ArticleCommunications biology2025
Extracellular vesicle-mediated transfer of MIR22HG inhibits the colonization of enteric neural crest cells in the colon by decreasing MPP3 expression.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hirschsprung's disease (HSCR) is a congenital malformation of the enteric nervous system (ENS) caused by deficient enteric neural crest cell (ENCC) colonization. However, the mechanisms inducing impaired ENCC colonization remain unclear. This study investigates the involvement of extracellular vesicles (EVs), pivotal mediators of intercellular communication, in ENS development and HSCR pathogenesis. We find that treatment with plasma-derived EVs from children with HSCR (HSCR-EV) significantly inhibits ENCC proliferation and migration. MIR22HG is identified as the key mediator of the HSCR-EV-induced suppression of ENCC proliferation and migration. Schwann cells within the aganglionic colon of HSCR children derive EVs containing upregulated MIR22HG. In vitro, Schwann cell-derived EV-MIR22HG inhibits ENCC proliferation and migration. In vivo, it blocks ENCC colonization in the distal colon and disrupts ENS formation. MPP3 is identified as a potential downstream target of MIR22HG, with MIR22HG downregulating its expression via the m
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