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About this book The book presents state-of-the-art developments in multiscale modeling and latest experimental data on multiscale mechanobiology of bone remodeling and adaptation including fracture healing applications. Show all. Show next xx. Recommended for you. PAGE 1. These time-varying components can strongly influence endothelial responses.

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Compared with steady flow with similar time-averaged magnitudes, pulsatile flow stimulates Erk activity more strongly Kadohama et al. Comparison of proinflammatory oscillatory flow with anti-inflammatory pulsatile-flow patterns at atherosclerosis-prone versus atherosclerosis-resistant sites in the human carotid artery identified specific frequency components that exerted pro- or anti-inflammatory effects Feaver et al. Of clinical interest, left ventricle assist devices for heart failure patients generate nonpulsatile flow that induces arterial-venous malformations Islam et al. Erk may mediate these effects, since it is strongly linked to arterial specification Deng et al.

These results imply that endothelial mechanosensors must decode subsecond-frequency characteristics, which necessitates rapid rates of both activation and inactivation. These kinetics, particularly the required inactivation rates, exclude even G protein signaling; however, ion channels can have very rapid activation and inactivation kinetics. Mechanosensitive Piezo channels have very rapid activation and inactivation rates Coste et al. The correlation between atherosclerosis-prone regions of arteries and disturbed flow led to the idea that oscillatory shear, where flow reverses during part of the cardiac cycle, promotes plaque formation Ku et al.

But how ECs sense flow direction is very poorly understood.

Interestingly, ECs in athero-prone regions fail to elongate and align in the direction of flow, and cells therefore experience flow at many angles, including perpendicular, whereas in athero-resistant regions of blood vessels, flow is parallel to the cell axis. In fact, recent studies suggest that plaque localization correlates more strongly with the perpendicular or transverse wall shear stress component than with oscillations Peiffer et al. These effects correlate with the ability of steady laminar or unidirectional pulsatile FSS to induce cell elongation and alignment in the flow direction in conjunction with suppression of inflammation, whereas low or oscillatory flow fails to induce alignment and promotes inflammatory pathways Mohan et al.

The fortuitous observation that the proteoglycan syndecan 4 Sdc4 is required for EC alignment in flow provided a way to test this idea. Yet in vitro, Sdc4 was not required for other flow responses, and thus appears to be specifically required for sensing flow direction, which is separable from sensing flow magnitude. Together, these results demonstrate that loss of alignment is causal for athero-susceptibility and that Sdc4 is a component of the flow direction sensor.

Hemodynamic forces control vessel specification and maturation during development and continue to regulate vessel remodeling during postnatal and adult life. The exquisite ability of ECs to sense multiple aspects of fluid shear stress patterns allows them to coordinate the complex ballet of events involving different cell types and signaling pathways, to constantly adjust vessel structure and function.

Identifying molecular mechanosensors behind the distinct sensing of FSS magnitude, direction, and pulsatility are major directions for future research. Further, characterizing how downstream signaling pathways and gene regulation events are integrated in the context of growth and disease is required to better understand the amazing plasticity of our blood vessels.

The finely tuned biomechanical responses discussed here govern health and disease in nearly every tissue from our first to our last heartbeat.

Biomechanics - Functional Adaption and Remodeling | Kozaburo Hayashi | Springer

Understanding these processes is a major, exciting challenge for biomedical research in the coming years. DOI: This article is distributed by The American Society for Cell Biology under license from the author s. Two months after publication it is available to the public under an Attribution—Noncommercial—Share Alike 3. Molecular Biology of the Cell Vol.

follow link Martin A. Schwartz 1 Address correspondence to: Martin A.

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Add to favorites Download Citations Track Citations. Abstract Flowing blood exerts a frictional force, fluid shear stress FSS , on the endothelial cells that line the blood and lymphatic vessels. Syndecan 4 is required for endothelial alignment in flow and atheroprotective signaling. Homeostasis: a plea for a unified approach. Adv Physiol Educ 28 , — Circulation Res , — PECAM-1 is necessary for flow-induced vascular remodeling.

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Arterioscler Thromb Vasc Biol 29 , — Effects of disturbed flow on vascular endothelium: pathophysiological basis and clinical perspectives. Physiol Rev 91 , — J Cell Biol , — Curr Biol 22 , — Curr Biol 23 , — Piezo1 and Piezo2 are essential components of distinct mechanically activated cation channels. Science , 55— Blood , — Lymph flow, shear stress, and lymphocyte velocity in rat mesenteric prenodal lymphatics.

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Microcirculation 13 , — Key role of the NO-pathway and matrix metalloprotease-9 in high blood flow-induced remodeling of rat resistance arteries. Arterioscler Thromb Vasc Biol 27 , — Human haemodynamic frequency harmonics regulate the inflammatory phenotype of vascular endothelial cells. J Cell Sci , — Gating the mechanical channel Piezo1: a comparison between whole-cell and patch recording. Channels 6 , — Experimental study of aortic flow in the ascending aorta via particle tracking velocimetry.

Exp Fluids 53 , — Molecular basis of the effects of mechanical stretch on vascular smooth muscle cells. J Biomechanics 40 , —