Document Type
Article
Publication Date
2-3-2021
Identifier
DOI: 10.3390/cells10020312
Abstract
The intestine is extremely dynamic and the epithelial cells that line the intestine get replaced every 3-5 days by highly proliferative intestinal stem cells (ISCs). The instructions for ISCs to self-renew or to differentiate come as cues from their surrounding microenvironment or their niche. A small number of evolutionarily conserved signaling pathways act as a critical regulator of the stem cells in the adult intestine, and these pathways are well characterized. However, the mechanisms, nutritional, and environmental signals that help establish the stem cell niche in the neonatal intestine are less studied. Deciphering the key signaling pathways that regulate the development and maintenance of the stem cells is particularly important to understanding how the intestine regenerates from necrotizing enterocolitis, a devastating disease in newborn infants characterized by inflammation, tissues necrosis, and stem cell injury. In this review, we piece together current knowledge on morphogenetic and immune pathways that regulate intestinal stem cell in neonates and highlight how the cross talk among these pathways affect tissue regeneration. We further discuss how these key pathways are perturbed in NEC and review the scientific knowledge relating to options for stem cell therapy in NEC gleaned from pre-clinical experimental models of NEC.
Journal Title
Cells
Volume
10
Issue
2
PubMed ID
33546361
Keywords
exosomes; immune signaling; intestinal stem cells; mesenchymal stem cell therapy; morphogentic pathways; necrotizing enterocolits
Recommended Citation
Venkatraman A, Yu W, Nitkin C, Sampath V. Intestinal Stem Cell Development in the Neonatal Gut: Pathways Regulating Development and Relevance to Necrotizing Enterocolitis. Cells. 2021;10(2):312. Published 2021 Feb 3. doi:10.3390/cells10020312
Comments
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Publisher's Link: https://www.mdpi.com/2073-4409/10/2/312
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