Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The actions of the neurotrophins are mediated through specific receptors. Nerve growth factor (NGF), the prototypic neurotrophin, binds to receptors of both high and low affinity. A protein 75 kDa in size (p75NGFR) binds NGF, as well as brain-derived neurotrophic factor and neurotrophin 3, with low affinity. Recent investigations suggest that this protein may also be a component of the high affinity NGF receptor complex. To study gene expression of the p75NGFR molecule, we used a sensitive reverse transcription-polymerase chain reaction (RT-PCR) assay to measure levels of its messenger RNA (mRNA) in small samples of total RNA. The assay is based on using a shortened p75NGFR cRNA as an internal RNA standard to control for variability in reverse transcription and polymerase chain amplification. We measured p75NGFR mRNA levels in the rat cerebellum during ontogeny to further study the transient developmental increase in receptor gene expression known to occur in this brain region during the early postnatal period. We found that p75NGFR mRNA levels were most abundant at postnatal day 2, and then declined to lower levels throughout postnatal development and in the adult. Northern blot analysis of the same total RNA samples used in our RT-PCR assay verified that p75NGFR expression is highest in the early postnatal period. These results confirm those of previous studies accomplished with much larger amounts of RNA using ribonuclease protection or northern blot assays. The use of an RT-PCR assay that utilized an internal standard also controls against changes in RNA complexity which can affect the measurement of message abundance across developmental stages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A reverse transcription-polymerase chain reaction study of p75 nerve growth factor receptor gene expression in developing rat cerebellum. 797 82

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

Previous studies have analyzed the expression of different members of the neurotrophin family and their trk receptors in glial cultures composed mainly or exclusively of type-1 astrocytes, whereas only partial data have been published on other cultured glial types. In this article we compare the mRNA levels for neurotrophins (NGF, BDNF, NT-3, NT-4) and their high-affinity receptors (trkA, trkB, trkC) in cultures enriched in specific glial types, such as microglia, type-1 astroglia, and cells of the O/2A lineage (type-2 astroglia and oligodendroglia). Relatively high levels of NGF mRNA (comparable to those observed in adult rat cerebral cortex) are present in all types of cultured glial cells, except for a low level of expression in cultures enriched in microglial cells. In contrast, BDNF mRNA is undetectable in all cultures examined. NT-3 and NT-4 mRNA molecules, at a level equal to that observed in adult rat cerebral cortex, are easily detected in type-1 astrocyte cultures, whereas their hybridization signals are undetectable in cells of the O/2A lineage and in microglial cultures. The analysis of neurotrophin receptor mRNAs confirms the absence of trkA mRNA, the presence of relatively high levels of trkB mRNA (70-100% of cerebral cortex values), and low levels of trkC mRNA (10-18% of cerebral cortex values) in both cultured astroglial and oligodendroglial cells. Only very low levels of trkB and trkC mRNAs are observed in microglial cultures. Although cultured glial cells express mainly mRNAs encoding for the truncated form of trkB and trkC, a low level of mRNA encoding for the full-length catalytic form of these receptors is detected by the sensitive ribonuclease protection assay.
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PMID:Neurotrophins and their trk receptors in cultured cells of the glial lineage and in white matter of the central nervous system. 886 Feb 35

Levels of mRNA for neurotrophins (brain-derived neurotrophic factor, BDNF; neurotrophin 3, NT-3; neurotrophin 4, NT-4) and their receptors (trkA, trkB, trkC) and for glial cell line-derived neurotrophic factor (GDNF) and its receptors (ret, GDNFR-alpha) were measured in rat thyroid tissue by ribonuclease protection assays. In thyroid tissue the NT-3 mRNA level was threefold lower and the NT-4 mRNA level sixfold higher than those detected in adult rat hippocampus, while BDNF mRNA was undetectable. Very low levels of mRNA for truncated trkB and trkC receptors and no catalytic trkA, trkB or trkC were found. In conclusion NT-3 and NT-4, but not the corresponding functional receptors, are expressed in the thyroid tissue. Therefore, it is unlikely that these factors serve a direct local autocrine or paracrine function in thyroid cell types, and a target-derived mode of action on neurons innervating the thyroid tissue is suggested. An opposite result has been found for the neurotrophic factor GDNF: thyroid tissue showed a high level of transcripts for the GDNF receptor subunits (GDNFR-alpha and Ret), while GDNF mRNA was undetectable. The in situ hybridization analysis of GDNFR-alpha and ret mRNA revealed an interesting difference in the cell distribution of these transcripts: ret mRNA is selectively expressed in a subpopulation of cells scattered in the follicular epithelium and in the interfollicular spaces, while GDNFR-alpha expression is more homogeneous and widespread, including the more abundant cell type of the thyroid gland: the follicular cell. Double-labeling in situ hybridization/immunocytochemistry experiments, with a specific marker (calcitonin), showed that parafollicular cells express ret but not GDNFR-alpha. This differential distribution of the GDNF receptor components (GDNFR-alpha and ret) may reflect a peculiar biological role in intercellular communication in the thyroid gland.
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PMID:Expression of neurotrophins, GDNF, and their receptors in rat thyroid tissue. 1002 66

Spinal cord injury and cyclophosphamide-induced cystitis dramatically alter lower urinary tract function and produce neurochemical, electrophysiological, and anatomical changes that may contribute to reorganization of the micturition reflex. Mechanisms underlying this neural plasticity may involve alterations in neurotrophic factors in the urinary bladder. These studies have determined neurotrophic factors in the urinary bladder that may contribute to reorganization of the micturition reflex following cystitis or spinal cord injury. A ribonuclease protection assay was used to measure changes in urinary bladder neurotrophic factor mRNA (betaNGF, BDNF, GDNF, CNTF, NT-3, and NT-4) following spinal cord injury (acute/chronic) or cyclophosphamide-induced cystitis (acute/chronic). The correlation between urinary bladder nerve growth factor mRNA and nerve growth factor protein expression was also determined. Each experimental paradigm resulted in significant (P </= 0.05-0.005) changes in urinary bladder neurotrophic factor mRNA, although the magnitude of the changes differed between paradigms. Urinary bladders from rats with acute spinal cord injury (4 days) exhibited the largest increase in neurotrophic factor mRNA levels (betaNGF, 21-fold increase; BDNF, 78-fold increase; GDNF, 11-fold increase; CNTF, 5.5-fold increase; NT-3, 10-fold increase; NT-4, 25-fold increase) relative to control urinary bladders. More modest but significant increases were demonstrated for urinary bladders from rats with chronic (4-6 weeks) spinal cord injury. Significant increases in urinary bladder neurotrophic factor mRNA levels of comparable magnitude were demonstrated following either acute or chronic cyclophosphamide-induced cystitis. Increased abundance of urinary bladder nerve growth factor mRNA was not always associated with increased total urinary bladder nerve growth factor. Total urinary bladder nerve growth factor decreased following acute or chronic cystitis despite increased abundance of nerve growth factor mRNA. Urinary bladder nerve growth factor mRNA correlates with protein measures 5-6 weeks following spinal cord injury but not earlier. The 5- to 6-week time point coincided with the reemergence of the spinal bladder-to-bladder reflex mechanisms following spinal cord injury. Discrepancies between two measures (mRNA and protein) may reflect retrograde axonal transport of nerve growth factor to the dorsal root ganglia (L6-S1). Retrogradely transported NGF may play a role in altered lower urinary tract function following spinal cord injury or cyclophosphamide-induced cystitis.
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PMID:Changes in urinary bladder neurotrophic factor mRNA and NGF protein following urinary bladder dysfunction. 1068 93

Interactions between neurotrophic factors and neurotransmitters participate in the formation and maintenance of appropriate connections, as well as in neurodegenerative processes. Here we have measured changes in the developmental expression pattern of BDNF and NT-3 in the striatum, cortex, and substantia nigra induced by intrastriatal injection of the N-methyl-d-aspartate glutamate receptor agonist quinolinic acid (QUIN). Animals were injected at different postnatal ages, and BDNF and NT-3 mRNA levels were determined 6 h after lesion using a ribonuclease protection assay. Our results show a biphasic increase in BDNF mRNA levels in striatum and in the ipsilateral cortex at postnatal day (P)5 and P21. In contrast, although NT-3 expression did not change in the striatum, it was down-regulated in the ipsilateral cortex at P5 and P30. Intrastriatal QUIN injection did not induce changes in either BDNF or NT-3 expression in the ipsilateral substantia nigra. These findings show that neurotrophin expression is developmentally regulated after excitotoxic injury, which suggests that this endogenous response may be involved in different neuronal maturation and vulnerability during development.
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PMID:Developmental regulation of BDNF and NT-3 expression by quinolinic acid in the striatum and its main connections. 1096 90

The capacity of the central nervous system for axonal growth decreases as the age of the animal at the time of injury increases. Changes in the expression of neurotrophic factors within embryonic and early postnatal spinal cord suggest that a lack of trophic support contributes to this restrictive growth environment. We examined neurotrophic factor gene profiles by ribonuclease protection assay in normal neonate and normal adult spinal cord and in neonate and adult spinal cord after injury. Our results show that in the normal developing spinal cord between postnatal days 3 (P3) and P10, compared to the normal adult spinal cord, there are higher levels of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), and glial-derived neurotrophic factor (GDNF) mRNA expression and a lower level of ciliary neurotrophic factor (CNTF) mRNA expression. Between P10 and P17, there is a significant decrease in the expression of NGF, BDNF, NT-3, and GDNF mRNA and a contrasting steady and significant increase in the level of CNTF mRNA expression. These findings show that there is a critical shift in neurotrophic factor expression in normal developing spinal cord between P10 and P17. In neonate spinal cord after injury, there is a significantly higher level of BDNF mRNA expression and a significantly lower level of CNTF mRNA expression compared to those observed in the adult spinal cord after injury. These findings suggest that high levels of BDNF mRNA expression and low levels of CNTF mRNA expression play important roles in axonal regrowth in early postnatal spinal cord after injury.
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PMID:Differences in neurotrophic factor gene expression profiles between neonate and adult rat spinal cord after injury. 1135 54