Cited by 53Neurogenesis and neuroplasticity mechanismsNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

CD38 positively regulates postnatal development of astrocytes cell-autonomously and oligodendrocytes non-cell-autonomously: HATTORI et al.

Hattori, Tsuyoshi, Kaji, Minoru, Ishii, Hiroshi, Jureepon, Roboon, Takarada-Iemata, Mika, Minh Ta, Hieu, Manh Le, Thuong, Konno, Ayumu +9 more·2017·Glia

Abstract

Glial development is critical for the function of the central nervous system. CD38 is a multifunctional molecule with ADP-ribosyl cyclase activity. While critical roles of CD38 in the adult brain such as oxytocin release and social behavior have been reported, those in the developing brain remain largely unknown. Here we demonstrate that deletion of Cd38 leads to impaired development of astrocytes and oligodendrocytes in mice. CD38 is highly expressed in the developing brains between postnatal day 14 (P14) and day 28 (P28). In situ hybridization and FACS analysis revealed that CD38 is expressed predominantly in astrocytes in these periods. Analyses of the cortex of Cd38 knockout (Cd38 -/- ) mice revealed delayed development of astrocytes and subsequently delayed differentiation of oligodendrocytes (OLs) at postnatal stages. In vitro experiments using primary OL cultures, mixed glial cultures, and astrocytic conditioned medium showed that astrocytic CD38 regulates the development of astrocytes in a cell-autonomous manner and the differentiation of OLs in a non-cell-autonomous manner. Further experiments revealed that connexin43 (Cx43) in astrocytes plays a promotive role for CD38-mediated OL differentiation. Finally, increased levels of NAD + , caused by CD38 deficiency, are likely to be responsible for the suppression of astrocytic Cx43 expression and OL differentiation. Our data indicate that CD38 is a positive regulator of astrocyte and OL development.

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Crossref · 10.1002/glia.23139

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Authors
Hattori, T., Kaji, M., Ishii, H., Jureepon, R., Takarada-Iemata, M., Minh Ta, H., Manh Le, T., Konno, A., Hirai, H., Shiraishi, Y., Ozaki, N., Yamamoto, Y., Okamoto, H., Yokoyama, S., Higashida, H., Kitao, Y., & Hori, O.
Affiliations
  • Kanazawa University (JP)
  • Department of Neuroanatomy, Graduate School of Medical Sciences; Kanazawa University; Kanazawa Ishikawa Japan
  • Gunma University (JP)
Corresponding author
Hattori, Tsuyoshi
Venue
Glia
Publisher
Wiley
Published
2017-03-13
Volume
65
Issue
6
Pages
974-989
ISSN
0894-1491 (ISSN-L)
OpenAlex
W2606970699
Cited by
53
References
8
Citations by year
2026: 2 · 2025: 3 · 2024: 10 · 2023: 7 · 2022: 7 · 2021: 4 · 2020: 8 · 2019: 5 · 2018: 3 · 2017: 4
FWCI
2.27
Type
journal article
Language
en
Open access
closed
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ministry of Education, Culture, Sports, Science and Technology (15K06753, 26430069, 15H01374, 15K18374)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
CD38, astrocyte development, oligodendrocyte differentiation, postnatal brain development, ADP-ribosyl cyclase, connexin 43, NAD+, glial development, CD38 knockout mice
MeSH terms
Animals, Astrocytes, Brain, Cell Differentiation, Cells, Cultured, Female, Male, Membrane Glycoproteins, Mice, Inbred ICR, NAD, Oligodendroglia, Rats, Wistar, Connexin 43, Mice, Knockout, Coculture Techniques, ADP-ribosyl Cyclase, ADP-ribosyl Cyclase 1

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