Disease relevance of Cntfr

• Further, CNTFR-alpha was transiently expressed in the cerebral cortex surrounding the hematoma, with a peak at 5 days [1].
• However, little is known about the expression of CNTF or that of its receptor (CNTFR-alpha) in cases of intracerebral hemorrhage (ICH) [1].
• Upregulation of ciliary neurotrophic factor (CNTF) and CNTF receptor alpha in rat kidney with ischemia-reperfusion injury [2].
• A delayed decrease in the 2.1 kb transcript of CNTFR alpha mRNA in the ischemic cortex was observed in rats subjected to 60 min ischemia followed by 72 h of reperfusion [3].
• In the present study, we examined the temporal and spatial expression profiles of CNTF and CNTF receptor alpha (CNTFR alpha) mRNAs in a focal cerebral ischemia model induced by transient occlusion of the right middle cerebral artery and both common carotid arteries [3].

High impact information on Cntfr

• Consistent with this notion, CNTFR alpha expression could be localized to neurons within all known peripheral targets of CNTF [4].
• Using the polymerase chain reaction, we also demonstrate the presence of CNTF and CNTF receptor alpha mRNA in these same thalamic nuclei [5].
• The widespread expression of CNTF and its principal binding protein, CNTF receptor alpha, in the central and peripheral nervous systems suggests a broader trophic role for this peptide [5].
• In the adult brain, the highest levels of CNTFR alpha immunoreactivity were found in the perikarya, dendrites and, occasionally, the axons of several distinct classes of neurons including hippocampal formation neurons, some sensory neurons, and many neurons involved in motor control [6].
• CNTFR alpha immunoreactivity also was concentrated in the following: perikarya, dendrites, and axons of ventral horn motor neurons in adult spinal cord; perikarya and axons of adult dorsal root ganglion neurons; and axons in adult peripheral nerve [6].

Biological context of Cntfr

• Adenoviral-mediated transfer of ciliary neurotrophic factor (CNTF) to the retina rescued retinal ganglion cells (RGCs) from axotomy-induced apoptosis, presumably via activation of the high affinity CNTF receptor alpha (CNTFRalpha) expressed on RGCs [7].
• Following 4 h of reperfusion, increased expression of CNTFR alpha mRNA was observed in the ipsilateral dentate gyrus, which is opposite to the down-regulation noted in the ischemic cortex [3].
• Analysis of 5HT levels showed no significant difference in the amount of serotonin between wild-type and CNTFR alpha knockout mice at birth, suggesting that the potential to switch phenotype mediated through CNTFR alpha is a latent property of neuroepithelial precursors in the raphe nucleus [8].
• Responsive and non-responsive neurons express comparable levels of STAT3.Therefore, in vivo ciliary neurotrophic factor receptor-initiated STAT3 signal transduction is regulated in a very cell-type-dependent manner [9].
• The neuroepithelium of the neonatal rat displayed a highly selective expression of ciliary neurotrophic factor receptor-alpha in areas which are known to exhibit high rates of postnatal cell proliferation in the germinal zones [10].

Anatomical context of Cntfr

• In situ, myenteric ganglia below the esophagus were CNTFR alpha-immunoreactive by E16-E18 [11].
• To investigate a potential role of CNTF in lesion-induced degeneration and reorganization, we have analyzed the expression of CNTF protein and CNTF receptor alpha (CNTFR alpha) mRNA in the rat dentate gyrus after unilateral entorhinal cortex lesions (ECLs), using immunocytochemistry and nonradioactive in situ hybridization, respectively [12].
• Differential regulation of ciliary neurotrophic factor (CNTF) and CNTF receptor alpha expression in astrocytes and neurons of the fascia dentata after entorhinal cortex lesion [12].
• Differential expression of ciliary neurotrophic factor receptor in skeletal muscle of chick and rat after nerve injury [13].
• To investigate, whether differences in the regulation of CNTF and CNTF receptor alpha (CNTFRalpha) contribute to the differences in PNS and CNS responses to injury, we have studied their expression on the mRNA and protein level in the rat optic nerve following a crush lesion to compare them with the situation in peripheral nerve [14].

Associations of Cntfr with chemical compounds

• Taken together, our findings provided the first extensive analysis on the mRNA expression of CNTFR alpha and the alpha subunit of the acetylcholine receptor in various skeletal muscles of the chick following nerve injury and regeneration [13].
• Expression and androgen regulation of the ciliary neurotrophic factor receptor (CNTFRalpha) in muscles and spinal cord [15].
• No significant changes were found in the proportion of surviving motoneurons expressing calcitonin gene-related peptide, galanin, receptor tyrosine kinase-C or the alpha subunit of the ciliary neurotrophic factor receptor [16].

Physical interactions of Cntfr

• To investigate the role of ciliary neurotrophic factor in the developing and mature brain by defining putative target cells the expression of the ligand-binding alpha-subunit of the ciliary neurotrophic factor receptor was studied in neonatal and adult rat brains using a digoxygenin-labelled probe for in situ hybridization [10].

Regulatory relationships of Cntfr

• In distinct contrast, several other classes of ciliary neurotrophic factor receptor expressing neurons fail to increase phospho-STAT3 levels following ciliary neurotrophic factor treatment, even when ciliary neurotrophic factor is applied at high concentrations [9].

Other interactions of Cntfr

• In many areas (e.g. in thalamic, midbrain and pontine nuclei) ciliary neurotrophic factor receptor-alpha expression became undetectable with maturation; however, there were other areas (e.g., olfactory bulb, cerebral cortex and hypothalamus) where expression was higher in the adult [10].

Analytical, diagnostic and therapeutic context of Cntfr

• The expression of CNTF and CNTFR alpha was monitored by reverse transcription-PCR, in situ hybridization, immunoblotting, immunohistochemistry, and electron microscopy [2].
• In situ hybridization studies revealed constitutive expression of CNTFR alpha mRNA in the majority of neurons in the brain [3].
• No signal of CNTFR alpha mRNA was detected within the infarct region following 3 days of reperfusion [3].
• These results indicate that survival of motoneurons after neonatal axotomy and CNTF treatment is associated with increased CNTF receptor alpha expression [17].
• We have used reverse transcription/polymerase chain reaction (RT-PCR) and Western blotting with an anti-peptide antibody to study the expression of the alpha-component of the receptor for ciliary neurotrophic factor (CNTFR alpha) in rat nervous tissue [18].

References