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Cathelicidins positively regulate pancreatic β-cell functions.

Jia Sun1, Meng Xu2, Henrik Ortsäter2

  • 1*State Key Laboratory of Food Science and Technology, School of Food Science and Technology and Synergetic Innovation Center of Food Safety and Nutrition, Jiangnan University, Wuxi, China; Biomedical Centre, Uppsala University, Uppsala, Sweden; Diabetes Research Unit, Department of Clinical Science and Education, Department of Physiology and Pharmacology, and The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, Stockholm, Sweden; Biomedical Center, University of Iceland, Reykjavik, Iceland; Institut National de la Santé et de la Recherche Médicale, Institute Necker-Enfants Malades, Centre National de la Recherche Scientifique, Paris, France; **Université Paris Descartes, Sorbonne Paris Cité, Paris, France; and Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden jiasun@jiangnan.edu.cn.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|November 4, 2015
PubMed
Summary

Cathelicidin-related antimicrobial peptide (CRAMP) is expressed by beta cells and promotes their survival and function. CRAMP administration improves glucose control, suggesting therapeutic potential for beta cell dysfunction.

Keywords:
CRAMPantimicrobial peptideendocrine cellsimmunomodulationtype 1 diabetes

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Area of Science:

  • Endocrinology
  • Immunology
  • Molecular Biology

Background:

  • Cathelicidins are antimicrobial peptides with immunomodulatory roles.
  • The function of cathelicidins in pancreatic beta cells remains largely unexplored.
  • Understanding beta cell regulation is crucial for diabetes research.

Purpose of the Study:

  • To investigate the expression and function of cathelicidin-related antimicrobial peptide (CRAMP) in pancreatic beta cells.
  • To determine CRAMP's role in beta cell survival, insulin secretion, and inflammatory responses.
  • To explore the therapeutic potential of CRAMP in models of diabetes.

Main Methods:

  • Quantitative analysis of CRAMP expression in beta cell lines and islets.
  • In vitro studies on beta cell survival and apoptosis modulation.
  • Ex vivo assessment of glucose-stimulated insulin secretion.
  • In vivo studies using CRAMP-deficient and prediabetic mouse models.

Main Results:

  • CRAMP is constitutively expressed and inducible in beta cells.
  • CRAMP enhances beta cell survival via EGFR and modulates Bcl-2 family proteins.
  • CRAMP stimulates glucose-stimulated insulin secretion and modulates inflammatory responses.
  • CRAMP deficiency impairs insulin secretion, while CRAMP administration improves glucose tolerance in vivo.

Conclusions:

  • Cathelicidins, specifically CRAMP, play a significant role in regulating beta cell function and survival.
  • CRAMP exhibits protective effects against inflammation-induced beta cell damage.
  • CRAMP represents a potential therapeutic target for diseases involving beta cell dysfunction.