作者: Ivana Bjelobaba , Jean Sévigny , Markus Kipp , Nadezda Nedeljkovic , Dusica Brisevac
DOI: 10.1007/S12031-015-0601-Y
关键词:
摘要: Extracellular ATP (eATP) acts as a danger-associated molecular pattern which induces reactive response of astrocytes after brain insult, including morphological remodeling astrocytes, proliferation, chemotaxis, and release proinflammatory cytokines. The responses induced by eATP are under control ecto-nucleotidases, catalyze sequential hydrolysis to adenosine. In the mammalian brain, ecto-nucleotidases comprise three enzyme families: ecto-nucleoside triphosphate diphosphohydrolases 1–3 (NTPDase1–3), ecto-nucleotide pyrophosphatase/phospodiesterases (NPP1–3), ecto-5′-nucleotidase (eN), crucially determine ATP/adenosine ratio in pericellular milieu. Altered expression has been demonstrated several experimental models human dysfunctions. present study, we have explored NTPDase1–3, NPP1–3, eN cultured cortical challenged with 1 mmol/L (eATP). At transcriptional level, upregulated NTPDase1, NTPDase2, NPP2, eN, while, at translational functional levels, these were paralleled only induction NTPDase2 eN. Additionally, altered membrane topology from clusters localized domains continuous distribution along cell membrane. Our results suggest that eATP, upregulating altering topology, affects local kinetics metabolism signal transduction may important roles process related inflammation gliosis.