Astrocyte activation is suppressed in both normal and injured brain by FGF signaling

Wenfei Kang, Francesca Balordi, Nan Su, Lin Chen, Gordon Fishell, Jean M. Hebert

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

In the brain, astrocytes are multifunctional cells that react to insults and contain damage. However, excessive or sustained reactive astrocytes can be deleterious to functional recovery or contribute to chronic inflammation and neuronal dysfunction. Therefore, astrocyte activation in response to damage is likely to be tightly regulated. Although factors that activate astrocytes have been identified, whether factors also exist that maintain astrocytes as nonreactive or reestablish their nonreactive state after containing damage remains unclear. By using loss- and gain-of-function genetic approaches, we show that, in the unperturbed adult neocortex, FGF signaling is required in astrocytes to maintain their nonreactive state. Similarly, after injury, FGF signaling delays the response of astrocytes and accelerates their deactivation. In addition, disrupting astrocytic FGF receptors results in reduced scar size without affecting neuronal survival. Overall, this study reveals that the activation of astrocytes in the normal and injured neocortex is not only regulated by proinflammatory factors, but also by factors such as FGFs that suppress activation, providing alternative therapeutic targets.

Original languageEnglish (US)
JournalProceedings of the National Academy of Sciences of the United States of America
Volume111
Issue number29
DOIs
StatePublished - Jul 22 2014

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Astrocytes
Brain
Neocortex
Fibroblast Growth Factor Receptors
Cicatrix
Inflammation
Wounds and Injuries

Keywords

  • Astrogliosis
  • Brain damage

ASJC Scopus subject areas

  • General

Cite this

Astrocyte activation is suppressed in both normal and injured brain by FGF signaling. / Kang, Wenfei; Balordi, Francesca; Su, Nan; Chen, Lin; Fishell, Gordon; Hebert, Jean M.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 111, No. 29, 22.07.2014.

Research output: Contribution to journalArticle

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