Open AccessConcise Review: Cellular and Molecular Mechanisms of Postnatal Injury‐Induced Enteric Neurogenesis
Author(s) -
Jonscher Raleigh,
BelkindGerson Jaime
Publication year - 2019
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.3045
Subject(s) - neurogenesis , enteric nervous system , biology , glial cell line derived neurotrophic factor , neural stem cell , stem cell , neurotrophic factors , progenitor cell , transdifferentiation , neuroscience , schwann cell , population , adult stem cell , immunology , microbiology and biotechnology , cellular differentiation , medicine , biochemistry , receptor , environmental health , gene
Although still controversial, there is increasing agreement that postnatal neurogenesis occurs in the enteric nervous system (ENS) in response to injury. Following acute colitis, there is significant cell death of enteric neurons and evidence suggests that subsequent neural regeneration follows. An enteric neural stem/progenitor cell population with neurogenic potential has been identified in culture; in vivo, compensatory neurogenesis is driven by enteric glia and may also include de‐differentiated Schwann cells. Recent evidence suggests that changes in the enteric microenvironment due to injury‐associated increases in glial cell‐derived neurotrophic factor (GDNF), serotonin (5‐hydroxytryptamine [HT]), products from the gut microbiome, and possibly endocannabinoids may lead to the transdifferentiation of mature enteric glia and may reprogram recruited Schwann cells. Targeting neurogenic pathways presents a promising avenue toward the development of new and innovative treatments for acquired damage to the ENS. In this review, we discuss potential sources of newly generated adult enteric neurons, the involvement of GDNF, 5‐HT, endocannabinoids, and lipopolysaccharide, as well as therapeutic applications of this evolving work. Stem Cells 2019;37:1136–1143