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 aim of the present study was to determine whether mRNA for the three endothelin peptides (endothelin-1, endothelin-2, and endothelin-3) and the two known receptor subtypes (ETA and ETB) was present in human endometrium at different stages of the menstrual cycle (menstrual, early and mid-proliferative, and early, mid-, and late secretory). Endometrium was obtained from women undergoing surgery for benign disease, and total RNA was extracted using a guanidinium isothiocyanate method. mRNA for endothelin peptide and receptor was detected using the reverse transcriptase-polymerase chain reaction with nested oligonucleotide primers. mRNA for endothelin-1, endothelin-2, and endothelin-3 was demonstrated throughout the menstrual cycle, and three splice variants of mRNA encoding endothelin-3 were found in all samples. The ratio of ETA to ETB receptor mRNA was found to change throughout the menstrual cycle. In the proliferative phase, amplified cDNA product was almost exclusively confined to the ETA receptor, whereas an increase in the amplified product of the ETB receptor cDNA was seen in the secretory and menstrual phases. These studies show that mRNA for endothelin-1, endothelin-2, and endothelin-3 is present in human endometrium at all stages of the menstrual cycle and suggest that different physiological actions of the endothelin peptides may be mediated through changes in the ratio of the ETA and ETB receptor subtypes.
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PMID:Presence of messenger ribonucleic acid for endothelin-1, endothelin-2, and endothelin-3 in human endometrium and a change in the ratio of ETA and ETB receptor subtype across the menstrual cycle. 146 62

Growth factors play a role in the cyclical growth and vascularization of normal endometrium. Abnormal endometrial proliferation and neovascularization may result in endometriosis. This study determines the presence and localization of acidic and basic fibroblast growth factors (aFGF and bFGF respectively) in endometrium of normal women, and in normal and ectopic endometrium of women with endometriosis. Endometrium was obtained at curettage or hysterectomy for benign disease, or laparoscopy for endometriosis. aFGF- and bFGF-immunoreactivity was detected at different phases of the menstrual cycle by immunohistochemistry using primary polyclonal rabbit antibodies. Expression of mRNA for aFGF and bFGF was determined in normal endometrium by nested reverse transcriptase polymerase chain reaction (RT-PCR). aFGF- and bFGF-immunoreactivity were both detected in endometrium from normal women, and in normal and ectopic endometrium of women with endometriosis. The pattern of staining with the two different FGFs was the same: immunoreactivity was predominantly confined to glandular epithelial cells and did not change throughout the menstrual cycle. Little or only light staining was seen in stromal cells and myometrium, and the pattern of staining did not differ between endometriotic and normal tissue. The presence of mRNA for aFGF and bFGF was demonstrated in normal endometrium. The detection of aFGF and bFGF mRNA in normal endometrium and aFGF- and bFGF-immunoreactivity in normal and endometriotic tissues suggests that these peptides may play a role in the proliferation and angiogenesis of normal and ectopic human endometrium.
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PMID:Immunohistochemical localization of acidic and basic fibroblast growth factors in normal human endometrium and endometriosis and the detection of their mRNA by polymerase chain reaction. 768 35

In previous studies we found expression of the protein colligin 2 (heat shock protein 47 (HSP47), SERPINH1) in glioma neovasculature while not in normal brain tissue. Generally, the regulation of heat shock gene expression in eukaryotes is mediated by heat shock factors (HSF). In mammals, three heat shock transcription factors, HSF-1, -2, and -4, have been isolated. Here we investigated the relation between the expression of colligin 2 and these heat shock factors at the mRNA level using real-time reverse transcriptase PCR (qRT-PCR) in different grades of astrocytic tumorigenesis, viz., low-grade glioma and glioblastoma. Endometrium samples, representing physiological angiogenesis, were included as controls. Since colligin 2 is a chaperon for collagens, the gene expression of collagen I (COL1A1) was also investigated. The blood vessel density of the samples was monitored by expression of the endothelial marker CD31 (PECAM1). Because NG2-immunopositive pericytic cells are involved in glioma neovascularization, the expression of NG2 (CSPG4) was also measured.We demonstrate overexpression of HSF2 in both stages of glial tumorigenesis (reaching significance only in low-grade glioma) and also minor elevated levels of HSF1 as compared to normal brain. There were no differences in expression of HSF4 between low-grade glioma and normal brain while HSF4 was downregulated in glioblastoma. In the endometrium samples, none of the HSFs were upregulated. In the low-grade gliomas SERPINH appeared to be slightly overexpressed with a parallel 4-fold upregulation of COL1A1, while in glioblastoma there was over 5-fold overexpression of SERPINH1 and more than 150-fold overexpression of COL1A1. In both the lowgrade gliomas and the glioblastomas overexpression of CSPG4 was found and overexpression of PECAM1 was only found in the latter. Our data suggest that the upregulated expression of colligin 2 in glioma is accompanied by upregulation of COL1A1, CSPG4, HSF2 and to a lesser extent, HSF1. Further studies will unravel the association of these factors with colligin 2 expression, possibly leading to keys for therapeutic intervention.
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PMID:Overexpression of Colligin 2 in Glioma Vasculature is Associated with Overexpression of Heat Shock Factor 2. 2107 23