and to a lesser extent by tumor necrosis factor-alpha (TNF-alpha). In situ, monoclonal antibodies to Thy-1 did not stain endothelial cells in normal skin, whereas endothelial cells in the synovial membrane of rheumatoid arthritis patients and endothelial cells surrounding melanoma express Thy-1. In summary, our data indicate that Thy-1 is present in soluble form in serum. Furthermore, Thy-1 seems to be a marker for endothelial cell activation. Therefore, activated endothelial cells as well as fibroblasts might be a possible source of sThy-1.
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PMID:Detection of human soluble Thy-1 in serum by ELISA. Fibroblasts and activated endothelial cells are a possible source of soluble Thy-1 in serum. 1057 Nov 19

Angiotensin I-converting enzyme (ACE, CD143, Kininase II, EC 3.4.15.1) occurs in two isoforms; whereas the somatic isoform (sACE) appears in certain endothelial cells and some other cell types, the testicular isoform (tACE) was found in humans and various mammals only during spermiogenesis. An expression of ACE was reported formerly in some human seminomas, but its isoform type, cellular distribution, and pathogenetic meaning are not known. Therefore we analyzed normal human testes, 22 different testicular tumors, and 23 fetal and postnatal tissues of different stages of testicular development. By reverse transcriptase-polymerase chain reaction, ACE mRNA isoforms were assessed in homogenized tissue sections and in germ cells selectively isolated by laser-assisted cell picking. Immunohistochemistry was performed on consecutive sections using monoclonal antibodies specific to the human somatic isoform or both, sACE and tACE. In adult men, tACE was detectable in spermatids and spermatozoa, but normal spermatogonia and spermatocytes were not found to express ACE in any isoform. By contrast, both mRNA and protein of sACE were detectable in the cells of intratubular germ cell neoplasm, seminomas, and other testicular tumor types. Because sACE was also found in fetal germ cells, our findings point to profound differences in the regulation of ACE expression in fetal, mature adult, and neoplastic germ cells. They are in agreement with the concept that neoplastic germ cells phenotypically reflect an embryonic stage of cellular differentiation. Laser-assisted cell picking proved to be a reliable method to investigate differently regulated mRNA of cells which reside in close neighborhood within complex tissues.
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PMID:Angiotensin-converting enzyme (CD143) in neoplastic germ cells. 1057 13


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