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Transplantation of enteric nervous system stem cells rescues nitric oxide synthase deficient mouse colon

Conor J. McCann, Julie E. Cooper, Dipa Natarajan, Benjamin Jevans, Laura E. Burnett, Alan J. Burns and Nikhil Thapar ()
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Conor J. McCann: Stem Cells and Regenerative Medicine, UCL Great Ormond Street Institute of Child Health
Julie E. Cooper: Stem Cells and Regenerative Medicine, UCL Great Ormond Street Institute of Child Health
Dipa Natarajan: Stem Cells and Regenerative Medicine, UCL Great Ormond Street Institute of Child Health
Benjamin Jevans: Stem Cells and Regenerative Medicine, UCL Great Ormond Street Institute of Child Health
Laura E. Burnett: Stem Cells and Regenerative Medicine, UCL Great Ormond Street Institute of Child Health
Alan J. Burns: Stem Cells and Regenerative Medicine, UCL Great Ormond Street Institute of Child Health
Nikhil Thapar: Stem Cells and Regenerative Medicine, UCL Great Ormond Street Institute of Child Health

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Enteric nervous system neuropathy causes a wide range of severe gut motility disorders. Cell replacement of lost neurons using enteric neural stem cells (ENSC) is a possible therapy for these life-limiting disorders. Here we show rescue of gut motility after ENSC transplantation in a mouse model of human enteric neuropathy, the neuronal nitric oxide synthase (nNOS−/−) deficient mouse model, which displays slow transit in the colon. We further show that transplantation of ENSC into the colon rescues impaired colonic motility with formation of extensive networks of transplanted cells, including the development of nNOS+ neurons and subsequent restoration of nitrergic responses. Moreover, post-transplantation non-cell-autonomous mechanisms restore the numbers of interstitial cells of Cajal that are reduced in the nNOS−/− colon. These results provide the first direct evidence that ENSC transplantation can modulate the enteric neuromuscular syncytium to restore function, at the organ level, in a dysmotile gastrointestinal disease model.

Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15937

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DOI: 10.1038/ncomms15937

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