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Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia
Piezo1 ion channels are mediators of mechanotransduction in several cell types including the vascular endothelium, renal tubular cells and erythrocytes. Gain-of-function mutations in PIEZO1 cause an autosomal dominant haemolytic anaemia in humans called dehydrated hereditary stomatocytosis. However,...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578306/ https://www.ncbi.nlm.nih.gov/pubmed/26387913 http://dx.doi.org/10.1038/ncomms9329 |
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author | Lukacs, Viktor Mathur, Jayanti Mao, Rong Bayrak-Toydemir, Pinar Procter, Melinda Cahalan, Stuart M. Kim, Helen J. Bandell, Michael Longo, Nicola Day, Ronald W. Stevenson, David A. Patapoutian, Ardem Krock, Bryan L. |
author_facet | Lukacs, Viktor Mathur, Jayanti Mao, Rong Bayrak-Toydemir, Pinar Procter, Melinda Cahalan, Stuart M. Kim, Helen J. Bandell, Michael Longo, Nicola Day, Ronald W. Stevenson, David A. Patapoutian, Ardem Krock, Bryan L. |
author_sort | Lukacs, Viktor |
collection | PubMed |
description | Piezo1 ion channels are mediators of mechanotransduction in several cell types including the vascular endothelium, renal tubular cells and erythrocytes. Gain-of-function mutations in PIEZO1 cause an autosomal dominant haemolytic anaemia in humans called dehydrated hereditary stomatocytosis. However, the phenotypic consequence of PIEZO1 loss of function in humans has not previously been documented. Here we discover a novel role of this channel in the lymphatic system. Through whole-exome sequencing, we identify biallelic mutations in PIEZO1 (a splicing variant leading to early truncation and a non-synonymous missense variant) in a pair of siblings affected with persistent lymphoedema caused by congenital lymphatic dysplasia. Analysis of patients' erythrocytes as well as studies in a heterologous system reveal greatly attenuated PIEZO1 function in affected alleles. Our results delineate a novel clinical category of PIEZO1-associated hereditary lymphoedema. |
format | Online Article Text |
id | pubmed-4578306 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-45783062015-10-21 Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia Lukacs, Viktor Mathur, Jayanti Mao, Rong Bayrak-Toydemir, Pinar Procter, Melinda Cahalan, Stuart M. Kim, Helen J. Bandell, Michael Longo, Nicola Day, Ronald W. Stevenson, David A. Patapoutian, Ardem Krock, Bryan L. Nat Commun Article Piezo1 ion channels are mediators of mechanotransduction in several cell types including the vascular endothelium, renal tubular cells and erythrocytes. Gain-of-function mutations in PIEZO1 cause an autosomal dominant haemolytic anaemia in humans called dehydrated hereditary stomatocytosis. However, the phenotypic consequence of PIEZO1 loss of function in humans has not previously been documented. Here we discover a novel role of this channel in the lymphatic system. Through whole-exome sequencing, we identify biallelic mutations in PIEZO1 (a splicing variant leading to early truncation and a non-synonymous missense variant) in a pair of siblings affected with persistent lymphoedema caused by congenital lymphatic dysplasia. Analysis of patients' erythrocytes as well as studies in a heterologous system reveal greatly attenuated PIEZO1 function in affected alleles. Our results delineate a novel clinical category of PIEZO1-associated hereditary lymphoedema. Nature Publishing Group 2015-09-21 /pmc/articles/PMC4578306/ /pubmed/26387913 http://dx.doi.org/10.1038/ncomms9329 Text en Copyright © 2015, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Lukacs, Viktor Mathur, Jayanti Mao, Rong Bayrak-Toydemir, Pinar Procter, Melinda Cahalan, Stuart M. Kim, Helen J. Bandell, Michael Longo, Nicola Day, Ronald W. Stevenson, David A. Patapoutian, Ardem Krock, Bryan L. Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia |
title | Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia |
title_full | Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia |
title_fullStr | Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia |
title_full_unstemmed | Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia |
title_short | Impaired PIEZO1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia |
title_sort | impaired piezo1 function in patients with a novel autosomal recessive congenital lymphatic dysplasia |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578306/ https://www.ncbi.nlm.nih.gov/pubmed/26387913 http://dx.doi.org/10.1038/ncomms9329 |
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