Serum response factor modulates neuron survival during peripheral axon injury
1 Department Molecular Biology, Interfaculty Institute for Cell Biology, Eberhard Karls University Tübingen, Auf der Morgenstelle 15, Tübingen, 72076, Germany
2 Current addresses: Institute for Physiological Chemistry, Ulm University, Ulm, 89081, Germany
3 Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Bonn, 53175, Germany
Journal of Neuroinflammation 2012, 9:78 doi:10.1186/1742-2094-9-78Published: 26 April 2012
The transcription factor SRF (serum response factor) mediates neuronal survival in vitro. However, data available so far suggest that SRF is largely dispensable for neuron survival during physiological brain function.
Here, we demonstrate that upon neuronal injury, that is facial nerve transection, constitutively-active SRF-VP16 enhances motorneuron survival. SRF-VP16 suppressed active caspase 3 abundance in vitro and enhanced neuron survival upon camptothecin induced apoptosis. Following nerve fiber injury in vitro, SRF-VP16 improved survival of neurons and re-growth of severed neurites. Further, SRF-VP16 enhanced immune responses (that is microglia and T cell activation) associated with neuronal injury in vivo. Genome-wide transcriptomics identified target genes associated with axonal injury and modulated by SRF-VP16.
In sum, this is a first report describing a neuronal injury-related survival function for SRF.