Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0027947 (
neutropenia
)
17,527
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Granulocyte colony-stimulating factor (G-CSF) has been used in the treatment of
neutropenia
in hematologic disorders. The neuroprotective and anti-inflammatory effects of G-CSF were reported in various neurological disease models. In this study, we examined whether G-CSF induces
functional recovery
after intracerebral hemorrhage (ICH). ICH was induced using collagenase injection in adult rats. Either G-CSF (50 microg/kg, i.p.) or saline was given from 2 h after ICH and every 24 h for 3 days. 72 h after ICH induction, the rats were sacrificed for histological analysis and measurement of brain edema. Behavioral tests were performed before and 1, 7, 14, 21, 28, and 35 days after ICH. We also measured the blood-brain barrier (BBB) permeability using Evans blue dye injection method. G-CSF-treated rats recovered better on rotarod and limb placing tests, starting from 14 days throughout 5 weeks after ICH. The brain water content and BBB permeability of G-CSF-treated group decreased in the lesioned hemispheres compared with those of ICH-only group. In G-CSF-treated group, the number of TUNEL+, myeloperoxidase+, and OX42+ cells was smaller than that of ICH-only group in the periphery of hematoma. These findings suggest that G-CSF induces long-term sensorimotor recovery after ICH with reduction of brain edema, inflammation, and perihematomal cell death.
...
PMID:Granulocyte colony-stimulating factor induces sensorimotor recovery in intracerebral hemorrhage. 1582 21
Granulocyte-colony stimulating factor (G-CSF) is a growth factor which stimulates proliferation, differentiation, and survival of hematopoietic progenitor cells. G-CSF is being used extensively in clinical practice to accelerate recovery of patients from
neutropenia
after cytotoxic therapy. However, growing evidences have suggested that G-CSF has important non-hematopoietic functions in central nervous system. Recent studies have shown the presence of G-CSF/G-CSF-receptor (G-CSFR) system in the brain, and their roles in neuroprotection and neural tissue repair as well as improvement in
functional recovery
. The increased expression of G-CSF/G-CSFR on neurons subjected to hypoxia provides evidence that G-CSF may have an autocrine protective signaling mechanism in response to neural injury. G-CSF exerts neuroprotective actions through the inhibition of apoptosis and inflammation and the stimulation of neurogenesis. Moreover, G-CSF has been shown to mobilize bone marrow stem cells into the injured brain improving neural plasticity. In this review, we summarize some of the recent studies on G-CSF and the corresponding signal transduction pathways regulated by G-CSF in neuroprotection.
...
PMID:Neuroprotective effect of granulocyte-colony stimulating factor. 1712 31
The clinical application of G-CSF is broadening. In addition to treating
neutropenia
and in bone marrow transplants, it is now being considered for
functional recovery
after myocardial infarction and stroke. It is thus very important that the effects of extended G-CSF administration on the skeleton are investigated. To simulate this potential clinical use of G-CSF in postmyocardial infarction or cerebral vascular accident, a 2-week course of administration was selected. Ten C57BL/6 mice at 22 weeks of age were given intraperitoneal injection of saline, and another nine of the same age were given G-CSF. Four weeks later, femurs were harvested and three-point-bend tests were performed until fracture. From the load-displacement curve recorded during the test, the stiffness, Young's modulus, fracture strength of the bone, fracture energy, and the total energy to break the femur were determined. The test data show that mice treated with G-CSF have significantly lower modulus in their femurs when compared to the controlled mice treated with saline. The stiffness demonstrates the largest decrease, by as much as 25%. As its clinical use increases, G-CSF effects on the mechanical properties of the skeleton become increasingly more important because many of these diseases occur in older patients with already compromised skeleton by osteopenia or osteoporosis. How G-CSF administration achieves these alterations in skeletal biomechanical properties is unclear. Although the current findings confirm its known temporary catabolic effects on bone homeostasis, it also suggests that a transient state of higher bone compliance following the end of G-CSF administration can be achieved that may have clinical benefits.
...
PMID:Granulocyte colony-stimulating factor administration alters femoral biomechanical properties in C57BL/6 mice. 1825 84
G-CSF is widely employed for the treatment of chemotherapy-induced
neutropenia
. Recently, neuroprotective effects of G-CSF in animal stroke models were discovered including infarct size reduction and enhancement of
functional recovery
. The underlying mechanisms of action of G-CSF in ischemia appear to be a direct anti-apoptotic activity in neurons and a neurogenesis inducing capacity. Additional effects may be based on the stimulation of new blood-vessel formation, the stimulation of immunocompetence and -modulation as well as on bone marrow mobilization. In addition to a discussion of these mechanisms, we will review the available preclinical studies and analyze their impact on the overall efficacy of G-CSF in experimental stroke.
...
PMID:Granulocyte-colony stimulating factor for stroke treatment: mechanisms of action and efficacy in preclinical studies. 2014 89