Expression of ciliary neurotrophic factor (CNTF) and its tripartite receptor complex by cells of the human optic nerve head. (1/16)

PURPOSE: Ciliary neurotrophic factor (CNTF) promotes gene expression, cell survival and differentiation in various types of peripheral and central neurons, glia and nonneural cells. The level of CNTF rises rapidly upon injury to neural tissue, suggesting that CNTF exerts its cytoprotective effects after release from cells via mechanisms induced by cell injury. The purpose of this study was to determine if cells in the optic nerve head express CNTF and its tripartite receptor complex. METHODS: Well-established optic nerve head astrocytes (ONHA) and lamina cribrosa (LC) cell cultures were derived from normal human donors. Total RNA was reverse transcribed and polymerase chain reaction (PCR) amplified for mRNA detection. Cytoplasmic protein expression was determined by immunocytochemistry and Western blot analysis of the cellular lysates. Serum free medium was concentrated and used for detecting extracellular proteins. CNTF complexed with CNTFR-alpha was assayed by immunoprecipitation. RESULTS: Cells isolated from the human optic nerve head express CNTF and its tripartite receptor complex members (CNTFR-alpha, gp130, LIFR-beta). CONCLUSIONS: Taken together, these data suggest a possible neuroprotective role of CNTF in the optic nerve head.  (+info)

Influence of maternal undernutrition and overfeeding on cardiac ciliary neurotrophic factor receptor and ventricular size in fetal sheep. (2/16)

Intrauterine nutrition status is reported to correlate with risk of cardiovascular diseases in adulthood. Either under- or overnutrition during early to mid gestation contributes to altered fetal growth and ventricular geometry. This study was designed to examine myocardial expression of ciliary neurotrophic factor receptor alpha (CNTFRalpha) and its downstream mediator signal transducer and activator of transcription 3 (STAT3) on maternal undernutrition- or overnutrition-induced changes in fetal heart weight. Multiparous ewes were fed with 50% [nutrient-restricted (NR)], 100% (control) or 150% [overfed (OF)] of National Research Council requirements from 28 to 78 days of gestation (dG; term, 148 dG). Ewes were euthanized on Day 78, and the gravid uteri and fetuses recovered. Ventricular protein expression of CNTFRalpha, STAT3, phosphorylated STAT3, insulin-like growth factor I receptor (IGF-1R), and IGF binding protein 3 (IGFBP3) were quantitated using Western blot. Plasma cortisol levels were higher in both NR and OF fetuses, whereas plasma IGF-1 levels were lower and higher in NR and OF fetuses. Fetal weights were reduced by 29.9% in NR ewes and were increased by 22.2% in fetuses from OF ewes compared to control group. Nutrient restriction did not affect fetal heart or ventricular weights, whereas overfeeding increased heart and ventricular weights. Protein expression of CNTFRalpha in fetal ventricular tissue was reduced in OF group, whereas STAT3 and phosphorylated STAT3 levels were reduced in both NR and OF groups. Expression of IGF-1R and IGFBP3 was unaffected in either NR or OF group. These data suggested that, compared with maternal undernutrition, intrauterine overfeeding during early to mid gestation is associated with increases in fetal blood concentrations of cortisol and IGF-1, in association with ventricular hypertrophy where reduced expression of CNTFRalpha and STAT3 may play a role.  (+info)

Co-administration of ciliary neurotrophic factor with its soluble receptor protects against neuronal death and enhances neurite outgrowth. (3/16)

Attempts to promote neuronal survival and repair with ciliary neurotrophic factor (CNTF) have met with limited success. The variability of results obtained with CNTF may, in part, reflect the fact that some of the biological actions of the cytokine are mediated by a complex formed between CNTF and its specific receptor, CNTFRalpha, which exists in both membrane-bound and soluble forms. In this study, we compared the actions of CNTF alone and CNTF complexed with soluble CNTFRalpha (hereafter termed "Complex") on neuronal survival and growth. Although CNTF alone produced limited effects, Complex protected against glutamate-mediated excitotoxicity via gap junction-dependent and -independent mechanisms. Further examination revealed that only Complex promoted neurite outgrowth. Differential gene expression analysis revealed that, compared with CNTF alone, Complex differentially regulates several neuroprotective and neurotrophic genes. Collectively, these findings indicate that CNTF exerts more robust effects on neuronal survival and growth when applied in combination with its soluble receptor.  (+info)

Neuroinflammation facilitates LIF entry into brain: role of TNF. (4/16)

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A putative physiological role of hypothalamic CNTF in the control of energy homeostasis. (5/16)

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CNTF-evoked activation of JAK and ERK mediates the functional expression of T-type Ca2+ channels in chicken nodose neurons. (6/16)

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Functional CNTF receptor alpha subunit restored by its recombinant in corneal endothelial cells in stored human donor corneas: connexin-43 upregulation. (7/16)

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Ciliary neurotrophic factor (CNTF) plus soluble CNTF receptor alpha increases cyclooxygenase-2 expression, PGE2 release and interferon-gamma-induced CD40 in murine microglia. (8/16)

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