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Fasudil reduces GFAP expression after hypoxic injury
Varun Kesherwani1, Shikha Tarang2, Robert Barnes1
1Division of Neurosurgery, Department of Surgery, University of Nebraska Medical Center, Omaha, NE 68198-7690, USA.
Neuroscience Letters
|June 7, 2014
Summary
Fasudil effectively reduces glial fibrillary acidic protein (GFAP) and astrogliosis following hypoxic injury in cell and spinal cord models. This inhibition of GFAP expression by Fasudil may promote axonal regeneration after spinal cord injury.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Spinal cord injury (SCI) triggers astrogliosis, characterized by increased glial fibrillary acidic protein (GFAP) expression, which can impede neuroregeneration.
- Fasudil (HA-1077), a Rho kinase II (ROCKII) inhibitor, is being investigated for SCI recovery due to its role in promoting axonal regeneration by inhibiting growth cone collapse.
Purpose of the Study:
- To investigate the effect of Fasudil on GFAP expression and astrogliosis in response to hypoxic injury.
- To determine if Fasudil can mitigate the increase in GFAP expression induced by hypoxia in both cell cultures and spinal cord tissue.
Main Methods:
- Hypoxic injury was induced in A172 astrocytic cell lines and rat spinal cord dorsal column white matter using cobalt chloride (CoCl2).
- Glial fibrillary acidic protein (GFAP) expression was quantified using real-time PCR, western blotting, and immunofluorescence staining.
- The impact of Fasudil treatment on GFAP levels and NF-κB activation was assessed.
Main Results:
- Hypoxia significantly increased GFAP protein and RNA expression in both A172 cells and spinal cord tissue.
- Fasudil treatment (20μM) markedly reduced GFAP expression in both models.
- Fasudil also decreased the activation of NF-κB in A172 cells following hypoxic injury.
Conclusions:
- Fasudil effectively reduces GFAP expression and subsequent astrogliosis in models of hypoxic CNS injury.
- By inhibiting GFAP and NF-κB activation, Fasudil shows potential therapeutic benefits for promoting neuroregeneration and functional recovery after spinal cord injury.
