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Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells
Bladder cells face a challenging biophysical environment: mechanical cues originating from urine flow and regular contraction to enable the filling voiding of the organ. To ensure functional adaption, bladder cells rely on high biomechanical compliance, nevertheless aging or chronic pathological con...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614373/ https://www.ncbi.nlm.nih.gov/pubmed/37904178 http://dx.doi.org/10.1186/s12964-023-01295-x |
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author | Gruber, Livia Jobst, Maximilian Kiss, Endre Karasová, Martina Englinger, Bernhard Berger, Walter Del Favero, Giorgia |
author_facet | Gruber, Livia Jobst, Maximilian Kiss, Endre Karasová, Martina Englinger, Bernhard Berger, Walter Del Favero, Giorgia |
author_sort | Gruber, Livia |
collection | PubMed |
description | Bladder cells face a challenging biophysical environment: mechanical cues originating from urine flow and regular contraction to enable the filling voiding of the organ. To ensure functional adaption, bladder cells rely on high biomechanical compliance, nevertheless aging or chronic pathological conditions can modify this plasticity. Obviously the cytoskeletal network plays an essential role, however the contribution of other, closely entangled, intracellular organelles is currently underappreciated. The endoplasmic reticulum (ER) lies at a crucial crossroads, connected to both nucleus and cytoskeleton. Yet, its role in the maintenance of cell mechanical stability is less investigated. To start exploring these aspects, T24 bladder cancer cells were treated with the ER stress inducers brefeldin A (10-40nM BFA, 24 h) and thapsigargin (0.1-100nM TG, 24 h). Without impairment of cell motility and viability, BFA and TG triggered a significant subcellular redistribution of the ER; this was associated with a rearrangement of actin cytoskeleton. Additional inhibition of actin polymerization with cytochalasin D (100nM CytD) contributed to the spread of the ER toward cell periphery, and was accompanied by an increase of cellular stiffness (Young´s modulus) in the cytoplasmic compartment. Shrinking of the ER toward the nucleus (100nM TG, 2 h) was related to an increased stiffness in the nuclear and perinuclear areas. A similar short-term response profile was observed also in normal human primary bladder fibroblasts. In sum, the ER and its subcellular rearrangement seem to contribute to the mechanical properties of bladder cells opening new perspectives in the study of the related stress signaling cascades. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01295-x. |
format | Online Article Text |
id | pubmed-10614373 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-106143732023-10-31 Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells Gruber, Livia Jobst, Maximilian Kiss, Endre Karasová, Martina Englinger, Bernhard Berger, Walter Del Favero, Giorgia Cell Commun Signal Research Bladder cells face a challenging biophysical environment: mechanical cues originating from urine flow and regular contraction to enable the filling voiding of the organ. To ensure functional adaption, bladder cells rely on high biomechanical compliance, nevertheless aging or chronic pathological conditions can modify this plasticity. Obviously the cytoskeletal network plays an essential role, however the contribution of other, closely entangled, intracellular organelles is currently underappreciated. The endoplasmic reticulum (ER) lies at a crucial crossroads, connected to both nucleus and cytoskeleton. Yet, its role in the maintenance of cell mechanical stability is less investigated. To start exploring these aspects, T24 bladder cancer cells were treated with the ER stress inducers brefeldin A (10-40nM BFA, 24 h) and thapsigargin (0.1-100nM TG, 24 h). Without impairment of cell motility and viability, BFA and TG triggered a significant subcellular redistribution of the ER; this was associated with a rearrangement of actin cytoskeleton. Additional inhibition of actin polymerization with cytochalasin D (100nM CytD) contributed to the spread of the ER toward cell periphery, and was accompanied by an increase of cellular stiffness (Young´s modulus) in the cytoplasmic compartment. Shrinking of the ER toward the nucleus (100nM TG, 2 h) was related to an increased stiffness in the nuclear and perinuclear areas. A similar short-term response profile was observed also in normal human primary bladder fibroblasts. In sum, the ER and its subcellular rearrangement seem to contribute to the mechanical properties of bladder cells opening new perspectives in the study of the related stress signaling cascades. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01295-x. BioMed Central 2023-10-30 /pmc/articles/PMC10614373/ /pubmed/37904178 http://dx.doi.org/10.1186/s12964-023-01295-x 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Gruber, Livia Jobst, Maximilian Kiss, Endre Karasová, Martina Englinger, Bernhard Berger, Walter Del Favero, Giorgia Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells |
title | Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells |
title_full | Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells |
title_fullStr | Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells |
title_full_unstemmed | Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells |
title_short | Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells |
title_sort | intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614373/ https://www.ncbi.nlm.nih.gov/pubmed/37904178 http://dx.doi.org/10.1186/s12964-023-01295-x |
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