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Cilia Action in Islets: Lessons From Mouse Models

Primary cilia as a signaling organelle have garnered recent attention as a regulator of pancreatic islet function. These rod-like sensors exist on all major islet endocrine cell types and transduce a variety of external cues, while dysregulation of cilia function contributes to the development of di...

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Autores principales: Cho, Jung Hoon, Hughes, Jing W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9260721/
https://www.ncbi.nlm.nih.gov/pubmed/35813631
http://dx.doi.org/10.3389/fendo.2022.922983
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author Cho, Jung Hoon
Hughes, Jing W.
author_facet Cho, Jung Hoon
Hughes, Jing W.
author_sort Cho, Jung Hoon
collection PubMed
description Primary cilia as a signaling organelle have garnered recent attention as a regulator of pancreatic islet function. These rod-like sensors exist on all major islet endocrine cell types and transduce a variety of external cues, while dysregulation of cilia function contributes to the development of diabetes. The complex role of islet primary cilia has been examined using genetic deletion targeting various components of cilia. In this review, we summarize experimental models for the study of islet cilia and current understanding of mechanisms of cilia regulation of islet hormone secretion. Consensus from these studies shows that pancreatic cilia perturbation can cause both endocrine and exocrine defects that are relevant to human disease. We discuss future research directions that would further elucidate cilia action in distinct groups of islet cells, including paracrine and juxtacrine regulation, GPCR signaling, and endocrine-exocrine crosstalk.
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spelling pubmed-92607212022-07-08 Cilia Action in Islets: Lessons From Mouse Models Cho, Jung Hoon Hughes, Jing W. Front Endocrinol (Lausanne) Endocrinology Primary cilia as a signaling organelle have garnered recent attention as a regulator of pancreatic islet function. These rod-like sensors exist on all major islet endocrine cell types and transduce a variety of external cues, while dysregulation of cilia function contributes to the development of diabetes. The complex role of islet primary cilia has been examined using genetic deletion targeting various components of cilia. In this review, we summarize experimental models for the study of islet cilia and current understanding of mechanisms of cilia regulation of islet hormone secretion. Consensus from these studies shows that pancreatic cilia perturbation can cause both endocrine and exocrine defects that are relevant to human disease. We discuss future research directions that would further elucidate cilia action in distinct groups of islet cells, including paracrine and juxtacrine regulation, GPCR signaling, and endocrine-exocrine crosstalk. Frontiers Media S.A. 2022-06-23 /pmc/articles/PMC9260721/ /pubmed/35813631 http://dx.doi.org/10.3389/fendo.2022.922983 Text en Copyright © 2022 Cho and Hughes https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Cho, Jung Hoon
Hughes, Jing W.
Cilia Action in Islets: Lessons From Mouse Models
title Cilia Action in Islets: Lessons From Mouse Models
title_full Cilia Action in Islets: Lessons From Mouse Models
title_fullStr Cilia Action in Islets: Lessons From Mouse Models
title_full_unstemmed Cilia Action in Islets: Lessons From Mouse Models
title_short Cilia Action in Islets: Lessons From Mouse Models
title_sort cilia action in islets: lessons from mouse models
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9260721/
https://www.ncbi.nlm.nih.gov/pubmed/35813631
http://dx.doi.org/10.3389/fendo.2022.922983
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