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Corticotropin-releasing factor receptor agonists decrease interstitial cells of Cajal in murine colon.

Xu Huang1, Jun-Ping Ao2, Han-Yue Fu1

  • 1Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Neurogastroenterology and Motility
|November 15, 2022
PubMed
Summary
This summary is machine-generated.

Peripheral corticotropin-releasing factor (CRF) activation of CRF receptor 1 in the colon reduces interstitial cells of Cajal (ICC) and may cause motility disorders. This suggests a new therapeutic target for stress-induced gastrointestinal issues.

Keywords:
CRF1CRF2ICCmurine colonstress

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Area of Science:

  • Gastroenterology
  • Neuroendocrinology
  • Cell Biology

Background:

  • Peripheral corticotropin-releasing factor (CRF) influences gastrointestinal (GI) motility via enteric nervous system (ENS) receptors.
  • The precise role of peripheral CRF in regulating interstitial cells of Cajal (ICC), crucial for GI motility, remains largely unexplored.

Purpose of the Study:

  • To investigate the impact of peripheral CRF signaling on colonic ICC in mice.
  • To explore the potential link between CRF receptor activation and stress-induced alterations in colonic motility.

Main Methods:

  • Mice received intraperitoneal injections of CRF receptor agonists (stressin1 for CRF1, sauvagine for CRF2).
  • Chronic heterotypic stress (CHeS) was applied to mice to assess endogenous CRF-CRF receptor signaling.
  • Expression of CRF receptors, c-Kit, Anoctamin-1 (ANO1), and stem cell factor (SCF) in colonic smooth muscle was analyzed.

Main Results:

  • Stressin1 (CRF1 agonist) decreased c-Kit, ANO1, and SCF expression in colonic smooth muscle.
  • Sauvagine (CRF2 agonist) also reduced ICC and ANO1 expression, while altering CRF1 and CRF2 expression.
  • CHeS mirrored these findings, showing reduced CRF1 and c-Kit expression in colonic ICC.

Conclusions:

  • Peripheral CRF, particularly via CRF receptor 1, may impair colonic motility by decreasing ICC number and function.
  • These findings highlight a potential therapeutic target for managing stress-related GI motility disorders.