INT8801

Context Info Confidence 0.74 First Reported 1991 Last Reported 2010 Negated 2 Speculated 3 Reported most in Body Documents 71 Total Number 74 Disease Relevance 45.60 Pain Relevance 10.83

extracellular space (Csf3) extracellular region (Csf3) enzyme binding (Csf3)

Anatomy Link Frequency motoneurons 12 granulocyte 7 macrophages 4 kidney 3 plasma 2 Csf3 (Mus musculus)

Pain Link Frequency Relevance Heat cytokine 145 100.00 Angina 1 99.84 Central nervous system 175 99.82 Sciatic nerve 375 99.48 Inflammatory response 192 99.44 Spinal cord 350 98.84 rheumatoid arthritis 120 98.76 Inflammation 334 96.96 ischemia 25 96.44 abdominal pain 3 95.64

Disease Link Frequency Relevance Heat Neutropenia 574 100.00 Coronary Artery Disease 4 100.00 Bladder Cancer 9 99.98 Cv General 3 Under Development 1 99.84 Targeted Disruption 436 99.78 Thrombophilia 1 99.64 Pancreatic Cancer 7 99.60 Motor Neuron Diseases 450 99.56 Infection 92 99.48 INFLAMMATION 557 99.44

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).

Spec (examined) Gene_expression (expression) of G-CSF in sciatic nerve associated with sciatic nerve

1) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.35 Pain Relevance 0.27

In conclusion, the G-CSF receptor is expressed at the neonatal stage and its expression is increased in response to axotomy.

Gene_expression (expressed) of G-CSF

2) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.75 Pain Relevance 0.31

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.

Gene_expression (express) of G-CSF

3) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.43 Pain Relevance 0.20

CNS- targeted overexpression of G-CSF protects motoneurons against cell death in neonatal pups

Gene_expression (overexpression) of G-CSF in motoneurons associated with central nervous system and death

4) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.79 Pain Relevance 0.28

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.

Gene_expression (overexpress) of G-CSF in motoneurons associated with targeted disruption and central nervous system

5) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.74 Pain Relevance 0.26

Overexpression of G-CSF protects lumbar motoneurons to an extent that is comparable to many of the classic neurotrophic factors.

Gene_expression (Overexpression) of G-CSF in motoneurons

6) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.28 Pain Relevance 0.04

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.

Gene_expression (overexpressing) of G-CSF in motoneurons associated with targeted disruption

7) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.40 Pain Relevance 0.09

On top of a relative increase of motoneuron numbers following overexpression of G-CSF, we also noted an increase of about 100 ?

Gene_expression (overexpression) of G-CSF in motoneuron

8) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.38 Pain Relevance 0.03

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].

Gene_expression (expression) of G-CSF in neurons associated with cv general 4 under development, ischemia, neurodegenerative disease and motor neuron diseases

9) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.41 Pain Relevance 0.24

;-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).

Gene_expression (overexpression) of G-CSF in forebrain associated with spinal cord

10) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.25 Pain Relevance 0.25

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.

Gene_expression (produced) of Recombinant granulocyte colony-stimulating factor in granulocyte

11) Confidence 0.66 Published 1991 Journal Drugs Section Abstract Doc Link 1717226 Disease Relevance 0.20 Pain Relevance 0.10

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).

Gene_expression (expression) of G-CSF

12) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.06 Pain Relevance 0.07

(B) Quantitative RT-PCR analysis of G-CSF expression normalized to GAPDH after LPS-stimulation of THP-1 cells.

Gene_expression (expression) of G-CSF in THP-1

13) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0 Pain Relevance 0

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).

Gene_expression (expression) of G-CSF

14) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.87 Pain Relevance 0.27

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).

Gene_expression (expression) of G-CSF

15) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.07 Pain Relevance 0.08

(A) Quantitative RT-PCR analysis of G-CSF expression normalized to ?

Gene_expression (expression) of G-CSF

16) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.06 Pain Relevance 0.06

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.

Gene_expression (expression) of G-CSF associated with inflammation

17) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.79 Pain Relevance 0.36

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).

Gene_expression (expression) of Csf3 gene

18) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.07 Pain Relevance 0.08

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.

Neg (not) Gene_expression (express) of G-CSF

19) Confidence 0.64 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.44 Pain Relevance 0.19

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.

Gene_expression (overexpressors) of G-CSF in motoneurons associated with targeted disruption

20) Confidence 0.64 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.89 Pain Relevance 0.03

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