Author
Listed:
- Yuki Miyamoto
(National Research Institute for Child Health and Development)
- Tomohiro Torii
(National Research Institute for Child Health and Development)
- Akito Tanoue
(National Research Institute for Child Health and Development)
- Junji Yamauchi
(National Research Institute for Child Health and Development
Laboratory of Molecular Neuroscience and Neurology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences)
Abstract
Oligodendrocytes differentiate to wrap their plasma membranes around axons, forming the myelin sheath. A neuronal cue is one of the regulator elements controlling this process. Here, we demonstrate that VCAM1, which plays a key role throughout the immune system, is also expressed in oligodendrocytes, where it regulates the initiation of myelination. VCAM1 knockout mice exhibit reduced myelin thickness. Decreased myelin thickness is also observed in mutant mice of α4 integrin, which is a neuronal VCAM1 ligand. Furthermore, CD69 is identified as one of the transcripts downregulated when VCAM1 is knocked down in oligodendrocytes. Knockdown of CD69 in mice indicates its role in myelination. Therefore, VCAM1 contributes not only to the initiation of myelination but also to its regulation through controlling the abundance of CD69, demonstrating that an intercellular molecule whose primary role is in the immune system can also play an unexpected role in the CNS.
Suggested Citation
Yuki Miyamoto & Tomohiro Torii & Akito Tanoue & Junji Yamauchi, 2016.
"VCAM1 acts in parallel with CD69 and is required for the initiation of oligodendrocyte myelination,"
Nature Communications, Nature, vol. 7(1), pages 1-16, December.
Handle:
RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13478
DOI: 10.1038/ncomms13478
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