Mechanobiology and Cellular Mechanotransduction: Basic Science and Clinical Implications

A special issue of Bioengineering (ISSN 2306-5354).

Deadline for manuscript submissions: closed (30 October 2021) | Viewed by 3854

Special Issue Editor


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Guest Editor
Clemson University, Department of Bioengineering, Clemson, SC, USA
Interests: cellular mechanotransduction; tissue engineering; hydrogels

Special Issue Information

Dear Colleagues,

For decades, scientists have observed that mechanical forces influence cellular biological events in physiology and pathology. Moreover, growing evidence indicates that the mechanical properties of the surrounding microenvironments also impact cellular function. Advancements in the study of mechanotransduction – the conversion of mechanical signal inputs into biological events – has improved our understanding of how mechanical stimuli affect our health and diseases through regulation of cellular behavior and tissue development. This Special Issue “Mechanobiology and Cellular Mechanotransduction: Basic Science and Clinical Implications” will publish original research and current review papers with the aim of providing the readers with the cutting-edge findings and innovative application of mechanobiology. 

Prof. Dr. Jiro Nagatomi
Guest Editor

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Keywords

  • Mechanobiology
  • Mechanotransduction
  • Cellular function
  • Tissue development
  • Cellular microenvironment
  • Cell mechanics
  • Ion channels
  • Signal transduction
  • Cytoskeleton
  • Extracellular matrix

Published Papers (1 paper)

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Research

17 pages, 4994 KiB  
Article
A Loss of Nuclear—Cytoskeletal Interactions in Vascular Smooth Muscle Cell Differentiation Induced by a Micro-Grooved Collagen Substrate Enabling the Modeling of an In Vivo Cell Arrangement
by Kazuaki Nagayama
Bioengineering 2021, 8(9), 124; https://doi.org/10.3390/bioengineering8090124 - 12 Sep 2021
Cited by 3 | Viewed by 3209
Abstract
Vascular smooth muscle cells (VSMCs) remodel vascular walls actively owing to mechanical cues and dedifferentiate to the synthetic phenotype from contractile phenotype in pathological conditions. It is crucial to clarify the mechanisms behind the VSMC phenotypic transition for elucidating their role in the [...] Read more.
Vascular smooth muscle cells (VSMCs) remodel vascular walls actively owing to mechanical cues and dedifferentiate to the synthetic phenotype from contractile phenotype in pathological conditions. It is crucial to clarify the mechanisms behind the VSMC phenotypic transition for elucidating their role in the vascular adaptation and repair and for designing engineered tissues. We recently developed novel micro-grooved collagen substrates with “wavy wrinkle” grooves to induce cell–substrate adhesion, morphological polarization, and a tissue-like cell arrangement with cytoskeletal rearrangements similar to those in vascular tissue in vivo. We found that cultivation with this micro-grooved collagen significantly induced VSMC contractile differentiation. Nonetheless, the detailed mechanism underlying the promotion of such VSMC differentiation by micro-grooved collagen has not been clarified yet. Here, we investigated the detailed mechanism of the cell arrangement into a tissue and contractile-differentiation improvement by our micro-grooved collagen substrates in terms of nuclear–cytoskeletal interactions that possibly affect the nuclear mechanotransduction involved in the activation of transcription factors. We found that VSMCs on micro-grooved collagen manifested significant cell arrangement into a tissue and nucleus slimming with a volume reduction in response to the remodeling of the actin cytoskeleton, with consequent inhibition of nuclear shuttling of a transcriptional coactivator, Yes-associated protein (YAP), and improved contractile differentiation. Furthermore, VSMC nuclei rarely deformed during macroscopic cell stretching and featured a loss of nesprin-1–mediated nuclear–cytoskeletal interactions. These results indicate that our micro-grooved collagen induces a cell alignment mimicking in vivo VSMC tissue and promotes contractile differentiation. In such processes of contractile differentiation, mechanical interaction between the nucleus and actin cytoskeleton may diminish to prevent a nuclear disturbance from the excess mechanical stress that might be essential for maintaining vascular functions. Full article
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