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Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition
Meibomian glands (MGs) are modified sebaceous glands producing the tear film’s lipids. Despite their critical role in maintaining clear vision, the mechanisms underlying MG morphogenesis in development and disease remain obscure. Cilia-mediate signals are critical for the development of skin adnexa,...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10023665/ https://www.ncbi.nlm.nih.gov/pubmed/36932132 http://dx.doi.org/10.1038/s42003-023-04632-5 |
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author | Portal, Céline Lin, Yvonne Rastogi, Varuni Peterson, Cornelia Yiu, Samuel Chi-Hung Foster, James W. Wilkerson, Amber Butovich, Igor A. Iomini, Carlo |
author_facet | Portal, Céline Lin, Yvonne Rastogi, Varuni Peterson, Cornelia Yiu, Samuel Chi-Hung Foster, James W. Wilkerson, Amber Butovich, Igor A. Iomini, Carlo |
author_sort | Portal, Céline |
collection | PubMed |
description | Meibomian glands (MGs) are modified sebaceous glands producing the tear film’s lipids. Despite their critical role in maintaining clear vision, the mechanisms underlying MG morphogenesis in development and disease remain obscure. Cilia-mediate signals are critical for the development of skin adnexa, including sebaceous glands. Thus, we investigated the role of cilia in MG morphogenesis during development. Most cells were ciliated during early MG development, followed by cilia disassembly during differentiation. In mature glands, ciliated cells were primarily restricted to the basal layer of the proximal gland central duct. Cilia ablation in keratine14-expressing tissue disrupted the accumulation of proliferative cells at the distal tip but did not affect the overall rate of proliferation or apoptosis. Moreover, impaired cellular patterning during elongation resulted in hypertrophy of mature MGs with increased meibum volume without altering its lipid composition. Thus, cilia signaling networks provide a new platform to design therapeutic treatments for MG dysfunction. |
format | Online Article Text |
id | pubmed-10023665 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-100236652023-03-19 Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition Portal, Céline Lin, Yvonne Rastogi, Varuni Peterson, Cornelia Yiu, Samuel Chi-Hung Foster, James W. Wilkerson, Amber Butovich, Igor A. Iomini, Carlo Commun Biol Article Meibomian glands (MGs) are modified sebaceous glands producing the tear film’s lipids. Despite their critical role in maintaining clear vision, the mechanisms underlying MG morphogenesis in development and disease remain obscure. Cilia-mediate signals are critical for the development of skin adnexa, including sebaceous glands. Thus, we investigated the role of cilia in MG morphogenesis during development. Most cells were ciliated during early MG development, followed by cilia disassembly during differentiation. In mature glands, ciliated cells were primarily restricted to the basal layer of the proximal gland central duct. Cilia ablation in keratine14-expressing tissue disrupted the accumulation of proliferative cells at the distal tip but did not affect the overall rate of proliferation or apoptosis. Moreover, impaired cellular patterning during elongation resulted in hypertrophy of mature MGs with increased meibum volume without altering its lipid composition. Thus, cilia signaling networks provide a new platform to design therapeutic treatments for MG dysfunction. Nature Publishing Group UK 2023-03-17 /pmc/articles/PMC10023665/ /pubmed/36932132 http://dx.doi.org/10.1038/s42003-023-04632-5 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Portal, Céline Lin, Yvonne Rastogi, Varuni Peterson, Cornelia Yiu, Samuel Chi-Hung Foster, James W. Wilkerson, Amber Butovich, Igor A. Iomini, Carlo Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition |
title | Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition |
title_full | Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition |
title_fullStr | Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition |
title_full_unstemmed | Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition |
title_short | Primary cilia control cellular patterning of Meibomian glands during morphogenesis but not lipid composition |
title_sort | primary cilia control cellular patterning of meibomian glands during morphogenesis but not lipid composition |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10023665/ https://www.ncbi.nlm.nih.gov/pubmed/36932132 http://dx.doi.org/10.1038/s42003-023-04632-5 |
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