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A Novel Human Epithelial Enteroid Model of Necrotizing Enterocolitis
Published on: April 10, 2019
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Liver damage, proliferation, and progenitor cell markers in experimental necrotizing enterocolitis
Hiromu Miyake1, Bo Li2, Carol Lee2
1Division of General and Thoracic Surgery, The Hospital for Sick Children, Toronto, ON, Canada; Department of Pediatric Surgery, Shizuoka Children's Hospital, Shizuoka, Japan.
Journal of Pediatric Surgery
|March 6, 2018
Summary
Necrotizing enterocolitis (NEC) impairs liver regeneration by reducing hepatic proliferation and LGR5 expression. Targeting LGR5+ progenitor cells may enhance recovery from NEC-induced liver injury.
Area of Science:
- Hepatology
- Neonatal Medicine
- Regenerative Medicine
Background:
- Necrotizing enterocolitis (NEC) is a severe intestinal disease affecting newborns.
- NEC can lead to multi-organ injury, including the liver.
- Liver regeneration is crucial for recovery from NEC-induced liver damage.
Purpose of the Study:
- To investigate hepatic proliferation in experimental NEC.
- To examine the expression of progenitor cell markers in NEC-affected livers.
- To understand the mechanisms of liver injury and regeneration in NEC.
Main Methods:
- NEC was induced in a mouse model using hypoxia, formula gavage, and LPS.
- Control group consisted of breastfed pups.
- Analysis included serum ALT, liver inflammatory cytokines, proliferation markers (Ki67, PCNA), and LGR5 expression (mRNA and protein).
Main Results:
- NEC group showed elevated serum ALT and liver inflammatory cytokines (IL6, TNF-α).
- Hepatic proliferation markers (Ki67, PCNA) were significantly decreased in NEC.
- LGR5 expression was markedly reduced in NEC livers at both mRNA and protein levels.
Conclusions:
- Experimental NEC causes significant liver inflammation and injury.
- Impaired hepatic proliferation and reduced LGR5 expression characterize NEC-induced liver damage.
- Modulating LGR5+ progenitor cells offers a potential therapeutic strategy for promoting liver regeneration in NEC.
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