Astrocytic GAP43 Induced by the TLR4/NF-κB/STAT3 Axis Attenuates Astrogliosis-Mediated Microglial Activation and Neurotoxicity.
Chia-Chi HungChun-Hua LinHsuan ChangChen-Yu WangShang-Hsuan LinPei-Chien HsuYu-Yo SunTeng-Nan LinFeng-Shiun ShieLung-Sen KaoChih-Ming ChouYi-Hsuan LeePublished in: The Journal of neuroscience : the official journal of the Society for Neuroscience (2016)
Astrogliosis is a complex state in which injury-stimulated astrocytes exert both protective and harmful effects on neuronal survival and plasticity. In this study, we demonstrated for the first time that growth-associated protein 43 (GAP43), a well known growth cone protein that promotes axonal regeneration, can be induced in rat brain astrocytes by the proinflammatory endotoxin lipopolysaccharide via both nuclear factor-κB and signal transducer and activator of transcription 3-mediated transcriptional activation. Importantly, LPS-induced GAP43 mediates plastic changes of astrocytes while attenuating astrogliosis-induced microglial activation and neurotoxicity. Hence, astrocytic GAP43 upregulation may serve to indicate beneficial astrogliosis after CNS injury.
Keyphrases
- lps induced
- nuclear factor
- inflammatory response
- toll like receptor
- lipopolysaccharide induced
- high glucose
- diabetic rats
- transcription factor
- cell proliferation
- stem cells
- signaling pathway
- drug induced
- immune response
- spinal cord injury
- amino acid
- gene expression
- oxidative stress
- heat shock
- neuropathic pain
- subarachnoid hemorrhage
- protein protein
- stress induced