Thrombocytes Modulate Neuroinflammation, Neuronal Plasticity and Recovery during Traumatic Brian Injury
Other conference paper

摘要Platelets (thrombocytes) are recognized as innate immune cells, which promote inflammation and tissue recovery on early stages after the trauma. Blood-brain barrier disruption occurs during large set of neurodegenerative and neurological disorders, including traumatic brain injury (TBI) and allows blood and immune cells enter the CNS. However, the role of platelets in neuroinflammation remains unclear.

Our research group has found previously that platelets could specifically recognize CNS-specific sialated glycolipids (gangliosides) within neuronal and astroglial lipid rafts [1]. ST3GalV knock-out (ST3KO) mice that are lack of major CNS-specific gangliosides exhibit impaired platelet - brain lipid raft interaction and reduced neuroinflammation during the onset of experimental autoimmune encephalitis. In the current study we investigated the role of platelet - CNS-specific ganglioside interaction in neuroinflammation and recovery in wild type (WT) and ST3KO mice TBI.

We found that ST3KO mice exhibited reduced level of microglia and macrophage activation, as well as lymphocyte infiltration to the brain after TBI. TBI was associated with more severe hemorrhage and neuronal damage at the brain trauma site of ST3KO, than WT, animals. Intracerebral injection of WT brain lipid rafts increased neuroinflammation and reduced hemorrhage initiated by TBI in ST3KO mice. Our results suggested that platelet-derived factors, such as serotonin, histamine and platelet-activating factor, were likely important mediators of platelet effect during TBI.
Moreover, platelets could directly interact with cortical neurons exhibiting neurotrophic and neuroprotective features. Platelets activated with WT, but not ST3KO, brain lipid rafts increased the expression of neuroplasticity markers PSD95, synapsin-1 and Trkβ and dendritic spine number in neuronal and brain organotypic culture and reduced the loss of these markers after TBI.

Our study demonstrated the essential role of thrombocyte – ganglioside interaction in regulation of neuroinflammation, hemorrhage, neuronal plasticity and recovery after TBI. In conclusion, we suggest that platelets can contribute to other neuroinflammatory and neuropsychiatric disorders, such as Alzheimer's disease, stroke and epilepsy.

1. Sotnikov I., Veremeyko T., Starossom S.C., Barteneva N., Weiner H.L., and Ponomarev E.D. Platelets Recognize Brain-Specific Glycolipid Structures, Respond to Neurovascular Damage and Promote Neuroinflammation. PLoS One. 2013; 8(3): e58979.
會議名稱The 4th International Anatomical Sciences and Cell Biology Conference (IASCBC)
會議地點Hong Kong SAR

上次更新時間 2018-23-01 於 04:40