Purification to Apparent Homogeneity and Biochemical Characterization of Human Pluripotent Hematopoietic Colony-Stimulating Factor

Welte, Karl; Platzer, E.; Gabrilove, Janice; Lü, Li; Levi, E.; Polivka, A; Mertelsmann, Roland; Moore, M. A. S.

doi:10.1007/978-3-642-70385-0_82

Cited by 11 publications

(10 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Granulocyte-colony-stimulating factor is a cytokine that stimulates the proliferation and the differentiation of myeloid precursors [1] and has been in clinical use for more than 10 years in indications related to counteracting chemotherapy-induced neutropenia or for bone-marrow transplantations [2]. We and others discovered that G-CSF also acts as a growth factor in the brain, and shows protective and regenerative properties in a number of CNS disease models [3-6].…”

Section: Introductionmentioning

confidence: 99%

G-CSF protects motoneurons against axotomy-induced apoptotic death in neonatal mice

et al. 2010

View full text Add to dashboard Cite

BackgroundGranulocyte colony stimulating factor (G-CSF) is a growth factor essential for generation of neutrophilic granulocytes. Apart from this hematopoietic function, we have recently uncovered potent neuroprotective and regenerative properties of G-CSF in the central nervous system (CNS). The G-CSF receptor and G-CSF itself are expressed in α motoneurons, G-CSF protects motoneurons, and improves outcome in the SOD1(G93A) transgenic mouse model for amyotrophic lateral sclerosis (ALS). In vitro, G-CSF acts anti-apoptotically on motoneuronal cells. Due to the pleiotrophic effects of G-CSF and the complexity of the SOD1 transgenic ALS models it was however not possible to clearly distinguish between directly mediated anti-apoptotic and indirectly protective effects on motoneurons. Here we studied whether G-CSF is able to protect motoneurons from purely apoptotic cell death induced by a monocausal paradigm, neonatal sciatic nerve axotomy.ResultsWe performed sciatic nerve axotomy in neonatal mice overexpressing G-CSF in the CNS and found that G-CSF transgenic mice displayed significantly higher numbers of surviving lumbar motoneurons 4 days following axotomy than their littermate controls. Also, surviving motoneurons in G-CSF overexpressing animals were larger, suggesting additional trophic effects of this growth factor.ConclusionsIn this model of pure apoptotic cell death the protective effects of G-CSF indicate direct actions of G-CSF on motoneurons in vivo. This shows that G-CSF exerts potent anti-apoptotic activities towards motoneurons in vivo and suggests that the protection offered by G-CSF in ALS mouse models is due to its direct neuroprotective activity.

show abstract

Section: Introductionmentioning

confidence: 99%

G-CSF protects motoneurons against axotomy-induced apoptotic death in neonatal mice

et al. 2010

View full text Add to dashboard Cite

show abstract

“…G‐CSF has been accepted to stimulate the proliferation, survival and maturation of cells committed to the granulocyte lineage through binding to the specific G‐CSF receptor 17 . G‐CSF has been widely used as adjunctive medication to chemotherapy and in mobilizing stem cells for bone marrow transplantation 34 .…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, we evaluated whether ex vivo treatments with granulocyte‐colony stimulating factor (G‐CSF) could modify biological properties of BMSC from aged rats and enhance its therapeutic effects in an animal model of traumatic brain injury. G‐CSF is a 20‐kDa glycoprotein and is well known to stimulate the proliferation, survival and maturation of cells committed to the neutrophil precursors and mature neutrophils through binding to specific G‐CSF receptors 17 . Hokari et al .…”

Section: Introductionmentioning

confidence: 99%

Impact of ageing on biological features of bone marrow stromal cells (BMSC) in cell transplantation therapy for CNS disorders: Functional enhancement by granulocyte‐colony stimulating factor (G‐CSF)

et al. 2011

View full text Add to dashboard Cite

This study was designed to clarify the effects of donor age on biological features of bone marrow stromal cells (BMSC), one of the candidates for cell transplantation therapy for CNS disorders, because many aged patients might require such therapy. This study was also aimed to test whether ex vivo treatments with granulocyte-colony stimulating factor (G-CSF) could modify biological properties of BMSC from aged donors and enhance its therapeutic effects in an animal model of traumatic brain injury. The BMSC were harvested from young (6-week-old) and aged (100-week-old) rats. The ageing significantly increased the senescence-associated β-galactosidase (SA-β-gal) activity of the cultured BMSC, and decreased their proliferative capacity and production of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF). As the next step, the rats were subjected to brain freezing injury by applying liquid nitrogen onto the neocortex through the thinned skull. The 6-week BMSC, 100-week BMSC, G-CSF-treated 100-week BMSC or vehicle were stereotactically injected into the ipsilateral striatum at 7 days post-injury. Transplantation of the 6-week BMSC, but not 100-week BMSC, significantly improved locomotor function. However, treatment of the 100-week BMSC with 0.1 µmol of G-CSF significantly improved their proliferation activity and growth factor production, and recovered therapeutic effects in the injured brain. In conclusion, donor age may largely determine biological aspects of BMSC. G-CSF may contribute to improve the outcome of BMSC transplantation therapy for CNS disorders in aged patients.

show abstract

“…Granulocyte-colony stimulating factor (G-CSF) is a cytokine first described as a hematopoietic growth factor that stimulates proliferation and differentiation of myeloid precursors [84]. Furthermore, G-CSF protects motor neurons, ameliorates functional outcomes, and improves lifespan of SOD-1(G93A) mice when administered subcutaneously [85].…”

Section: Delivery Of Factors For Neuroprotectionmentioning

confidence: 99%

Research advances in gene therapy approaches for the treatment of amyotrophic lateral sclerosis

Nizzardo

Simone

Falcone

et al. 2011

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease of motor neurons that causes progressive muscle weakness, paralysis, and premature death. No effective therapy is available. Research in the motor neuron field continues to grow, and recent breakthroughs have demonstrated the possibility of completely achieving rescue in animal models of spinal muscular atrophy, a genetic motor neuron disease. With adeno-associated virus (AAV) vectors, gene transfer can be achieved with systemic non-invasive injection and minimal toxicity. In the context of this success, we review gene therapy approaches for ALS, considering what has been done and the possible future directions for effective application of the latest generation of vectors for clinical translation. We focus on recent developments in the areas of RNA/antisense-mediated silencing of specific ALS causative genes like superoxide dismutase-1 and other molecular pathogenetic targets, as well as the administration of neuroprotective factors with viral vectors. We argue that gene therapy offers new opportunities to open the path for clinical progress in treating ALS.

show abstract

Purification to Apparent Homogeneity and Biochemical Characterization of Human Pluripotent Hematopoietic Colony-Stimulating Factor

Cited by 11 publications

References 16 publications

G-CSF protects motoneurons against axotomy-induced apoptotic death in neonatal mice

G-CSF protects motoneurons against axotomy-induced apoptotic death in neonatal mice

Impact of ageing on biological features of bone marrow stromal cells (BMSC) in cell transplantation therapy for CNS disorders: Functional enhancement by granulocyte‐colony stimulating factor (G‐CSF)

Research advances in gene therapy approaches for the treatment of amyotrophic lateral sclerosis

Contact Info

Product

Resources

About