Effects of weaning on intestinal longitudinal muscle-myenteric plexus function in piglets

Li, Jing; Liu, Fenfen; Mo, Kaibin; Ni, Hengjia; Yin, Yulong

doi:10.1007/s11427-022-2391-x

Cited by 3 publications

(1 citation statement)

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“…Maternal separation (MS), also regarded as weaning in mammals, is a familiar ELS paradigm [5][6][7]. Meanwhile, weaning is a basic process that most mammalian newborns, including humans, must undergo [8,9]. In rodents, MS is now a valid animal model of IBS because it exhibits the characteristic phenotype of IBS: severe IEI and gut-brain-microbiome (GBM) axis system disorder [2,6].…”

Section: Introductionmentioning

confidence: 99%

Role of the GLP2–Wnt1 axis in silicon-rich alkaline mineral water maintaining intestinal epithelium regeneration in piglets under early-life stress

Chen,

Dai,

Zhao

et al. 2024

Cell. Mol. Life Sci.

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Stress-induced intestinal epithelial injury (IEI) and a delay in repair in infancy are predisposing factors for refractory gut diseases in adulthood, such as irritable bowel syndrome (IBS). Hence, it is necessary to develop appropriate mitigation methods for mammals when experiencing early-life stress (ELS). Weaning, as we all know, is a vital procedure that all mammalian newborns, including humans, must go through. Maternal separation (MS) stress in infancy (regarded as weaning stress in animal science) is a commonly used ELS paradigm. Drinking silicon-rich alkaline mineral water (AMW) has a therapeutic effect on enteric disease, but the specific mechanisms involved have not been reported. Herein, we discover the molecular mechanism by which silicon-rich AMW repairs ELS-induced IEI by maintaining intestinal stem cell (ISC) proliferation and differentiation through the glucagon-like peptide (GLP)2–Wnt1 axis. Mechanistic study showed that silicon-rich AMW activates GLP2-dependent Wnt1/β-catenin pathway, and drives ISC proliferation and differentiation by stimulating Lgr5+ ISC cell cycle passage through the G1–S-phase checkpoint, thereby maintaining intestinal epithelial regeneration and IEI repair. Using GLP2 antagonists (GLP23−33) and small interfering RNA (SiWnt1) in vitro, we found that the GLP2–Wnt1 axis is the target of silicon-rich AMW to promote intestinal epithelium regeneration. Therefore, silicon-rich AMW maintains intestinal epithelium regeneration through the GLP2–Wnt1 axis in piglets under ELS. Our research contributes to understanding the mechanism of silicon-rich AMW promoting gut epithelial regeneration and provides a new strategy for the alleviation of ELS-induced IEI.

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