An introductory review of cell mechanobiology. Biomech. Model. Mechanobiol. 5:1-16

MechanoBiology Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, 210 Lothrop St. BST, E1640, Pittsburgh, PA 15213, USA.
Biomechanics and Modeling in Mechanobiology (Impact Factor: 3.15). 04/2006; 5(1):1-16. DOI: 10.1007/s10237-005-0012-z
Source: PubMed


Mechanical loads induce changes in the structure, composition, and function of living tissues. Cells in tissues are responsible for these changes, which cause physiological or pathological alterations in the extracellular matrix (ECM). This article provides an introductory review of the mechanobiology of load-sensitive cells in vivo, which include fibroblasts, chondrocytes, osteoblasts, endothelial cells, and smooth muscle cells. Many studies have shown that mechanical loads affect diverse cellular functions, such as cell proliferation, ECM gene and protein expression, and the production of soluble factors. Major cellular components involved in the mechanotransduction mechanisms include the cytoskeleton, integrins, G proteins, receptor tyrosine kinases, mitogen-activated protein kinases, and stretch-activated ion channels. Future research in the area of cell mechanobiology will require novel experimental and theoretical methodologies to determine the type and magnitude of the forces experienced at the cellular and sub-cellular levels and to identify the force sensors/receptors that initiate the cascade of cellular and molecular events.

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Available from: James Wang, Feb 05, 2015
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    • "In comparison, mechanical behavior of MSCs during differentiation to a vascular cell fate, such as SMCs, is less well defined and more controversial. It is reported that many physiological cell activities such as motility, differentiation, migration and proliferation are influenced by cell structural integrity and consequently cell mechanical properties (Wang and Thampatty, 2006). "
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    ABSTRACT: Human mesenchymal stem cells (hMSCs) have shown promising potential in the field of regenerative medicine particularly in vascular tissue engineering. Optimal growing of MSCs into specific lineage requires a thorough understanding of the role of mechanobiology in MSC metabolism. Although effects of external physical cues (mechanical stimuli through external loading and scaffold properties) on regulation of MSC differentiation into Smooth muscle (SM) lineage have attracted widespread attention, fewer studies are available on mechanical characterization of single engineered MSCs which is vital in tissue development through proper mechanotransductive cell–environment interactions. In this study, we investigated effects of uniaxial tensile strain and transforming growth factor-β1 (TGF-β1) stimulations on mechanical properties of engineered MSCs and their F-actin cytoskeleton organization. Micropipette aspiration technique was used to measure mechanical properties of MSCs including mean Young׳s modulus (E) and the parameters of standard linear viscoelastic model. Compared to control samples, MSCs treated by uniaxial strain either with or without TGF-β1 indicated significant increases in E value and considerable drop in creep compliance curve, while samples treated by TGF-β1 alone met significant decreases in E value and considerable rise in creep compliance curve. Among treated samples, uniaxial tensile strain accompanied by TGF-β1 stimulation not only caused higher stimulation in MSC differentiation towards SM phenotype at transcriptional level, but also created more structural integrity in MSCs due to formation of thick bundled F-actin fibers. Results can be applied in engineering of MSCs towards functional target cells and consequently tissue development.
    Journal of the Mechanical Behavior of Biomedical Materials 03/2015; 43. DOI:10.1016/j.jmbbm.2014.12.013 · 3.42 Impact Factor
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    • "The media is separated from the intima by the internal elastic lamina and contains a three-dimensional network of elastin fibres and, vascular smooth muscle cells (VSMCs) and collagen fibres which form a fibrous helix with near circumferential orientation [9]. Elastin, a rubber-like, highly extensible protein, gives elasticity to arterial tissue, whilst VSMCs regulate arterial diameter via vasoconstriction and vasodilation [10]. The adventitia is composed predominantly of collagen fibres maintained by fibroblast cells. "
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    ABSTRACT: Intracranial aneurysms (IAs) are abnormal dilatations of the cerebral vasculature. Computational modelling may shed light on the aetiology of the disease and lead to improved criteria to assist diagnostic decisions. We briefly review models of aneurysm evolution to date and present a novel fluid-solid-growth (FSG) framework for patient-specific modelling of IA evolution. We illustrate its application to 4 clinical cases depicting an IA. The section of arterial geometry containing the IA is removed and replaced with a cylindrical section: this represents an idealised section of healthy artery upon which IA evolution is simulated. The utilisation of patient-specific geometries enables G&R to be explicitly linked to physiologically realistic spatial distributions and magnitudes of haemodynamic stimuli. In this study, we investigate the hypothesis that elastin degradation is driven by locally low wall shear stress (WSS). In 3 out of 4 cases, the evolved model IA geometry is qualitatively similar to the corresponding in vivo IA geometry. This suggests some tentative support for the hypothesis that low WSS plays a role in the mechanobiology of IA evolution.
    12/2014; 10:396–409. DOI:10.1016/j.piutam.2014.01.034
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    • "Cells of multicellular organisms experience mechanical stimuli that range from the direct mechanical impact of pulling and stretching to changes in osmotic and hydrostatic pressure. Mechanical stretch or pressure activates ion channels in the plasma membrane, resulting in depolarization, increased intracellular Ca2+ concentration and changes in gene expression, cell shape and cytoskeletal organization (Bourque, 2008; Loukin et al., 2010a; Loukin et al., 2010b; Naruse et al., 1998; Thodeti et al., 2009; Wang and Thampatty, 2006). "
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    ABSTRACT: How the neural retina is held in its place in the human physiological living body) Bratislava 2014 Original self-publishing first edition of the monograph, entitled " Gergely's retinal linkage (How the neural retina is held in its place in the human physiological living body) " by Gergely K (contact:; affiliation: Faculty of Medicine in Bratislava, Comenius University in Bratislava, Slovak Republic; This work may not be translated or copied in whole or in part without the written permission of the publisher Květoslava Gergelyova, MD; Prague, Czech Republic (contact:, except for brief excerpts in connection with scientific articles or scholarly analysis [regular citation: Gergely K. Gergely's retinal linkage (How the neural retina is held in its place in the human physiological living body). Publisher Gergelyova, 2014]. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights.
    1. 12/2014; Gergelyova Kvetoslava,, ISBN: 978-80-260-6819-8
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