2011
DOI: 10.1186/1742-2094-8-74
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Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis

Abstract: BackgroundGranulocyte colony stimulating factor (GCSF) is protective in animal models of various neurodegenerative diseases. We investigated whether pegfilgrastim, GCSF with sustained action, is protective in a mouse model of amyotrophic lateral sclerosis (ALS). ALS is a fatal neurodegenerative disease with manifestations of upper and lower motoneuron death and muscle atrophy accompanied by inflammation in the CNS and periphery.MethodsHuman mutant G93A superoxide dismutase (SOD1) ALS mice were treated with peg… Show more

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Cited by 63 publications
(70 citation statements)
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“…Additionally, it is not known whether the previously described markers for muscle degeneration/regeneration, some of which correlate with longevity in in SOD1-G93A animals [25,26], could be affected by G-CSF analogs in vivo. Here we have confirmed the results of Pollari et al [19] by showing the prosurvival and HSC-stimulatory capacity of PEGF in SOD1-G93A mice. Furthermore, we have demonstrated the effect of long-term PEGF treatment on modulating the expression of various mRNA markers in vivo as well as the direct effect of G-CSF on SOD1-G93A SKM myoblast proliferation in vitro.…”
Section: Introductionsupporting
confidence: 81%
See 1 more Smart Citation
“…Additionally, it is not known whether the previously described markers for muscle degeneration/regeneration, some of which correlate with longevity in in SOD1-G93A animals [25,26], could be affected by G-CSF analogs in vivo. Here we have confirmed the results of Pollari et al [19] by showing the prosurvival and HSC-stimulatory capacity of PEGF in SOD1-G93A mice. Furthermore, we have demonstrated the effect of long-term PEGF treatment on modulating the expression of various mRNA markers in vivo as well as the direct effect of G-CSF on SOD1-G93A SKM myoblast proliferation in vitro.…”
Section: Introductionsupporting
confidence: 81%
“…Current evidence suggests a multiphased immune response where an early neuroprotective function responsible for clearance of cellular debris shifts towards a cytotoxic/neurodegenerative response when the disease aggravates [17,18]. G-CSF is thought to exert its effects through the inhibition of neuroinflammation and, consistently, PEGF has been shown to attenuate both astro- and microgliosis and increase survival of SOD1-G93A ALS mice [12,19,20]. …”
Section: Introductionmentioning
confidence: 99%
“…Our results show that G-CSF treatment abolished the DHCA-dependent increases in IL-6 and TNF-α, two proteins for which an increase is correlated with increased brain injury. This result is consistent with the work of Pollari et al [63] who reported that, in vitro, exposure of cell cultures to G-CSF reduced their TNF-α production. In our study treatment with G-CSF also decreased the levels of MIP-3 and NAP-2, two cytokines believed to play a role in neuronal cell injury.…”
Section: Discussionsupporting
confidence: 83%
“…The time to clinical endstage is increased by 10% in SOD1 G93A mice receiving G-CSF. Importantly, while G-CSF was initially used for its neuroprotective effects and its ability to readily cross the blood-brain barrier [203,204], further characterization of treated SOD1 G93A mice shows a reduced spinal cord astrocytosis and microgliosis as well as an increased availability of migratory healing monocytes, suggesting that G-CSF may be beneficial in ALS via its modulation of neuroinflammation [205].…”
Section: Advances and Possible Applications Of Protein Therapymentioning
confidence: 99%