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LSR targets YAP to modulate intestinal Paneth cell differentiation.

Yanan An1, Chao Wang2, Baozhen Fan3

  • 1Department of Physiology, Binzhou Medical University, Yantai, Shandong, China; Shandong Engineering Research Center of Molecular Medicine for Renal Diseases, Yantai, Shandong, China.

Cell Reports
|September 13, 2023
PubMed
Summary

Lipolysis-stimulated lipoprotein receptor (LSR) is crucial for Paneth cell differentiation in the intestine. LSR deficiency impairs Paneth cell development and exacerbates necrotizing enterocolitis.

Keywords:
CP: Cell biologyCP: Stem cell researchLSRPaneth cellYAPintestinal stem cell

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Area of Science:

  • Cell Biology
  • Gastroenterology
  • Molecular Biology

Background:

  • Lipolysis-stimulated lipoprotein receptor (LSR) is known for its roles in epithelial tight junctions and lipoprotein metabolism.
  • Its function in intestinal epithelium homeostasis and disease remains largely unexplored.

Purpose of the Study:

  • To investigate the role of LSR in intestinal epithelium homeostasis.
  • To determine LSR's contribution to the pathogenesis of intestinal diseases, specifically necrotizing enterocolitis.

Main Methods:

  • Conditional deletion mouse models and ex vivo organoid cultures were employed.
  • Mechanistic studies involved assessing YAP protein levels, phosphorylation, and proteasomal degradation.
  • Gain- and loss-of-function studies were conducted to evaluate LSR's impact on disease models.

Main Results:

  • LSR elimination in intestinal stem cells led to the disappearance of Paneth cells.
  • LSR deficiency increased YAP abundance by modulating its phosphorylation and proteasomal degradation.
  • LSR protected against necrotizing enterocolitis by enhancing Paneth cell differentiation.

Conclusions:

  • LSR is an essential factor for Paneth cell differentiation in the small intestinal epithelium.
  • LSR acts as an upstream negative regulator of YAP activity.
  • LSR represents a potential therapeutic target for necrotizing enterocolitis.