central-nervous-system-2016_posters-accepted-abstracts

16 / 42

Notes:
Page 72
CNS 2016
December 05-07, 2016
Volume 7, Issue 5(Suppl) J Neurol Neurophysiol
ISSN: 2155-9562 JNN, an open access journal
conferenceseries .com
December 05-07, 2016 Dubai, UAE
2nd International Conference on
Central Nervous System Disorders & Therapeutics
Stephanie Nadine Reichel et al., J Neurol Neurophysiol 2016, 7:5(Suppl)
The Role of Glia-specific NF-κB Activation in Traumatic Brain Injury
Stephanie Nadine Reichel
Institute of Physiological Chemistry, Ulm University, 89081 Ulm
The transcription factor NF-κB is a central regulator of various cellular processes, including cell survival and inflammation.
Inflammation in the CNS is mediated by both astroglia and microglia, which become activated and crosstalk upon CNS
damage, such as traumatic brain injury (TBI). There is increasing evidence that IKK/NF-κB activation in astrocytes and
microglia is part of the secondary pathophysiology in TBI. However, neither the cell-type-specific activation kinetics after
TBI nor the exact associated cellular functions induced by NF-κB in this context is properly understood so far. We used
the closed head injury model in transgenic NF-κB reporter gene mice, which allow monitoring of NF-κB activation by GFP
expression. Interestingly, we found increasing NF-κB activation in both astrocytes and microglia on the ipsilateral site after
TBI, however with different kinetics. Notably, also on the contralateral site microglia showed NF-κB activation, suggesting
that the TBI triggered inflammatory response can indeed spread from local site of damage to the uninjured hemisphere.
Using conditional mouse models allowing conditional astrocyte-specific activation or inhibition of NF-κB, we found first
evidence that NF-κB activation in astrocytes prior to TBI promotes development of neurological deficits post TBI. In contrast,
animals with astrocyte-specific NF-κB inhibition show less neurological impairments suggesting beneficial effects of NF-κB
suppression in astrocytes. Currently, we focus on the molecular mechanisms underlying this differential TBI outcome using
immunohistochemical, biochemical and gene expression analyses as well as investigation of the blood-brain-barrier integrity
and edema formation. This research is supported by a grant of the Deutsche Forschungsgemeinschaft (DFG SFB 1194).
Biography
Stephanie Nadine Reichel studied Molecular Medicine at the Eberhard-Karls University in Tübingen. Since January 2014 she is doing her PhD at the Institute of
Physiological Chemistry of the University of Ulm. Besides, she is a student representative in the International Graduate School in Molecular Medicine Ulm (IGradU)
and a member of the biotechnological student initiative (bts e.V.) Ulm.