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Critical Reviews™ in Immunology
Fator do impacto: 1.404 FI de cinco anos: 3.347 SJR: 0.706 SNIP: 0.55 CiteScore™: 2.19

ISSN Imprimir: 1040-8401
ISSN On-line: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2015012127
pages 77-84

Lipocalin-2 in the Inflammatory Activation of Brain Astrocytes

Shinrye Lee
Korea Brain Research Institute (KBRI), Daegu, Republic of Korea
Mithilesh Kumar Jha
Department of Pharmacology, Brain Science & Engineering Institute, Department of Biomedical Science, BK21 PLUS KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea
Kyoungho Suk
Department of Pharmacology, Brain Science & Engineering Institute, Department of Biomedical Science, BK21 PLUS KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea

RESUMO

Lipocalin-2 (LCN2), a secretory protein, regulates diverse cellular processes such as cell death/survival, cell migration/invasion, cell differentiation, iron delivery, inflammation, insulin resistance, and tissue regeneration. Recently, we reported that LCN2 is secreted by brain astrocytes under inflammatory conditions and that it promotes apoptosis, morphological changes, and migration in astrocytes both in vitro and in vivo. Activated astrocytes release LCN2 not only to induce the morphological transformation associated with reactive astrocytosis, but also to promote their own death. Under inflammatory conditions, activated astrocytes also show functional dichotomy similar to the M1/M2 phenotypes of microglia and macrophages. LCN2 is thought to be a chemokine inducer and an autocrine promoter of the classical proinflammatory activation of astrocytes. This article summarizes the current knowledge regarding the role of astrocyte-derived LCN2 as a proinflammatory mediator in the central nervous system and discusses LCN2's role in neuroinflammatory disorders.


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