Novel C1q receptor-mediated signaling controls neural stem cell behavior and neurorepair

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dc.contributor.authorBenavente, Francisca
dc.contributor.authorPiltti, Katja M.
dc.contributor.authorHooshmand, Mitra J.
dc.contributor.authorNava, Aileen A.
dc.contributor.authorLakatos, Anita
dc.contributor.authorFeld, Brianna G.
dc.contributor.authorCreasman, Dana
dc.contributor.authorGershon, Paul D.
dc.contributor.authorAnderson, Aileen
dc.date.accessioned2021-07-27T16:08:06Z
dc.date.available2021-07-27T16:08:06Z
dc.date.issued2020-09
dc.description.abstractC1q plays a key role as a recognition molecule in the immune system, driving autocatalytic complement cascade activation and acting as an opsonin. We have previously reported a non-immune role of complement C1q modulating the migration and fate of human neural stem cells (hNSC); however, the mechanism underlying these effects has not yet been identified. Here, we show for the first time that C1q acts as a functional hNSC ligand, inducing intracellular signaling to control cell behavior. Using an unbiased screening strategy, we identified five transmembrane C1q signaling/receptor candidates in hNSC (CD44, GPR62, BAI1, c-MET, and ADCY5). We further investigated the interaction between C1q and CD44 , demonstrating that CD44 mediates C1q induced hNSC signaling and chemotaxis in vitro, and hNSC migration and functional repair in vivo after spinal cord injury. These results reveal a receptor-mediated mechanism for C1q modulation of NSC behavior and show that modification of C1q receptor expression can expand the therapeutic window for hNSC transplantation.es
dc.identifier.citationeLife, 2020 september, vol.9:e55732es
dc.identifier.urihttps://doi.org/10.7554/eLife.55732es
dc.identifier.urihttp://hdl.handle.net/11447/4199
dc.language.isoenes
dc.subjectComplement C1qes
dc.subjectMousees
dc.subjectNeural stem cell transplantses
dc.subjectRegenerative medicinees
dc.subjectSpinal cord injuryes
dc.subjectStem cellses
dc.titleNovel C1q receptor-mediated signaling controls neural stem cell behavior and neurorepaires
dc.typeArticlees

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