Reactive astrocytes function as phagocytes after brain ischemia via ABCA1-mediated pathway

Yosuke M. Morizawa, Yuri Hirayama, Nobuhiko Ohno, Shinsuke Shibata, Eiji Shigetomi, Yang Sui, Junichi Nabekura, Koichi Sato, Fumikazu Okajima, Hirohide Takebayashi, Hideyuki Okano and Schuichi Koizumi ()
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Yosuke M. Morizawa: University of Yamanashi
Yuri Hirayama: University of Yamanashi
Nobuhiko Ohno: National Institute for Physiological Sciences
Shinsuke Shibata: Keio University School of Medicine
Eiji Shigetomi: University of Yamanashi
Yang Sui: National Institute for Physiological Sciences
Junichi Nabekura: National Institute for Physiological Sciences
Koichi Sato: Gunma University
Fumikazu Okajima: Gunma University
Hirohide Takebayashi: Niigata University
Hideyuki Okano: Keio University School of Medicine
Schuichi Koizumi: University of Yamanashi

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Astrocytes become reactive following various brain insults; however, the functions of reactive astrocytes are poorly understood. Here, we show that reactive astrocytes function as phagocytes after transient ischemic injury and appear in a limited spatiotemporal pattern. Following transient brain ischemia, phagocytic astrocytes are observed within the ischemic penumbra region during the later stage of ischemia. However, phagocytic microglia are mainly observed within the ischemic core region during the earlier stage of ischemia. Phagocytic astrocytes upregulate ABCA1 and its pathway molecules, MEGF10 and GULP1, which are required for phagocytosis, and upregulation of ABCA1 alone is sufficient for enhancement of phagocytosis in vitro. Disrupting ABCA1 in reactive astrocytes result in fewer phagocytic inclusions after ischemia. Together, these findings suggest that astrocytes are transformed into a phagocytic phenotype as a result of increase in ABCA1 and its pathway molecules and contribute to remodeling of damaged tissues and penumbra networks.

Date: 2017
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DOI: 10.1038/s41467-017-00037-1

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