4.5 Article

Acetylation and phosphorylation of STAT3 are involved in the responsiveness of microglia to beta amyloid

期刊

NEUROCHEMISTRY INTERNATIONAL
卷 81, 期 -, 页码 48-56

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2015.01.007

关键词

STAT3; 14-3-3epsilon; Alzheimer's disease; Amyloid beta peptides; Microglia

资金

  1. Italian grant from MIUR [PRIN 2010HEBBB8_002]
  2. Sapienza University grant [C26A124WCR]
  3. Istituto Pasteur-Fondazione Cenci Bolognetti
  4. Credito Cooperativo Cassa Rurale ed Artigiana di Paliano

向作者/读者索取更多资源

Microglia are macrophages within the central nervous system playing a central role in neurodegenerative disorders. Although the initial engagement of microglia seems to be neuroprotective, many lines of evidence indicate that its persistent activation contributes to dismantle neuronal activity and to induce neuronal loss. The molecular pathways that lead from amyloid interaction with membrane receptors to the microglial activation have been extensively investigated, although a definitive picture is not yet at hand. In this work, primary and immortalized microglial cells were treated with a synthetic form of All peptides, and relative abundance of acetylated and phosphorylated STAT3 were assayed. Results highlight, for the first time, three distinctive sequential events: i) an earlier event marked by the increase in the level of STAT3 acetylated species, followed by ii) a later increase in the level of STAT3 phosphorylated form, and finally iii) an involvement of phosphorylated STAT3 in the increase in expression of the 14-3-3 epsilon, a protein frequently associated with neurodegenerative diseases and known to be a marker of All-activated microglia. These data outline a complex, time-dependent modification of STAT3 signalling triggered by amyloid in the microglial compartments, that once confirmed by in vivo experiments will broaden the knowledge of the molecular basis of amyloid neurotoxicity. (C) 2015 Elsevier Ltd. All rights reserved.

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