Stress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening rats

Abstract Hypertension causes aortic wall thickening until the original wall stress is restored. We hypothesized that this regulation involves stress fiber (SF) tension transmission to the nucleus in smooth muscle cells (SMCs) and investigated the strain in the SF direction as a condition required fo...

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Main Authors: Shukei Sugita, Rintaro Kawai, Yoshihiro Ujihara, Masanori Nakamura
Format: Article
Language:English
Published: Nature Portfolio 2024-11-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-024-81229-w
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author Shukei Sugita
Rintaro Kawai
Yoshihiro Ujihara
Masanori Nakamura
author_facet Shukei Sugita
Rintaro Kawai
Yoshihiro Ujihara
Masanori Nakamura
author_sort Shukei Sugita
collection DOAJ
description Abstract Hypertension causes aortic wall thickening until the original wall stress is restored. We hypothesized that this regulation involves stress fiber (SF) tension transmission to the nucleus in smooth muscle cells (SMCs) and investigated the strain in the SF direction as a condition required for this transmission. Thoracic aortas from Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHRs) were examined. SFs in aortic SMCs were fluorescently labeled and observed under a confocal microscope while stretched along the circumferential (θ) axis. Three conditions were studied: WKY physiological (WKYphys; blood pressure changes from diastolic to systolic for WKY), high-strain state (WKYhigh; diastolic to hypertensive level for WKY simulating initial hypertension), and SHR physiological (SHRphys; diastolic to systolic for SHR simulating after wall-thickening). SF strain and direction were measured. The SF inclination angle from the θ axis was 18° ± 3° in WKYphys, 13° ± 2° in WKYhigh, and 20° ± 1° in SHRphys. SF strain was 0.01 ± 0.02 in WKYphys, 0.20 ± 0.04 in WKYhigh, and 0.02 ± 0.02 SHRphys. SF strain was minimal in WKYphys, significantly increased in WKYhigh, and reduced to approximately zero in SHRphys. These findings support SFs function as mechanosensors in response to hypertension.
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spelling doaj-art-e960d58beec14e099c96e9d68207bcb12025-08-20T01:57:49ZengNature PortfolioScientific Reports2045-23222024-11-0114111210.1038/s41598-024-81229-wStress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening ratsShukei Sugita0Rintaro Kawai1Yoshihiro Ujihara2Masanori Nakamura3Department of Electrical and Mechanical Engineering, Nagoya Institute of TechnologyDepartment of Electrical and Mechanical Engineering, Nagoya Institute of TechnologyDepartment of Electrical and Mechanical Engineering, Nagoya Institute of TechnologyDepartment of Electrical and Mechanical Engineering, Nagoya Institute of TechnologyAbstract Hypertension causes aortic wall thickening until the original wall stress is restored. We hypothesized that this regulation involves stress fiber (SF) tension transmission to the nucleus in smooth muscle cells (SMCs) and investigated the strain in the SF direction as a condition required for this transmission. Thoracic aortas from Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHRs) were examined. SFs in aortic SMCs were fluorescently labeled and observed under a confocal microscope while stretched along the circumferential (θ) axis. Three conditions were studied: WKY physiological (WKYphys; blood pressure changes from diastolic to systolic for WKY), high-strain state (WKYhigh; diastolic to hypertensive level for WKY simulating initial hypertension), and SHR physiological (SHRphys; diastolic to systolic for SHR simulating after wall-thickening). SF strain and direction were measured. The SF inclination angle from the θ axis was 18° ± 3° in WKYphys, 13° ± 2° in WKYhigh, and 20° ± 1° in SHRphys. SF strain was 0.01 ± 0.02 in WKYphys, 0.20 ± 0.04 in WKYhigh, and 0.02 ± 0.02 SHRphys. SF strain was minimal in WKYphys, significantly increased in WKYhigh, and reduced to approximately zero in SHRphys. These findings support SFs function as mechanosensors in response to hypertension.https://doi.org/10.1038/s41598-024-81229-wHypertensionFluorescent microscopyVascular smooth muscle cellsStress fiberNormal strain
spellingShingle Shukei Sugita
Rintaro Kawai
Yoshihiro Ujihara
Masanori Nakamura
Stress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening rats
Scientific Reports
Hypertension
Fluorescent microscopy
Vascular smooth muscle cells
Stress fiber
Normal strain
title Stress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening rats
title_full Stress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening rats
title_fullStr Stress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening rats
title_full_unstemmed Stress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening rats
title_short Stress fiber strain is zero in normal aortic smooth muscle, elevated in hypertensive stretch, and minimal in wall thickening rats
title_sort stress fiber strain is zero in normal aortic smooth muscle elevated in hypertensive stretch and minimal in wall thickening rats
topic Hypertension
Fluorescent microscopy
Vascular smooth muscle cells
Stress fiber
Normal strain
url https://doi.org/10.1038/s41598-024-81229-w
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