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Activated T cells induce proliferation of oligodendrocyte progenitor cells via release of vascular endothelial cell growth factor‐A
Author(s) -
Choi Elliot H.,
Xu Yadi,
Medynets Marie,
Monaco Maria Chiara G.,
Major Eugene O.,
Nath Avindra,
Wang Tongguang
Publication year - 2018
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.23501
Subject(s) - biology , microbiology and biotechnology , progenitor cell , neural stem cell , haematopoiesis , stem cell , oligodendrocyte , cell growth , hematopoietic growth factor , immunology , central nervous system , neuroscience , myelin , genetics
Neuroinflammatory diseases such as multiple sclerosis are characterized by infiltration of lymphocytes into the central nervous system followed by demyelination and axonal degeneration. While evidence suggests that activated T lymphocytes induce neurotoxicity and impair function of neural stem cells, the effect of T cells on oligodendrocyte progenitor cells (OPCs) is still uncertain, partly due to the difficulty in obtaining human OPCs. Here we studied the effect of activated T cells on OPCs using OPCs derived from human hematopoietic stem cells or from human fetal brain. OPCs were exposed to supernatants (sups) from activated T cells. Cell proliferation was determined by EdU incorporation and CellQuanti‐Blue assays. Surprisingly, we found that sups from activated T cells induced OPC proliferation by regulating cell cycle progression. Vascular endothelial growth factor A (VEGF‐A) transcripts were increased in T cells after activation. Immunodepletion of VEGF‐A from activated T cell sups significantly attenuated its effect on OPC proliferation. Furthermore, VEGF receptor 2 (VEGFR2) was expressed on OPCs and its inhibition also attenuated activated T cell‐induced OPC proliferation. Thus, activated T cells have a trophic role by promoting OPC proliferation via the VEGFR2 pathway.