Silencing of TGFβ signalling in microglia results in impaired homeostasis

Tanja Zöller, Artur Schneider, Christian Kleimeyer, Takahiro Masuda, Phani Sankar Potru, Dietmar Pfeifer, Thomas Blank, Marco Prinz, Björn Spittau

研究成果: Contribution to journalArticle査読

42 被引用数 (Scopus)

抄録

TGFβ1 has been implicated in regulating functional aspects of several distinct immune cell populations including central nervous system (CNS) resident microglia. Activation and priming of microglia have been demonstrated to contribute to the progression of neurodegenerative diseases and, thus, underlie stringent control by endogenous regulatory factors including TGFβ1. Here, we demonstrate that deletion of Tgfbr2 in adult postnatal microglia does neither result in impairment of the microglia-specific gene expression signatures, nor is microglial survival and maintenance affected. Tgfbr2-deficient microglia were characterised by distinct morphological changes and transcriptome analysis using RNAseq revealed that loss of TGFβ signalling results in upregulation of microglia activation and priming markers. Moreover, protein arrays demonstrated increased secretion of CXCL10 and CCL2 accompanied by activation of immune cell signalling as evidenced by increased phosphorylation of TAK1. Together, these data underline the importance of microglial TGFβ signalling to regulate microglia adaptive changes.

本文言語英語
論文番号4011
ジャーナルNature communications
9
1
DOI
出版ステータス出版済み - 12 1 2018
外部発表はい

All Science Journal Classification (ASJC) codes

  • 化学 (全般)
  • 生化学、遺伝学、分子生物学(全般)
  • 物理学および天文学(全般)

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