Article ; Online: Deletion of PTEN in microglia ameliorates chronic neuroinflammation following repetitive mTBI.
Molecular and cellular neurosciences
2023 Volume 125, Page(s) 103855
Abstract: Traumatic brain injury is a leading cause of morbidity and mortality in adults and children in developed nations. Following the primary injury, microglia, the resident innate immune cells of the CNS, initiate several inflammatory signaling cascades and ... ...
| Abstract | Traumatic brain injury is a leading cause of morbidity and mortality in adults and children in developed nations. Following the primary injury, microglia, the resident innate immune cells of the CNS, initiate several inflammatory signaling cascades and pathophysiological responses that may persist chronically; chronic neuroinflammation following TBI has been closely linked to the development of neurodegeneration and neurological dysfunction. Phosphoinositide 3-kinases (PI3Ks) are a family of lipid kinases that have been shown to regulate several key mechanisms in the inflammatory response to TBI. Increasing evidence has shown that the modulation of the PI3K/AKT signaling pathway has the potential to influence the cellular response to inflammatory stimuli. However, directly targeting PI3K signaling poses several challenges due to its regulatory role in several cell survival pathways. We have previously identified that the phosphatase and tensin homolog deleted on chromosome 10 (PTEN), the major negative regulator of PI3K/AKT signaling, is dysregulated following exposure to repetitive mild traumatic brain injury (r-mTBI). Moreover, this dysregulated PI3K/AKT signaling was correlated with chronic microglial-mediated neuroinflammation. Therefore, we interrogated microglial-specific PTEN as a therapeutic target in TBI by generating a microglial-specific, Tamoxifen inducible conditional PTEN knockout model using a CX3CR1 Cre recombinase mouse line PTEN |
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| MeSH term(s) | Animals ; Mice ; Brain Injuries, Traumatic/metabolism ; Disease Models, Animal ; Inflammation/metabolism ; Mice, Inbred C57BL ; Microglia/metabolism ; Neuroinflammatory Diseases ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism | |||||
| Chemical Substances | Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Pten protein, mouse (EC 3.1.3.67) | |||||
| Language | English | |||||
| Publishing date | 2023-04-20 | |||||
| Publishing country | United States | |||||
| Document type | Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. | |||||
| ZDB-ID | 1046640-x | |||||
| ISSN | 1095-9327 ; 1044-7431 | |||||
| ISSN (online) | 1095-9327 | |||||
| ISSN | 1044-7431 | |||||
| DOI | 10.1016/j.mcn.2023.103855 | |||||
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| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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