CURRENT RESEARCH:
Neuroprotection of Granulocyte Colony-stimulating factor on retinal ischemia-reperfusion injury
Ischemic insult to the mammalian retina is frequently observed in open-angle glaucoma, diabetic retinopathies, and hypertensive retinopathies. They are major causes of blindness worldwide. Current therapies for ischemic neurodegenerations are retardant and are not sufficient to restore visual function.
Granulocyte-colony-stimulating factor (G-CSF) is a member of the cytokine family of growth factors. It was originally reported that G-CSF could stimulate the differentiation and function of hematopoietic cells. G-CSF also stimulates the proliferation, survival, and maturation of cells committed to the neutrophilic granulocyte (NG) lineage through the specific G-CSF receptor (G-CSFR). G-CSF exhibits a significant neuroprotective effect in cell cultures and in vivo after intravenous administration after stroke. G-CSF treatment increase signal transducer(s) and activator(s) of transcription (STAT3) expression mediated by G-CSFR. In addition, treatment with G-CSF in experimental spinal cord contusion injury improve functional outcome and reduce apoptosis in the injured spinal cord. G-CSF has trophic effects on neuronal cells. G-CSF is typically used for treatment of different kinds of neutropenia in humans. It is one of the few growth factors approved for clinical use for almost twenty years with a very good safety record.
Adminstration of G-CSF is neuroprotective in rat optic nerve crush model. We found G-CSF receptor expression in retinal ganglion cell layer and inner nuclear layer in vivo, we propose that G-CSF treatment will protect against acute retinal ischemia-reperfusion injury. | 
