scholarly journals A human in vitro 3D neo-cartilage model to explore the response of OA risk genes to hyper-physiological mechanical stress

2021 ◽  
pp. 100231
Author(s):  
Ritchie G.M. Timmermans ◽  
Niek G.C. Bloks ◽  
Margo Tuerlings ◽  
Marcella van Hoolwerff ◽  
Rob G.H.H. Nelissen ◽  
...  
Keyword(s):  
Mechanical Stress ◽  
Risk Genes

scholarly journals Exosomal Vimentin from Adipocyte Progenitors Protects Fibroblasts against Osmotic Stress and Inhibits Apoptosis to Enhance Wound Healing

2021 ◽  
Vol 22 (9) ◽  
pp. 4678
Author(s):  
Sepideh Parvanian ◽  
Hualian Zha ◽  
Dandan Su ◽  
Lifang Xi ◽  
Yaming Jiu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Osmotic Stress ◽  
Mechanical Stress ◽  
Impaired Wound Healing ◽  
In Vivo Experiments ◽  
Adipocyte Progenitors ◽  
Osmotic Balance ◽  
Induced Apoptosis

Mechanical stress following injury regulates the quality and speed of wound healing. Improper mechanotransduction can lead to impaired wound healing and scar formation. Vimentin intermediate filaments control fibroblasts’ response to mechanical stress and lack of vimentin makes cells significantly vulnerable to environmental stress. We previously reported the involvement of exosomal vimentin in mediating wound healing. Here we performed in vitro and in vivo experiments to explore the effect of wide-type and vimentin knockout exosomes in accelerating wound healing under osmotic stress condition. Our results showed that osmotic stress increases the size and enhances the release of exosomes. Furthermore, our findings revealed that exosomal vimentin enhances wound healing by protecting fibroblasts against osmotic stress and inhibiting stress-induced apoptosis. These data suggest that exosomes could be considered either as a stress modifier to restore the osmotic balance or as a conveyer of stress to induce osmotic stress-driven conditions.

Mechanical stress and osteogenesis in vitro

1992 ◽  
Vol 7 (S2) ◽  
pp. S397-S401 ◽  
Author(s):  
Elisabeth H. Burger ◽  
Jenneke Klein-Nulend ◽  
J. Paul Veldhuijzen
Keyword(s):  
Mechanical Stress ◽  
Osteogenesis In Vitro

In vitro mechanical stress

Cell ◽  
1989 ◽  
Vol 56 (5) ◽  
pp. v
Keyword(s):  
Mechanical Stress

scholarly journals Estimation of nitric oxide generation by endothelial cells EA.hy926 under flow-induced mechanical stress in a microfluidic system

2020 ◽  
pp. 71-77
Author(s):  
А.А. Московцев ◽  
А.Н. Мыльникова ◽  
Д.В. Колесов ◽  
А.А. Микрюкова ◽  
Д.М. Зайченко ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Mechanical Stress ◽  
Microfluidic System ◽  
Hydrodynamic Characteristics ◽  
No Production ◽  
Hydrodynamic Conditions ◽  
Cellular Mechanisms ◽  
Vascular Walls

Эндотелиальные клетки, выстилающие стенки сосудов, преобразовывают деформацию собственных структур, вызванную током крови, в химические сигналы, одним из которых является важный регулятор просвета сосуда - оксид азота (NO). К настоящему моменту накоплен большой объём данных о клеточных механизмах активации продукции NO, однако сведений о динамике генерации оксида азота эндотелиальными клетками в зависимости от гидродинамических условий недостаточно. В этой связи разработка микрофлюидных систем in vitro, имитирующих кровеносное русло, и изучение в них эндотелия в сложных гидродинамических условиях является актуальной задачей. В данной работе для создания контролируемых гидродинамических условий для монослоя эндотелиоцитоподобных клеток EA.hy926 была спроектирована и разработана микрофлюидная система, имитирующая линейные участки микрососудистого русла. Методом непрямого определения содержания оксида азота (II) NO с использованием флуоресцентного зонда 4,5-диаминофлуоресцеина DAF-2 впервые получены данные об увеличении продукции NO клетками EA.hy926 при механическом стрессе, создаваемом потоком ростовой среды. Представлены расчетные гидродинамические характеристики микрофлюидной системы, а также методика измерения продукции NO. Возможность исследования функциональной активности эндотелия позволяет использовать разработанную микрофлюидную модельную систему как для изучения клеточно-автономных регуляторных свойств эндотелия при действии ряда вазоактивных фармакологических препаратов и других методов воздействия на эндотелий, так и при моделируемой дисфункции эндотелия. Endothelial cells lining vascular walls transform the flow-induced deformation of their own structures into chemical signals, one of which, nitric oxide (NO), is an important regulator of the vascular lumen diameter. By present, a large amount of data on cellular mechanisms for activation of NO production has been accumulated. However, there is insufficient information on changes in endothelial NO generation under different hydrodynamic conditions. Therefore, development of microfluidic systems that model blood vessels in vitro and using them to study the endothelium under complex hydrodynamic conditions are relevant tasks. In this study, a microfluidic system was developed to create controlled hydrodynamic conditions for a monolayer of endotheliocyte-like cells EAhy.926. This system simulates linear sections of the microvasculature. By indirect measurement of NO (II) content with a fluorescent 4,5-diaminofluorescein (DAF-2) probe, we showed an increase in the NO production by EAhy.926 cells under mechanical stress generated by the medium flow. The article presents the method for measuring NO production and the calculated hydrodynamic characteristics of the microfluidic system. The results showed that the developed microfluidic model system is promising for studying cell-autonomous regulatory properties of the endothelium both under the action of vasoactive agents and in simulated endothelial dysfunction.

Mechanical Stress Activates Platelets at a Subhemolysis Level: An In Vitro Study

2007 ◽  
Vol 31 (4) ◽  
pp. 316-323 ◽  
Author(s):  
Ihsan Bakir ◽  
Marc F. Hoylaerts ◽  
Thomas Kink ◽  
Luc Foubert ◽  
Peter Luyten ◽  
...  
Keyword(s):  
Mechanical Stress ◽  
In Vitro Study ◽  
Vitro Study

Repetitive tensile stress to rat caudal vertebrae inducing cartilage formation in the spinal ligaments: a possible role of mechanical stress in the development of ossification of the spinal ligaments

2006 ◽  
Vol 5 (3) ◽  
pp. 234-242 ◽  
Author(s):  
Nobuaki Tsukamoto ◽  
Takeshi Maeda ◽  
Hiromasa Miura ◽  
Seiya Jingushi ◽  
Akira Hosokawa ◽  
...  
Keyword(s):  
Tensile Stress ◽  
Mechanical Stress ◽  
Tensile Force ◽  
Bone Morphogenetic Protein 2 ◽  
Woven Bone ◽  
Morphogenetic Protein ◽  
Caudal Vertebrae ◽  
Spinal Ligaments

Object Mechanical stress has been considered one of the important factors in ossification of the spinal ligaments. According to previous clinical and in vitro studies, the accumulation of tensile stress to these ligaments may be responsible for ligament ossification. To elucidate the relationship between such mechanical stress and the development of ossification of the spinal ligaments, the authors established an animal experimental model in which the in vivo response of the spinal ligaments to direct repetitive tensile loading could be observed. Methods The caudal vertebrae of adult Wistar rats were studied. After creating a novel stimulating apparatus, cyclic tensile force was loaded to rat caudal spinal ligaments at 10 N in 600 to 1800 cycles per day for up to 2 weeks. The morphological responses were then evaluated histologically and immunohistochemically. After the loadings, ectopic cartilaginous formations surrounded by proliferating round cells were observed near the insertion of the spinal ligaments. Several areas of the cartilaginous tissue were accompanied by woven bone. Bone morphogenetic protein–2 expression was clearly observed in the cytoplasm of the proliferating round cells. The histological features of the rat spinal ligaments induced by the tensile loadings resembled those of spinal ligament ossification observed in humans. Conclusions The findings obtained in the present study strongly suggest that repetitive tensile stress to the spinal ligaments is one of the important causes of ligament ossification in the spine.

scholarly journals Mechanical stress impairs pheromone signaling via Pkc1-mediated regulation of the MAPK scaffold Ste5

2019 ◽  
Vol 218 (9) ◽  
pp. 3117-3133 ◽  
Author(s):  
Frank van Drogen ◽  
Ranjan Mishra ◽  
Fabian Rudolf ◽  
Michal J. Walczak ◽  
Sung Sik Lee ◽  
...  
Keyword(s):  
Mechanical Stress ◽  
Cell Fusion ◽  
Polarized Growth ◽  
Conserved Residues ◽  
Cellular Processes ◽  
Pheromone Signaling ◽  
Stress Signals ◽  
Cell Cell

Cells continuously adapt cellular processes by integrating external and internal signals. In yeast, multiple stress signals regulate pheromone signaling to prevent mating under unfavorable conditions. However, the underlying crosstalk mechanisms remain poorly understood. Here, we show that mechanical stress activates Pkc1, which prevents lysis of pheromone-treated cells by inhibiting polarized growth. In vitro Pkc1 phosphorylates conserved residues within the RING-H2 domains of the scaffold proteins Far1 and Ste5, which are also phosphorylated in vivo. Interestingly, Pkc1 triggers dispersal of Ste5 from mating projections upon mechanically induced stress and during cell–cell fusion, leading to inhibition of the MAPK Fus3. Indeed, RING phosphorylation interferes with Ste5 membrane association by preventing binding to the receptor-linked Gβγ protein. Cells expressing nonphosphorylatable Ste5 undergo increased lysis upon mechanical stress and exhibit defects in cell–cell fusion during mating, which is exacerbated by simultaneous expression of nonphosphorylatable Far1. These results uncover a mechanical stress–triggered crosstalk mechanism modulating pheromone signaling, polarized growth, and cell–cell fusion during mating.

scholarly journals Integrin β1 Gene Therapy Enhances in Vitro Creation of Tissue-Engineered Cartilage Under Periodic Mechanical Stress

2015 ◽  
Vol 37 (4) ◽  
pp. 1301-1314 ◽  
Author(s):  
Wenwei Liang ◽  
Chunhui Zhu ◽  
Feng Liu ◽  
Weiding Cui ◽  
Qing Wang ◽  
...  
Keyword(s):  
Mechanical Stress ◽  
Type Ii Collagen ◽  
Cell Types ◽  
Signal Pathways ◽  
Matrix Synthesis ◽  
Integrin Β1 ◽  
Chondrocyte Proliferation ◽  
Engineered Cartilage

Background/Aims: Periodic mechanical stress activates integrin β1-initiated signal pathways to promote chondrocyte proliferation and matrix synthesis. Integrin β1 overexpression has been demonstrated to play important roles in improving the activities and functions of several non-chondrocytic cell types. Therefore, in the current study, we evaluated the effects of integrin β1 up-regulation on periodic mechanical stress-induced chondrocyte proliferation, matrix synthesis and ERK1/2 phosphorylation in chondrocyte monolayer culture, and evaluated the quality of tissue-engineered cartilage constructed in vitro under periodic mechanical stress combined with integrin β1 up-regulation. Methods and Results: Our results revealed that under periodic mechanical stress, pre-treatment with integrin β1-wild type vector significantly enhanced chondrocyte proliferation and matrix synthesis and promoted ERK1/2 phosphorylation in comparison to mock transfectants. Furthermore, when chondrocytes were seeded in PLGA scaffolds, more accumulated GAG and type II collagen tissue were detected after Lv-integrin β1 transfection compared with sham controls exposed to periodic mechanical stress. In contrast, in the Lv-shRNA-integrin β1 group, the opposite results were observed. Conclusion: Our findings collectively suggest that in addition to periodic mechanical stress, integrin β1 up-regulation in chondrocytes could further improve the quality of tissue-engineered cartilage.

Mechanical Stretching of Mouse Calvarial Osteoblasts In Vitro Models Changes in MMP-2 and MMP-9 Expression at the Bone-Implant Interface

2016 ◽  
Vol 42 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Richard A. Nichols ◽  
Frank D. Niagro ◽  
James L. Borke ◽  
Michael F. Cuenin
Keyword(s):  
Mechanical Stress ◽  
Mechanical Loading ◽  
Tooth Movement ◽  
Active Form ◽  
Orthodontic Tooth Movement ◽  
Biological Response ◽  
Gelatin Zymography ◽  
Joint Disease ◽  
Mechanical Stretching

Bone to mechanical loading elicits a biological response that has clinical significance for several areas in dental medicine, including orthodontic tooth movement, tempromandibular joint disease, and endosseous dental implant osseointegration. Human orthopedic studies of failed hip implant sites have identified increased mRNA expression of several collagen-degrading matrix metalloproteinases (MMPs), while in vitro experiments have shown increases in MMP secretion after exposure to inflammatory mediators. This investigation evaluates the effects of mechanical deformation on in vitro osteoblasts by assessing changes in MMP gene expression and enzyme activity. We seeded mouse neonatal calvarial osteoblasts onto flexible 6-well plates and subjected to continuous cyclic mechanical stretching. The expression and activity of mRNA for several MMPs (2, 3, 9, and 10) was assessed. When subjected to mechanical stress in culture, only mRNA specific for MMP-9 was significantly increased compared to nonstretched controls (P < .005). Measurement of MMP activity by gelatin zymography demonstrated that none of the MMPs showed increased activity with stretching; however, MMP-2 activity decreased. Our results suggest that in response to stretch, MMP-2 responds rapidly by inhibiting conversion of a MMP-2 to the active form, while a slower up-regulation of MMP-9 may play a role in the long-term remodeling of extracellular matrix in response to continuous mechanical loading. This study suggests that the regulation of metalloproteinases at both the mRNA and protein level are important in the response of bone to mechanical stress.

scholarly journals In Vitro Weight-Loaded Cell Models for Understanding Mechanodependent Molecular Pathways Involved in Orthodontic Tooth Movement: A Systematic Review

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Mila Janjic ◽  
Denitsa Docheva ◽  
Olivera Trickovic Janjic ◽  
Andrea Wichelhaus ◽  
Uwe Baumert
Keyword(s):  
Systematic Review ◽  
Mechanical Stress ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Compressive Force ◽  
Cell Types ◽  
Dental Stem Cells ◽  
Protein Protein Interaction ◽  
Different Cell Types

Cells from the mesenchymal lineage in the dental area, including but not limited to PDL fibroblasts, osteoblasts, and dental stem cells, are exposed to mechanical stress in physiological (e.g., chewing) and nonphysiological/therapeutic (e.g., orthodontic tooth movement) situations. Close and complex interaction of these different cell types results in the physiological and nonphysiological adaptation of these tissues to mechanical stress. Currently, different in vitro loading models are used to investigate the effect of different types of mechanical loading on the stress adaptation of these cell types. We performed a systematic review according to the PRISMA guidelines to identify all studies in the field of dentistry with focus on mechanobiology using in vitro loading models applying uniaxial static compressive force. Only studies reporting on cells from the mesenchymal lineage were considered for inclusion. The results are summarized regarding gene expression in relation to force duration and magnitude, and the most significant signaling pathways they take part in are identified using protein-protein interaction networks.

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