Granulocyte-Colony Stimulating Factor (G-CSF) for stroke: an individual patient data meta-analysis

England, Timothy J.; Sprigg, Nikola; Алашеев, А. М.; Belkin, Andrey; Kumar, Amit; Prasad, Kameshwar; Bath, Philip M

doi:10.1038/srep36567

Cited by 33 publications

(26 citation statements)

References 35 publications

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“…It has the potential to accelerate repair and regeneration of damaged organs. A number of studies have revealed its accelerating effects on the recovery process of acute myocardial infarction [24,25] and cerebral stroke [26,27]. With regard to the liver, G-CSF was previously shown to stimulate the mobilization and proliferation of HPC in both rodents [10] and humans [11,12] suffering from advanced liver diseases.…”

Section: Discussionmentioning

confidence: 99%

“…This is particularly crucial in patients with liver cirrhosis who are already associated with splenomegaly as a result of portal hypertension. Acute tissue injuries such as myocardial infusion and cerebral stroke need only a single G-CSF injection for their repair [24][25][26][27]. In marked contrast to this, liver fibrosis/cirrhosis is a chronic progressive disease that may require repeated G-CSF administration, increasing the risk of splenic rupture as the total number of G-CSF injections increases.…”

Section: Discussionmentioning

confidence: 99%

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Identification of a Novel Bone Marrow Cell-Derived Accelerator of Fibrotic Liver Regeneration Through Mobilization of Hepatic Progenitor Cells in Mice

et al. 2018

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Granulocyte colony stimulating factor (G-CSF) has been reported to ameliorate impaired liver function in patients with advanced liver diseases through mobilization and proliferation of hepatic progenitor cells (HPCs). However, the underlying mechanisms remain unknown. We previously showed that G-CSF treatment increased the number of bone marrow (BM)-derived cells migrating to the fibrotic liver following repeated carbon tetrachloride (CCl 4 ) injections into mice. In this study, we identified opioid growth factor receptor-like 1 (OGFRL1) as a novel BM cellderived accelerator of fibrotic liver regeneration in response to G-CSF treatment. Endogenous Ogfrl1 was highly expressed in the hematopoietic organs such as the BM and spleen, whereas the liver contained a relatively small amount of Ogfrl1 mRNA. Among the peripheral blood cells, monocytes were the major sources of OGFRL1. Endogenous Ogfrl1 expression in both the peripheral blood monocytes and the liver was decreased following repeated CCl 4 injections. An intrasplenic injection of cells overexpressing OGFRL1 into CCl 4 -treated fibrotic mice increased the number of HPC and stimulated proliferation of hepatic parenchymal cells after partial resection of the fibrotic liver. Furthermore, overexpression of OGFRL1 in cultured HPC accelerated their differentiation as estimated by increased expression of liver-specific genes such as hepatocyte nuclear factor 4α, cytochrome P450, and fatty acid binding protein 1, although it did not affect the colony forming ability of HPC. These results indicate a critical role of OGFRL1 in the mobilization and differentiation of HPC in the fibrotic liver, and administration of OGFRL1-expressing cells may serve as a potential regenerative therapy for advanced liver fibrosis. STEM CELLS 2019; 37:89-101 SIGNIFICANT STATEMENTThe liver is well-known to possess high regenerative capacity in response to injury. However, its regeneration is impaired in the case of advanced liver fibrosis when mature hepatocytes can hardly self-proliferate. Hepatic progenitor cells (HPCs) have been implicated as a source of hepatocytes in regeneration of the fibrotic liver, and efficient mobilization of HPC represents an important strategy to treat liver fibrosis. This study identified a novel blood cell-derived factor that accelerates regeneration of the fibrotic liver through mobilization of HPC. Administration of cells overexpressing this factor may serve as a potential regenerative therapy for advanced liver fibrosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Identification of a Novel Bone Marrow Cell-Derived Accelerator of Fibrotic Liver Regeneration Through Mobilization of Hepatic Progenitor Cells in Mice

et al. 2018

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“…These authors found that G-CSF was not different from placebo on the primary end-point, modified Rankin scale score at day 90. A meta-analysis of studies introducing G-CSF days to years post-stroke did not find favorable effects [ 61 ].…”

Section: Therapies To Promote Neural Repair After Strokementioning

confidence: 99%

Treatments to Promote Neural Repair after Stroke

Cramer

2018

J Stroke

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Stroke remains a major cause of human disability worldwide. In parallel with advances in acute stroke interventions, new therapies are under development that target restorative processes. Such therapies have a treatment time window measured in days, weeks, or longer and so have the advantage that they may be accessible by a majority of patients. Several categories of restorative therapy have been studied and are reviewed herein, including drugs, growth factors, monoclonal antibodies, activity-related therapies including telerehabilitation, and a host of devices such as those related to brain stimulation or robotics. Many patients with stroke do not receive acute stroke therapies or receive them and do not derive benefit, often surviving for years thereafter. Therapies based on neural repair hold the promise of providing additional treatment options to a majority of patients with stroke.

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“…In particular, granulocytecolony stimulating factor (G-CSF) was evaluated in the AX200 for Ischemic Stroke Study (AXIS). The AXIS study concluded that G-CSF is tolerated when given within 12 hours of an ischemic stroke, however, a meta-analysis conducted after the AXIS study discovered that administration of G-CSF at any time span, days to years, post-stroke had unfavorable effects [21][22][23][24].…”

Section: Growth Factors Stimulate Angiogenesis Cell Proliferation Cmentioning

confidence: 99%

Monoclonal Antibody as an Emerging Therapies for Ischemic Stroke

Woods¹,

Jiang²,

Chu³

2019

Preprint

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Acute ischemic strokes are the third leading cause of death and the leading cause of neurological disability worldwide. The oxygen and glucose deprivation associated with ischemic strokes not only leads to neuronal cell death, but also increases the inflammatory response and decreases functional output of the brain. The only intervention approved by US Federal Drug and Food Administration for treatment of ischemic strokes is tissue plasminogen activator (tPA), however, such treatment can only be given within 4.5 hours of the onset of stroke-like symptoms. This narrow time-range limits its application, and it also might induce detrimental rather than beneficial effects to stroke patients by treatment of the tPA. In order to reduce the infarct volume of an acute ischemic stroke while increasing the time period for treatment, emerging therapies reveal great potential by targeting inflammation, growth factors, ion channels, and neurotransmitter receptors with monoclonal antibody (MAB). With successfully application in the treatment of cancer patient by MAB, in this review, we will focus on recent advances on stroke therapy by using MAB on the treatment of stroke by targeting inflammation, growth factors, ion channels, and neurotransmitter receptors. Therefore, developing specific MAB targeting the signaling pathway of stroke will contribute to stroke therapy.

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Granulocyte-Colony Stimulating Factor (G-CSF) for stroke: an individual patient data meta-analysis

Cited by 33 publications

References 35 publications

Identification of a Novel Bone Marrow Cell-Derived Accelerator of Fibrotic Liver Regeneration Through Mobilization of Hepatic Progenitor Cells in Mice

Identification of a Novel Bone Marrow Cell-Derived Accelerator of Fibrotic Liver Regeneration Through Mobilization of Hepatic Progenitor Cells in Mice

Treatments to Promote Neural Repair after Stroke

Monoclonal Antibody as an Emerging Therapies for Ischemic Stroke

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