Granulocyte-colony stimulating factor in experimental stroke and its effects on infarct size and functional outcome: A systematic review

England, Timothy J.; Gibson, Claire L.; Bath, Philip M.W.

doi:10.1016/j.brainresrev.2009.09.002

Cited by 60 publications

(45 citation statements)

References 56 publications

(66 reference statements)

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“…Additionally, there were acinar and ductal diameters significant decrease than MTX group and nonsignificant increase versus group I. These findings are supported by the previously reported therapeutic effect of G-CSF on liver, kidney and brain lesions and irradiated salivary glands [15,[57][58][59] . Such G-CSF preservative influence was explained by its BMHSCs mobilizing effect [60] supported in this work by BMHSCs significant increase in Neupogen-treated group compared to MTX group.…”

Section: Discussionsupporting

confidence: 87%

Therapeutic mechanisms of granulocyte-colony stimulating factor in methotrexate-induced parotid lesion in adult rats and possible role of telocytes: A histological study

Omar

Yousry

Farag

2018

Egyptian Journal of Histology

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Background: Worldwide, Methotrexate (MTX) is used to treat neoplastic and non-neoplastic diseases despite its severe side-effects. One of these adverse effects is salivary dysfunction that can aggravate MTX mucotoxic effects. Such effects interfere with the patients' quality of life and increase morbidities and mortalities. Available treatments for salivary dysfunction have many drawbacks. Mobilization of bone marrow haematopoietic stem cells (BMHSCs) by human Granulocyte-Colony Stimulating Factor (G-CSF) used in many diseases showed promising results. Aim of the work: To detect the therapeutic effect of G-CSF on MTX-induced parotid lesion highlighting its possible mechanisms and the role of telocytes. Materials and Methods: Forty-one albino rats were divided into 3 groups; control, MTX and Neupogen-treated groups. All animals were weighed and sacrificed after 6 days. Parotid homogenates of 6 rats from each group were used to measure total protein concentration, amylase activity and malondialdehyde (MDA) value. The right parotids of the remaining animals of each group were processed to Paraffin blocks while, the left ones were processed to resin blocks. Paraffin sections stained with Hematoxylin and Eosin and immunohistochemical stains for CD34 and platelet-derived growth factor receptor-alpha (PDGFR-α) as well as resin semithin and ultrathin sections were examined. Body weight, biochemical results, number of immune-positive cells, difference between numbers of CD34+ and PDGFR-α+ cells (stem cells number), acini and ducts numbers and diameters were statistically analysed. Results: MTX group revealed diarrhoea, decreased body weight in addition to, degenerated acinar and ductal cells, and telocytes. However, Neupogen-treated group demonstrated almost normal histological features. Immunohistochemically, the treated group showed significant increase in CD34+ cells, PDGFR-α + cells and stem cells number versus MTX group. Conclusions: G-CSF had a therapeutic effect on MTX-induced parotid degeneration through its direct effects, BMHSCs mobilization and telocytes preservation.

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Section: Discussionsupporting

confidence: 87%

Therapeutic mechanisms of granulocyte-colony stimulating factor in methotrexate-induced parotid lesion in adult rats and possible role of telocytes: A histological study

Omar

Yousry

Farag

2018

Egyptian Journal of Histology

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“…The regenerative potential by G-CSF, apart from its neuroprotective power in the acute phase of stroke, has been shown in various studies. [13][14][15] In the present study, we can show that postischemic G-CSF treatment, in fact, causes an increased functional outcome concerning motor and sensorimotor qualities. However, its combination with CIMT, by concurrent application as well as by sequential treatment, failed to further enhance the beneficial effect.…”

Section: Discussionsupporting

confidence: 58%

Successful Regeneration After Experimental Stroke by Granulocyte-Colony Stimulating Factor Is Not Further Enhanced by Constraint-Induced Movement Therapy Either in Concurrent or in Sequential Combination Therapy

Diederich

Quennet

Bauer

et al. 2012

Stroke

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Background and Purpose— Both application of granulocyte-colony stimulating factor (G-CSF) and constraint-induced movement therapy (CIMT) have been shown to improve outcome after experimental stroke. The aim of the present study was to determine whether concurrent or sequential combination of both therapies will further enhance therapeutic benefit and whether specific modifications in the abundance of various neurotransmitter receptors do occur. Methods— Adult male Wistar rats were subjected to photothrombotic ischemia and assigned to the following treatment groups (n=20 each): (1) ischemic control (saline); (2) CIMT (CIMT between poststroke Days 2 and 11; (3) G-CSF (10 μg/kg G-CSF daily between poststroke Days 2 and 11; (4) combined concurrent group (CIMT plus 10 μg/kg G-CSF daily between poststroke Days 2 and 11; and (5) combined sequential group (CIMT between poststroke Days 2 and 11 and 10 μg/kg G-CSF daily between poststroke Days 12 and 21, respectively). Rats were functionally tested before and up to 4 weeks after ischemia. Quantitative receptor autography was performed for N -methyl- d -aspartate, AMPA, and GABA A receptors. Results— Significant improvement of functional outcome was seen in all groups treated with G-CSF alone and in either combination with CIMT, whereas CIMT alone failed to enhance recovery. Infarct sizes and remaining cortical tissue did not differ in the various treatment groups. Failure of significant benefit in the CIMT group was associated with a shift toward inhibition in perilesional and remote cortical regions. Conclusions— Our findings disclose G-CSF as the major player for enhanced recovery after experimental stroke, preventing a shift toward inhibition as seen in the CIMT group.

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“…To date, G-CSF PBSC mobilization has been generally regarded as a practical and feasible source of cells for therapeutic angiogenesis [27][28][29]. However, a recent metaanalysis reported that G-CSF infusion alone had no significant clinical benefit in myocardial infarction [30], and it was reported that G-CSF-mobilized PBSCs were less effective in inducing ulcer healing than were BMSCs [31].…”

Section: Introductionmentioning

confidence: 99%

Granulocyte colony‐stimulating factor (G‐CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells for vascular regeneration therapy

Tura

Crawford

Barclay

et al. 2010

Journal of Thrombosis and Haemostasis

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Summary. Background: The most common source of hematopoietic progenitor cells (HPCs) for hematopoietic reconstitution comprises granulocyte colony‐stimulating factor (G‐CSF)‐mobilized peripheral blood stem cells (PBSCs). It has been proposed that endothelial progenitor cells (EPCs) share precursors with HPCs, and that EPC release may accompany HPC mobilization to the circulation following G‐CSF administration. Objective: To investigate EPC activity following HPC mobilization, and the direct effects of exogenous G‐CSF administration on human umbilical vein endothelial cells (HUVECs) and endothelial outgrowth cells (EOCs), using in vitro and in vivo correlates of angiogenesis. Patients/Methods: Heparinized venous blood samples were collected from healthy volunteers and from cord blood at parturition. G‐CSF‐mobilized samples were collected before administration, at apheresis harvest, and at follow‐up. PBSCs were phenotyped by flow cytometry, and cultured in standard colony‐forming unit (CFU)‐EPC and EOC assays. The effect of exogenous G‐CSF was investigated by addition of it to HUVECs and EOCs in standard tubule formation and aortic ring assays, and in an in vivo sponge implantation model. Results: Our data show that G‐CSF mobilization of PBSCs produces a profound, reversible depression of circulating CFU‐EPCs. Furthermore, G‐CSF administration did not mobilize CD34+CD133− cells, which include precursors of EOCs. No EOCs were cultured from any mobilized PBSCs studied. Exogenous G‐CSF inhibited CFU‐EPC generation, HUVEC and EOC tubule formation, microvessel outgrowth, and implanted sponge vascularization in mice. Conclusions: G‐CSF administration depresses both endothelial cell angiogenesis and monocyte proangiogenic activity, and we suggest that any angiogenic benefit observed following implantation of cells mobilized by G‐CSF may come only from a paracrine effect from HPCs.

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Granulocyte-colony stimulating factor in experimental stroke and its effects on infarct size and functional outcome: A systematic review

Abstract: Background

Cited by 60 publications

References 56 publications

Therapeutic mechanisms of granulocyte-colony stimulating factor in methotrexate-induced parotid lesion in adult rats and possible role of telocytes: A histological study

Therapeutic mechanisms of granulocyte-colony stimulating factor in methotrexate-induced parotid lesion in adult rats and possible role of telocytes: A histological study

Successful Regeneration After Experimental Stroke by Granulocyte-Colony Stimulating Factor Is Not Further Enhanced by Constraint-Induced Movement Therapy Either in Concurrent or in Sequential Combination Therapy

Granulocyte colony‐stimulating factor (G‐CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells for vascular regeneration therapy

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