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)

By northern blot analysis and ribonuclease protection assay, we observed the presence of a high level of trkB mRNA in primary brain cultures devoid of neuronal cells and highly enriched in glial fibrillary acidic protein-positive astroglial cells prepared from newborn rat cerebral hemispheres, cerebral cortex, hippocampus, and striatum. In primary astroglial cultures, the more abundant trkB transcripts code for the truncated receptor without tyrosine kinase activity; probes specific for the full-length trkB mRNA did not detect any signal in northern blot analysis. By the sensitive ribonuclease protection assay, we could show the presence of trkC mRNA in cultured astrocytes, whereas no trkA mRNA was detected. We confirmed the presence of relatively high levels of nerve growth factor and neurotrophin-3 mRNA, and very low basal level of brain-derived neurotrophic factor mRNA. Moreover, we demonstrated that another member of the neurotrophin family, neurotrophin-4, is also expressed in cultured astroglial cells. In view of the fact that many functional receptors for conventional neurotransmitters or neuropeptides present on astroglial cells may act via the adenylate cyclase system, we studied also the effect of agents able to increase the intracellular cyclic AMP concentration. A sharp increase in the trkB mRNA level was observed after treatment of primary astroglial cultures with dibutyryl cyclic AMP, 8-bromo-cyclic AMP, or the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine. On the contrary, trkC mRNA levels were unaffected by treatment with cyclic AMP-elevating agents. All the neurotrophin mRNAs examined, except neutrophin-4, were increased by 3-isobutyl-1-methylxanthine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of neurotrophins and their receptors in primary astroglial cultures: induction by cyclic AMP-elevating agents. 751 99

The structure of the mouse neurotrophin-3 (NT-3) gene has been analysed using genomic cloning and the rapid amplification of cDNA ends (RACE) method. The gene consists of two small upstream exons (exons IA and IB) and a larger downstream exon (exon II) that encodes the mature protein. Two classes of NT-3 transcripts, termed transcripts A and B, are generated by alternative splicing of exon IA or exon IB to the common exon II. The NT-3 gene also contains several transcription start sites in both upstream exons, and three different polyadenylation sites in exon II, as shown by RNase protection assays and by RACE, giving rise to multiple NT-3 mRNA variants of slightly different lengths. Cerebellar granule neurons express both classes of NT-3 transcripts, but only transcript B is regulated by tri-iodothyronine (T3) in these neurons. The effect of T3 on NT-3 mRNA is primarily due to transcription enhancement, as shown in nuclear run-on experiments. The levels of NT-3 mRNA are much lower in cultured mouse astrocytes and are undetectable in the human neuroblastoma cell line IMR 32. A TATA box is present in the upstream region of exon IB but not in that of exon IA. Promoter analysis using the chloramphenicol acetyltransferase reporter gene fused to different NT-3 upstream regions showed the presence of two active NT-3 promoters in cerebellar granule neurons. However, in IMR 32 cells, NT-3 promoter activity decreased dramatically with increasing length of the 5' flanking region. This suggests that expression of the NT-3 gene is regulated both by positive influences, such as T3, and by negative silencing elements present in the upstream regions of the NT-3 promoter.
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PMID:Two promoters direct transcription of the mouse NT-3 gene. 795 96

The expression of neurotrophin and neurotrophin receptor mRNAs was examined using RNase protection assays and Northern-blot analysis in rat thymus, spleen tissue and immunocompetent mononuclear cells purified from these two organs. Nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4 mRNAs were all expressed in thymus and spleen tissue although at different levels, while immunocompetent cells expressed neurotrophin-3 and neurotrophin-4 mRNAs. Thymus and spleen tissue expressed mRNAs encoding the low-affinity nerve-growth-factor receptor, the non-neuronal TrkA I receptor, the truncated (kinase deficient) and full-length TrkB, and the TrkC receptor. Low-affinity nerve-growth-factor receptor and non-neuronal TrkA I mRNAs were detected in both thymus and spleen immunocompetent cells. In addition, thymus cells expressed neuronal TrkA II mRNA and spleen cells expressed truncated TrkB mRNA. The expression of TrkA I and TrkA II mRNAs was enhanced in both thymus and spleen cells after cell culture. Enhanced levels of neurotrophin-4 mRNA were observed in spleen immunocompetent cells after adrenalectomy. Moreover, the expression of neurotrophin-4 mRNA was up-regulated after stimulation of immune cells with the mitogens concanavalin A or lipopolysaccharide or with the inflammatory mediator leukotriene B4. This suggests that neurotrophin-4 could be secreted by immunocompetent cells and may be involved in inflammatory processes.
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PMID:Expression of mRNA encoding neurotrophins and neurotrophin receptors in rat thymus, spleen tissue and immunocompetent cells. Regulation of neurotrophin-4 mRNA expression by mitogens and leukotriene B4. 805 49

Degenerate primers directed against conserved regions of the trk and trkB amino acid sequences were used in the polymerase chain reaction to isolate a 455 bp fragment from embryonic day 3 chicken cDNA encoding the trkC. This fragment was subsequently used to synthesize an anti-sense trkC cRNA probe which was used in a RNase protection assay of total RNA from chicken embryos. trkC mRNA was found in the E2 embryo with increasing levels later in development. In the E9 embryo highest levels were found in brain and spinal cord with intermediate levels in eye, heart, gut and muscle. Low levels were found in kidney, liver, skin and yolk sac. Using the 455 bp trkC fragment as a probe in RNA blot analyses of poly A+ RNA, a major transcript of 6.3 kb and two minor transcripts of 3 kb and 10 kb were found. In situ hybridization was performed on embryos taken at three stages of development (embryonic day 3, 9 and 19), using a 48-mer antisense oligonucleotide probe for chicken trkC. Within the sensory nervous system trkC mRNA expression at all ages was confined to the ventrolateral neurons of the spinal sensory and trigeminal ganglia as well as distal ganglia associated with the VIIth, IXth and Xth cranial nerves. Labelling for trkC mRNA was also observed within the developing CNS at E3 and the ganglion of Remak at E19. A barely detectable level of expression was observed in the sympathetic chain and no labelling was evident in the proximal ganglia of the cranial nerves. These results suggest that neurons have a very early capacity to respond to neurotrophin-3 which continues throughout embryonic development. The early expression of trkC mRNA also support the growing evidence suggesting a role for neurotrophins in neuronal differentiation.
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PMID:Molecular cloning and cellular localization of trkC in the chicken embryo. 826 14

The presence of the neurotrophin, nerve growth factor, brain derived neurotrophic factor, neurotrophin-3 and neurotrophin-4 (NGF, BDNF, NT-3 and NT-4) and their receptors of the tyrosine kinase family (trkA, trkB and trkC) have been investigated in the choroid plexus and dura mater of the adult rat by ribonuclease protection assay. The choroid plexus contained high levels of mRNAs for NGF and NT-4, and low levels of NT-3 and BDNF mRNA; and high levels of trkB mRNA, and undetectable levels of trkA and trkC mRNA. In the dura mater there were high levels of NT-3 and NGF, and low levels of BDNF and NT-4 mRNAs; and high levels of trkC mRNA, and relatively high amount of trkB mRNA, while levels of trkA mRNA was undetectable. The present analysis revealed a different distribution of neurotrophins and their related receptors in the choroid plexus and dura mater.
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PMID:Expression of mRNAs for neurotrophins and their receptors in the rat choroid plexus and dura mater. 858 Apr 26

Using the RNase protection assay, we have found that nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) are expressed in the avian retina during development. The expression peaks around embryonic days 12-15, with decreasing levels at later stages of development. Abundant levels of NGF and BDNF but low levels of NT-3 mRNA were found in the adult retina. We also found that light/darkness regulated the levels of NGF and BDNF mRNAs but not the levels of NT-3 mRNA in the 5-day-old chicken retina. It was demonstrated that NGF and BDNF mRNA levels were up-regulated by light exposure. The cellular localization of mRNA expression for the neurotrophins and neurotrophin receptors TrkA, TrkB, and TrkC in the retina was studied using in situ hybridization. The patterns of NGF and trkA mRNA expression were very similar and were localized to the external part of the inner nuclear layer on the border with the outer plexiform layer and corresponded to the localization of horizontal cells. NT-3 labeling was also found over the external part of the inner nuclear layer, whereas trkC mRNA was found over all layers in the retina. BDNF labeling was found over all layers in the retina, whereas TrkB labeling was intense over cells in the ganglion cell layer, which is in agreement with the response of ganglion cells to BDNF stimulation. Functional neurotrophin receptors were suggested by the response of retinal explants to neurotrophin stimulation. These data indicate that the neurotrophins play local roles in the retina that involve interactions between specific neuronal populations, which were identified by the localization of the Trk receptor expression. The data also suggest that NGF and BDNF expression is regulated by normal neuron usage in the retina.
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PMID:Expression of neurotrophins and trk receptors in the avian retina. 882 53

The expression of neurotrophin and neurotrophin receptor mRNAs in human granulocytes and bone marrow cells was examined using ribonuclease protection assay and reverse transcription-polymerase chain reaction. The granulocytes expressed mRNA coding for nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-4 (NT-4), but not neurotrophin-3 (NT-3). Moreover, the inflammatory mediator leukotriene B4 (LTB4) up-regulated the expression of NT-4 mRNA in granulocytes, but did not affect the expression of other neurotrophin mRNAs. Granulocytes generally lacked expression of mRNA coding for neurotrophin receptors. In contrast, human bone marrow cells consistently expressed mRNA for trkB (the BDNF and NT-4 receptor) and displayed variable expression of mRNA coding for trkA (the tyrosine kinase NGF receptor) and LNGFR (the low-affinity NGF receptor), whereas mRNA for trkC (the NT-3 receptor) was not expressed. Contrary to granulocytes, normal bone marrow cells generally expressed only low levels of mRNA encoding BDNF and NT-4. Expression of mRNA encoding NGF and NT-3 was not detected. However, significantly increased expression of BDNF mRNA was observed when bone marrow cells from patients with chronic myeloproliferative disorders (MPD) were analyzed. The results suggest that neurotrophins may act as granulocyte-derived effector molecules and that human bone marrow cells may be targets for these compounds, in particular BDNF and NT-4.
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PMID:Expression of mRNA encoding neurotrophins and neurotrophin receptors in human granulocytes and bone marrow cells--enhanced neurotrophin-4 expression induced by LTB4. 971 63

Dexamethasone (DEX) increases the expression of neurotrophin-3 (NT-3) in normal rat hippocampal neurons, whereas transient forebrain ischemia reduces the NT-3 mRNA level. The effect of DEX on the expression of NT-3 mRNA in injured brain cells after ischemia has not been investigated, however. Using in situ hybridization and ribonuclease protection assay methods, we studied NT-3 mRNA expression in rats with and without DEX administration after transient forebrain ischemia. Without DEX treatment, NT-3 mRNA was down-regulated in the hippocampal neurons at 2, 4, 12 h and returned to basal levels 24 h following ischemia. With DEX treatment, however, NT-3 mRNA showed no change at 2, 4 and 12 h and increased 24 h after ischemia. The results indicate that DEX inhibits ischemia-induced NT-3 mRNA down-regulation during the first 12 h and up-regulates NT-3 mRNA 24 h after ischemia. DEX administration might be effective in influencing some of the pathophysiological effects of ischemia in the hippocampus.
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PMID:Dexamethasone inhibits ischemia-induced transient reduction of neurotrophin-3 mRNA in rat hippocampal neurons. 985 2

These studies were performed to determine the developmental expression pattern of neurotrophic factor (NTF: nerve growth factor (betaNGF), brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), ciliary neurotrophic factor (CNTF), neurotrophin-3 (NT-3) and NT-4 mRNA and NGF, NT-3 and NT-4 protein in the urinary bladder of the postnatal Wistar rat. It was hypothesized that NTFs may contribute to the development of the spinobulbospinal micturition reflex that represents the adult micturition pattern. Changes in NTF mRNA or protein expression in the urinary bladder at the time of development of the mature micturition reflex (postnatal days (P) 16-18) may suggest an involvement of target-derived NTFs in this maturation process. Developmental ages, prior to (P5, P10, P15) or following (P20, P30, adult P90) the development of the spinobulbospinal micturition reflex were selected and the urinary bladder was analyzed for levels of neurotrophic factor mRNA or protein. Results from ribonuclease protection assays demonstrated a similar developmental pattern among each neurotrophic factor examined. Neurotrophic factor mRNA levels increased by P10 and reach a maximum by P15. Subsequently, NTF mRNA levels declined to adult levels that were less than the earliest postnatal time examined (P5). NTF mRNA expression was significantly (p</=0.05-0.001) greater at P10, P15, P20 and P40 (NT-4 mRNA) compared to adult levels for each NTF examined except GDNF mRNA. In general, NGF, NT-3 and NT-4 urinary bladder protein levels in early postnatal development, as determined by ELISA, were similar when compared to the corresponding mRNA expression. Differences in the correlation between NT-3 and NT-4 mRNA and protein expression were demonstrated in the adult urinary bladder where significantly (p</=0. 001) greater levels of protein were revealed despite relatively low abundance of NT-3 and NT-4 mRNA. The developmental expression pattern (maximum expression at the second to third postnatal week) of NTFs in the urinary bladder is consistent with a potential role in the development of the spinobulbospinal reflex. Relatively high expression of NT-3 and NT-4 protein in the adult urinary bladder suggests a potential importance of these factors in the adult lower urinary tract.
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PMID:Developmental expression of urinary bladder neurotrophic factor mRNA and protein in the neonatal rat. 1067 71

Fischer 344 rats were exposed to 60 Hz magnetic fields (EMFs) during gestation and lactation. Rats received continuous exposure to 2-, 200- or 1000-microT magnetic fields for 18.5 h per day, 7 days a week, or sham exposure (sham controls). During postnatal development, on postnatal days 1, 3, 6, 9, 15 and 20, forebrain tissue from male pups was examined for alterations in mRNA level for developmentally regulated central nervous system-specific proteins. Alterations in these factors during critical periods of development could result in alterations in the final neural network. Gap43 (growth-associated protein 43) mRNA was measured by Northern hybridization as a developmental indicator of axonal growth during the development of the neuron. Between postnatal days 1 and 9, detectable levels of Gap43 mRNA displayed a similar pattern across all sham control and exposure groups. In addition to Gap43, mRNA levels for the nervous system-specific growth factors ciliary neurotrophic factor (Cntf), brain-derived neurotrophic factor (Bdnf), beta nerve growth factor (Ngfb), neurotrophin-3 (Ntf3), and neurotrophin-4 (Ntf4) were examined by RNase protection assay. While there is public concern for developmental neurotoxicity associated with exposure to EMFs, these data, generated from animals exposed to 2-, 200- or 1000-microT magnetic fields during both gestational and lactational periods of development, suggest that under these conditions no significant alterations in these critical factors for brain development occur.
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PMID:Developmental profiles of growth-associated protein (Gap43), Ngfb, Bndf and Ntf4 mRNA levels in the rat forebrain after exposure to 60 Hz magnetic fields. 1079 Feb 87


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