INT8801
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
We therefore examined expression of the G-CSF receptor by quantitative PCR of whole spinal cords 4 days following neonatal axotomy of the right sciatic nerve (i.e. on postnatal day 9). | |||||||||||||||
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In conclusion, the G-CSF receptor is expressed at the neonatal stage and its expression is increased in response to axotomy.
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The three groups are a.) mice not harbouring any transgene ("wt"), b.) mice harbouring only the BEG2 transgene (which do not express G-CSF), and c.) mice harbouring both the BEG2 transgene and the CaMKII-tTA driver, that do express G-CSF. | |||||||||||||||
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CNS- targeted overexpression of G-CSF protects motoneurons against cell death in neonatal pups | |||||||||||||||
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We chose to use transgenic mice that overexpress G-CSF in the CNS as an endogenous "delivery system" to study effects of increased concentration of G-CSF on the lesioned motoneurons. | |||||||||||||||
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Overexpression of G-CSF protects lumbar motoneurons to an extent that is comparable to many of the classic neurotrophic factors. | |||||||||||||||
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This analysis revealed that only 50 - 60% of the motoneurons survived in the genotypes lacking the CaMK-tta driver transgene, whereas close to 90% of the motoneurons survived in the double transgenic mice (i.e. in animals overexpressing G-CSF) (BEG -/T CaMK-/T (88.76 ± 4.32%) vs. | |||||||||||||||
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On top of a relative increase of motoneuron numbers following overexpression of G-CSF, we also noted an increase of about 100 ? | |||||||||||||||
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The expression of G-CSF receptor is induced by neurons under neurodegenerative conditions such as after cerebral ischemia or in ALS, presumably as an endogenous protective response [6,7]. | |||||||||||||||
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;-promoter directed G-CSF overexpression in the forebrain leads to a strong elevation of G-CSF levels in the neonatal brain and spinal cord (P9; 28.00 ± 11.60 vs 0.24 ± 0.23 pg/mg tissue protein; p < 0.05) (Figure 3). | |||||||||||||||
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Recombinant granulocyte colony-stimulating factor (rG-CSF) is a glycoprotein hormone which has been produced in mammalian cells and, in a nonglycosylated form, in the bacterium Escherichia coli through recombinant DNA technology. | |||||||||||||||
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Interestingly, among the immune response genes induced by LPS treatment, expression of the Csf3 gene encoding G-CSF was significantly down-regulated in LNA-antimiR-treated cells compared to the untreated and LNA controls (P = 0.014 and P = 0.008, respectively, Student's t-test, two-sided), implying that the regulation of G-CSF expression is mediated by miR-155 (Figure 5A, Supplementary table S1). | |||||||||||||||
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(B) Quantitative RT-PCR analysis of G-CSF expression normalized to GAPDH after LPS-stimulation of THP-1 cells. | |||||||||||||||
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Thus, it is possible that c/ebp Beta, which is modulated by miR-155, acts in part by fine-tuning G-CSF expression levels, consistent with a c/ebp Beta binding motif in the promoter of G-CSF (15,32). | |||||||||||||||
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Interestingly, among the immune response genes induced by LPS treatment, expression of the Csf3 gene encoding G-CSF was significantly down-regulated in LNA-antimiR-treated cells compared to the untreated and LNA controls (P = 0.014 and P = 0.008, respectively, Student's t-test, two-sided), implying that the regulation of G-CSF expression is mediated by miR-155 (Figure 5A, Supplementary table S1). | |||||||||||||||
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(A) Quantitative RT-PCR analysis of G-CSF expression normalized to ? | |||||||||||||||
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Moreover, we report that miR-155 mediates regulation of G-CSF expression, thereby underscoring the role of miR-155 in fine-tuning important regulatory networks during inflammation.
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Interestingly, among the immune response genes induced by LPS treatment, expression of the Csf3 gene encoding G-CSF was significantly down-regulated in LNA-antimiR-treated cells compared to the untreated and LNA controls (P = 0.014 and P = 0.008, respectively, Student's t-test, two-sided), implying that the regulation of G-CSF expression is mediated by miR-155 (Figure 5A, Supplementary table S1). | |||||||||||||||
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The three groups are a.) mice not harbouring any transgene ("wt"), b.) mice harbouring only the BEG2 transgene (which do not express G-CSF), and c.) mice harbouring both the BEG2 transgene and the CaMKII-tTA driver, that do express G-CSF. | |||||||||||||||
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Although we do not see significant effects on the number of contralateral motoneurons in the different transgenic crosses, there is an interesting trend (p = 0.1) towards more motoneurons contralaterally in the G-CSF overexpressors compared to littermates not transgenic for the CaMKII tta driver. | |||||||||||||||
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