Background: Glial Maturation Factor Beta (GMFB) is a highly conserved brain-enriched
protein implicated in immunoregulation, neuroplasticity and apoptosis, processes central to neural injury
and repair following cerebral ischaemia. Therefore, we examined if changes in neurocellular GMFB
expression and release can be used to assess brain injury following ischaemia.
Methods and Results: Immunofluorescence staining, Western blotting, immunohistochemistry and
ELISA were used to measure GMFB in cultured neurons and astrocytes, rat brain tissues and plasma
samples from stroke model rats and stroke patients, while cell viability assays, TTC staining and micro-
PET were used to assess neural cell death and infarct severity. Immunofluorescence and immunohistochemistry
revealed GMFB expression mainly in astrocyte and neuronal nuclei but also in neuronal
axons and dendrites. Free GMFB concentration increased progressively in the culture medium during
hypoxia-hypoglycaemia treatment. Plasma GMFB concentration increased in rats subjected to middle
cerebral artery occlusion (MCAO, a model of stroke-reperfusion) and in stroke patients. Plasma
GMFB in MCAO model rats was strongly correlated with infarct size (R2=0.9582). Plasma GMFB
concentration was also markedly elevated in stroke patients within 24 h of onset and remained elevated
for more than one week. Conversely, plasma GMFB elevations were not significant in myocardial infarct
patients and stroke patients without infarction.
Conclusion: GMFB has the prerequisite stability, expression specificity and response dynamics to
serve as a reliable indicator of ischaemic injury in animal models and stroke patients. Plasma GMFB
may be a convenient non-invasive adjunct to neuroimaging for stroke diagnosis and prognosis.