| First Author | Dai SS | Year | 2010 |
| Journal | J Neurochem | Volume | 113 |
| Issue | 6 | Pages | 1536-44 |
| PubMed ID | 20367749 | Mgi Jnum | J:163571 |
| Mgi Id | MGI:4822309 | Doi | 10.1111/j.1471-4159.2010.06716.x |
| Citation | Dai SS, et al. (2010) Adenosine A2A receptors in both bone marrow cells and non-bone marrow cells contribute to traumatic brain injury. J Neurochem 113(6):1536-44 |
| abstractText | Adenosine A2A receptors (A(2A)Rs) in bone marrow-derived cells (BMDCs) are involved in regulation of inflammation and outcome in several CNS injuries; however their relative contribution to traumatic brain injury (TBI) is unknown. In this study, we created a mouse cortical impact model, and BMDC A(2A)Rs were selectively inactivated in wild-type (WT) mice or reconstituted in global A(2A)R knockout (KO) mice (i.e. inactivation of non-BMDC A(2A)Rs) by bone marrow transplantation. When compared with WT mice, selective inactivation of BMDC A(2A)Rs significantly attenuated the neurological deficits, brain water content and cell apoptosis at 24 h post-TBI as global A(2A)R KO did. However, compared with the A(2A)R KO mice, selective reconstitution of BMDC A(2A)Rs failed to reinstate brain injury, indicating the contribution of the non-BMDC A(2A)R to TBI. Furthermore, the protective outcome by selective inactivation of BMDC A(2A)R or broad inactivation of non-BMDC A(2A)Rs was accompanied with reduced CSF glutamate level and suppression of the inflammatory cytokines interleukin-1, or interleukin-1 and tumor necrosis factor-alpha. These findings demonstrate that inactivation of A(2A)Rs in either BMDCs or non-BMDCs is sufficient to confer the protective effect as global A(2A)R KO against TBI, indicating the A(2A)R involvement in TBI by multiple cellular mechanisms of A(2A)R involvement including inhibition of glutamate release and inflammatory cytokine expressions. |
