| First Author | Sun H | Year | 2016 |
| Journal | Neuroscience | Volume | 317 |
| Pages | 65-75 | PubMed ID | 26774050 |
| Mgi Jnum | J:231155 | Mgi Id | MGI:5767021 |
| Doi | 10.1016/j.neuroscience.2016.01.003 | Citation | Sun H, et al. (2016) Aquaporin-4 mediates communication between astrocyte and microglia: Implications of neuroinflammation in experimental Parkinson's disease. Neuroscience 317:65-75 |
| abstractText | Aquaporin-4 (AQP4), a water-selective membrane transport protein, is up-regulated in astrocytes in various inflammatory lesions, including Parkinson disease (PD). However, the exact functional roles of AQP4 in neuroinflammation remain unknown. In the present study, we investigated how AQP4 participates in the neuroinflammation of PD using AQP4 knockout (KO) mice and astrocyte-microglial co-cultures. We found that AQP4 KO mice exhibited increased basal and inducible canonical NF-kappaB activity, and showed significantly enhanced gliosis (astrocytosis and microgliosis) in chronic MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)/probenecid PD models, companying with the increase in the production of IL-1beta and TNF-alpha in the midbrain. Similarly, AQP4 deficiency augmented the activation of the NF-kappaB pathway and the production of IL-1beta and TNF-alpha in midbrain astrocyte cultures treated with MPP(+) (1-methyl-4-phenylpyridinium). Furthermore, AQP4 deficiency promoted activation of microglial cells in the co-cultured system. Our data provide the first evidence that AQP4 modulates astrocyte-to-microglia communication in neuroinflammation, although its effect on astrocyte inflammatory activation remains to be explored. |
