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:3.1.27.1 (RNase)
16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When the ovaries of 23-day-old juvenile rats are transplanted to an ectopic site, they recover within 1 week the ability to control gonadotropin secretion via steroid negative feedback. Vascular corrosion casting followed by scanning electron microscopy revealed that the transplanted ovary becomes profusely revascularized within 48 h after transplantation. Vascular ingrowth was accompanied by a 40- to 60-fold increase in expression of the genes encoding two angiogenic factors, vascular endothelial growth factor (VEGF) and transforming growth factor-beta 1 (TGF beta 1), as assessed by RNA blot hybridization of the corresponding mRNAs. Although TGF beta 3 mRNA levels also increased, no changes in the levels of mRNAs encoding other putative angiogenic factors, such as TGF alpha, basic fibroblast growth factor, and TGF beta 2, were observed. Hybridization histochemistry demonstrated that in intact ovaries, VEGF mRNA is mainly expressed in granulosa cells of the cumulus oophorus and thecal cells of large antral follicles. Transplantation is followed by an increase in mRNA abundance and a dramatic shift in cellular localization, so that the mRNA becomes predominantly expressed in cells of the outer ovarian cortex. In intact ovaries, low levels of TGF beta 1 mRNA were detected in thecal-interstitial cells; after transplantation, its expression also became more predominant in the ovarian outer cortex, but this change was not as marked as in the case of VEGF. Because ovarian autotransplantation is followed by a rapid increase in serum gonadotropin levels, experiments were conducted to determine the importance of this rise in the activation of VEGF and TGF beta 1 gene expression. After transplantation, some animals were treated with the LHRH antagonist Nal-Glu LHRH (50 micrograms/rat, once a day for 2 days) to prevent the posttransplantation rise in serum gonadotropins. Quantitation of VEGF and TGF beta 1 mRNA by RNase protection assay 48 h later showed that suppression of gonadotropin secretion diminished the increase in both VEGF and TGF beta 1 gene expression. Concomitant treatment with PMSG (8 IU/rat, single injection), which mainly bypasses the suppression of endogenous FSH levels, restored the TGF beta 1 mRNA response, but had no effect on VEGF mRNA. The results suggest that the increase in gonadotropin secretion following ovarian transplantation contributes to revascularization of the graft by up-regulating the gene expression of two major angiogenic factors.
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PMID:Immature rat ovaries become revascularized rapidly after autotransplantation and show a gonadotropin-dependent increase in angiogenic factor gene expression. 811 53

Expression of the vascular permeability factor/vascular endothelial growth factor (VEGPF) gene was investigated in human central nervous system (CNS) neoplasms and normal brain. Adsorption of capillary permeability activity from human glioblastoma multiforme (GBM) cell conditioned medium and GBM cyst fluids by anti-VEGPF antibodies demonstrated that VEGPF is secreted by GBM cells and is present in sufficient quantities in vivo to induce vascular permeability. Cloning and sequencing of polymerase chain reaction-amplified GBM and normal brain cDNA demonstrated three forms of the VEGPF coding region (567, 495, and 363 nucleotides), corresponding to mature polypeptides of 189, 165, and 121 amino acids, respectively. VEGPF mRNA levels in CNS tumors vs. normal brain were investigated by the RNase protection assay. Significant elevation of VEGPF gene expression was observed in 81% (22/27) of the highly vascular and edema-associated CNS neoplasms (6/8 GBM, 8/8 capillary hemangioblastomas, 6/7 meningiomas, and 2/4 cerebral metastases). In contrast, only 13% (2/15) of those CNS tumors that are not commonly associated with significant neovascularity or cerebral edema (2/10 pituitary adenomas and 0/5 nonastrocytic gliomas) had significantly increased levels of VEGPF mRNA. The relative abundance of the forms of VEGPF mRNA was consistent in tumor and normal brain: VEGPF495 > VEGPF363 > VEGPF567. In situ hybridization confirmed the presence of VEGPF mRNA in tumor cells and its increased abundance in capillary hemangioblastomas. Our results suggest a significant role for VEGPF in the development of CNS tumor neovascularity and peritumoral edema.
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PMID:Expression of the vascular permeability factor/vascular endothelial growth factor gene in central nervous system neoplasms. 838 Aug 10

Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF), exists as multiple forms due to alternative splicing of mRNA. VEGF165/164 (human/rodent homologue) is often assumed to be the predominant form, although truly quantitative assessments are lacking. We have used the RNase protection assay to directly quantitate the relative abundance of VEGF mRNA forms in five rat tissues (brain, kidney, lung, spleen, and heart) and two rat glioma cell lines (C6 and 9L). The three major forms, which code for proteins of 188, 164, and 120 amino acids, were observed in all of the tissues and cells examined. However, the relative abundance differed among the samples. VEGF188 was the predominant form (> 50% of total VEGF mRNA) in heart and lung, but was the least abundant form (6-15%) in all other samples. VEGF164 was lower (approximately 25%) in heart and lung, but was predominant (> 50%) in brain and kidney. VEGF164 and VEGF120 were present in equimolar amounts (each form approximately 46% of total) in the spleen, C6, and 9L. VEGF120 was also present in kidney (38%) and lung (27%) and was least abundant (approximately 15%) in brain and heart. A rat homologue of VEGF206 was not observed. VEGF mRNA splicing occurs in a tissue-specific manner. The assumption that the predominant physiologic form of VEGF is a VEGF165/164 homodimer should be viewed with caution.
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PMID:Differential expression of vascular endothelial growth factor (vascular permeability factor) forms in rat tissues. 852 59

The human endometrium undergoes a complex process of vascular and glandular proliferation, differentiation, and regeneration with each menstrual cycle in preparation for implantation. Vascular endothelial growth factor (VEGF) is an endothelial cell-specific angiogenic protein that appears to play an important role in both physiological and pathological neovascularization. To investigate whether VEGF may regulate human endometrial angiogenesis, we examined VEGF messenger ribonucleic acid (mRNA) and protein throughout the menstrual cycle and studied the regulation of VEGF by reproductive steroids in isolated human endometrial cells. By ribonuclease protection analysis, VEGF mRNA increased relative to early proliferative phase expression by 1.6-,2.0-, and 3.6-fold in midproliferative, late proliferative, and secretory endometrium, respectively. In histological sections, VEGF mRNA and protein were localized focally in glandular epithelial cells and more diffusely in surrounding stroma, with greatest VEGF expression in secretory endometrium. Consistent with these in vivo results, the treatment of isolated human endometrial cells with estradiol (E2), medroxyprogesterone acetate (MPA), or E2 plus MPA significantly increased VEGF mRNA expression over the control value by 3.1-, 2.8-, and 4.7-fold, respectively. The VEGF response to E2 was rapid, with steady state levels of VEGF mRNA reaching 85% maximum 1 h after the addition of steroid. E2 also caused a 46% increase in secreted VEGF protein, and the combination of E2 and MPA caused an 18% increase. VEGF expression in endometriosis, an angiogenesis-dependent, estrogen-sensitive disease was similar to that seen in eutopic endometrium. Peritoneal fluid concentrations of VEGF were significantly higher in women with moderate to severe endometriosis than in women with minimal to mild endometriosis or no disease. VEGF, therefore, may be important in both physiological and pathological angiogenesis of human endometrium, as it is an estrogen-responsive angiogenic factor that varies throughout the menstrual cycle and is elevated in women with endometriosis.
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PMID:Ovarian steroid regulation of vascular endothelial growth factor in the human endometrium: implications for angiogenesis during the menstrual cycle and in the pathogenesis of endometriosis. 876 83

There is accumulating evidence from in vitro experiments that the gene expression of the vascular endothelial growth factor (VEGF) is, like that of the erythropoietin (EPO) gene, regulated by the oxygen tension and by divalent cations such as cobalt. Since the information about the regulation of VEGF gene expression in vivo is rather scarce, this study aimed to examine the influence of hypoxia and of cobalt on VEGF gene expression in different rat organs and to compare it with that on EPO gene expression. To this end male Sprague-Dawley rats were exposed to carbon monoxide (0.1% CO), hypoxia (8% O2 ) or to cobalt chloride (12 and 60 mg/kg s.c.) for 6 h. mRNA levels for VEGF- 188, -164, and -120 amino acid isoforms in lungs, hearts, kidneys and livers were semiquantitated by RNase protection. For these organs we found a rank order of VEGF mRNA abundance of lung >> heart > kidney = liver. EPO mRNA levels were semiquantitated in kidneys and livers. Hypoxia, CO and cobalt increased EPO mRNA levels 60-fold, 140-fold and 5-fold, respectively, in the kidneys, and 11-fold, 11-fold and 3-fold, respectively, in the livers. None of these manoeuvres caused significant changes of VEGF mRNA in lung, heart or kidneys. Only in the livers did hypoxia lead to a significant (50%) increase of VEGF mRNA. These findings suggest that, in contrast to the in vitro situation, the expression of the VEGF gene in normal rat tissues is rather insensitive to hypoxia. In consequence, the in vivo regulation of the VEGF and the EPO genes appear to differ substantially, suggesting that the regulation of the VEGF and EPO genes may not follow the same essential mechanisms in vivo.
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PMID:Divergent regulation of vascular endothelial growth factor and of erythropoietin gene expression in vivo. 892 8

The corpus luteum undergoes tremendous growth, development and regression each oestrous or menstrual cycle. These changes are reflected by equally impressive growth and regression of the luteal vasculature. We have previously shown that angiogenic factors from corpora lutea are primarily heparin binding and that one of these factors is similar to vascular endothelial growth factor (VEGF). In an effort to identify this factor, and to define its role in luteal vascular development, the cDNA for the coding region of ovine VEGF was sequenced and a sensitive RNase protection assay was developed to quantitate mRNA encoding VEGF in luteal tissues from ewes in the early (days 2-4), mid- (day 8) and late (days 14-15) stages of the oestrous cycle. In addition, an N-terminal peptide was synthesized from the translated ovine cDNA sequence for VEGF and an antiserum was raised against this peptide for use in western immunoblotting procedures. Nested reverse transcriptase (RT)-PCR of RNA from ovine corpora lutea resulted in three products that correspond in size to the alternatively spliced variants of VEGF (VEGF120, VEGF164, and VEGF188) predicted from other species. The RNase protection assay revealed that the proportion of mRNA encoding VEGF was 2- to 3-fold greater on days 2-4 than on day 8 or days 14-15. Densitometric analysis of gels from the RNase protection assay showed that VEGF120 represented approximately one third of the total mRNA encoding VEGF in the corpus luteum and that this proportion did not vary with stage of the oestrous cycle. SDS-PAGE and western immunoblot analysis of a homogenate from corpora lutea showed a single 18 kDa protein. These data demonstrate that VEGF is expressed in luteal tissue throughout the ovine oestrous cycle and that expression of mRNA encoding VEGF is upregulated during the period of rapid luteal development, when luteal vascular growth is at its maximum.
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PMID:Characterization and expression of vascular endothelial growth factor (VEGF) in the ovine corpus luteum. 895 42

Erectile dysfunction is often associated with problems in vascular perfusion to the erectile components of the penis. In order to better understand the factors that control vascular formation and perfusion in the erectile tissues of the penis, we have begun to characterize the expression of vascular endothelial growth factor (VEGF) in penis tissues. VEGF is one of several polypeptides that have significant angiogenic activity in vitro and in vivo. Extensive characterization of the VEGF gene and its products has shown that several different mature mRNA transcripts exist, originating from alternative splicing of the basic VEGF transcript. These variant transcripts can encode peptides with different biological activities. Penile tissue was obtained from adult rats and from human patients undergoing penile prosthesis implantation. Analysis of the forms of VEGF transcripts was performed using a reverse transcription-polymerase chain reaction technique with primer pairs derived from the first and eighth exon of the VEGF gene. The expression levels of the various isoforms in the rat penis were then quantified using RNase protection assays. Four previously described splice variants of VEGF mRNA (VEGF 120, 144, 164, 188) were detected in rat and human penile tissues. In contrast to what is seen in the rat lung, where the most abundant form of VEGF mRNA is the 188 splice isoform, VEGF 164 is the most abundant transcript detected in the penis. Finally, sequence analysis of numerous VEGF cDNA clones obtained from the rat penis demonstrated the presence of a previously undescribed VEGF splice variant that could give rise to a protein of 110 amino acid residues (VEGF 110, GenBank accession no. AF080594). In summary, a number of VEGF mRNA isoforms are expressed in the rat and human penis, with the splice variant encoding a 164-amino acid protein present in greatest abundance. This study is a prelude to attempts to genetically manipulate VEGF expression in the penis as a therapy for erectile dysfunction.
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PMID:Expression of messenger ribonucleic acid splice variants for vascular endothelial growth factor in the penis of adult rats and humans. 991 7

Evenomation by arachnids of the genus Loxosceles frequently results in disfiguring necrotic skin lesions. The cellular and molecular mechanisms which contribute to lesion development are incompletely defined but appear to involve participation of several pro-inflammatory mediators. We have recently observed that Loxosceles deserta venom induces the production of chemokines in human umbilical vein endothelial cells (HUVECs) and human pulmonary epithelial cells. In the present study we observed that Loxosceles deserta venom induces the expression of vascular endothelial growth factor (VEGF) in human keratinocytes but little in smooth muscle cells and none in pulmonary epithelial cells. A potent endothelial cell-specific mitogen, VEGF induces angiogenesis and vascular permeability in vivo. RNase protection assay data indicate that VEGF mRNA concentrations in keratinocytes are significantly increased at 2 h following venom exposure. These data suggest that keratinocyte-derived VEGF may contribute to the vasodilation, edema and erythema which occur following Loxosceles evenomation.
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PMID:Loxosceles deserta spider venom induces the expression of vascular endothelial growth factor (VEGF) in keratinocytes. 1070 59

Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen that promotes angiogenesis during embryonic development and the progression of certain pathologies. This study examined the regulation of VEGF expression by adenosine receptor (AR) activation in PC12 rat pheochromocytoma cells. Treatment of cells with the AR agonist CGS21680 reduced the VEGF mRNA level to approximately 20% of that in control cells with an EC(50) value of 0.47 nM, indicative of mediation by the A(2A)AR. Down-regulation of VEGF mRNA by CGS21680 was abolished by pretreatment of cells with the AR antagonist ZM241385. Additionally, ZM241385 alone increased VEGF mRNA by 2.8-fold above basal. RNase protection assays indicated that CGS21680 down-regulated VEGF(121), VEGF(165), and VEGF(189) transcripts. VEGF protein secretion was similarly decreased by CGS21680. Under hypoxic conditions, VEGF mRNA expression was reduced by 85.7% after pretreatment with CGS21680. The down-regulation response appears to be mediated predominately by coupling of the A(2A)AR to G(s) because cholera toxin treatment also reduced VEGF expression. The decrease in VEGF mRNA steady-state levels after A(2A)AR activation is apparently due to a decrease in the VEGF gene transcription rate and not to a decrease in mRNA stability. Thus, depending on the cell type, adenosine may have an inhibitory effect on VEGF production, which may have implications in blood vessel development.
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PMID:Down-regulation of vascular endothelial growth factor expression after A(2A) adenosine receptor activation in PC12 pheochromocytoma cells. 1086 76

The presence of vascular endothelial growth factor (VEGF) in the ovary has been reported in a number of species. The objective of the present study was to demonstrate the expression of VEGF, VEGF receptor (R)-1, and VEGFR-2 in detail by different methodological approaches in bovine corpora lutea (CL) obtained from different stages of the estrous cycle and during pregnancy. VEGF and VEGF receptor transcripts were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and ribonuclease protection assay. All components of the VEGF system were found in the bovine CL during the estrous cycle and pregnancy. Analysis of VEGF transcript by RT-PCR shows that CL tissues expressed predominantly the smallest isoforms (VEGF(121) and VEGF(165)). The highest mRNA expression for VEGF and VEGFR-2 mRNA was detected during the early luteal phase, followed by a significant decrease of expression during the mid and late luteal phase and a further decrease of VEGF mRNA after regression. During pregnancy, high levels of expression were always present. In contrast, no significant change in VEGFR-1 mRNA expression during the estrous cycle and pregnancy was found. The VEGF protein concentration in CL tissue was significantly higher (20.9-23.4 ng/g wet weight) during the early luteal phase (Days 1-7), followed by a decrease at the late luteal phase (14.3-18.7 ng/g wet weight) and, especially, after CL regression (2.8 ng/g wet weight). However, relatively high levels were found during pregnancy (10.1 ng/g wet weight). As achieved by immunohistochemistry, VEGF protein was localized predominantly in luteal cells. High VEGF protein and transcript concentrations and increased VEGFR-2 expression during the early luteal phase coincided with luteal vascularization. These results suggest an important role of VEGF in angiogenesis of the newly formed CL. The high VEGF mRNA expression and protein levels during matured vasculature in the mid-stage CL and pregnancy also suggest also a survival function for endothelial cells.
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PMID:Expression and tissue concentration of vascular endothelial growth factor, its receptors, and localization in the bovine corpus luteum during estrous cycle and pregnancy. 1099 33


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