Mechanobiology of cardiomyocyte development

Jacot, Jeffrey G.; Martin, Jody; Hunt, Darlene L.

doi:10.1016/j.jbiomech.2009.09.014

Cited by 194 publications

(185 citation statements)

References 61 publications

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“…The contractile forces for myocytes plated on ECM-coated substrates increased with stiffness and correlated well with myocyte striation data. Other studies have also established this correlation for ECM substrates (14,15,26). Contractile forces measured through cadherin adhesions also increased with stiffness; however, they plateaued after 5 kPa, which is consistent with the morphological data, which show optima in striation at 5 kPa.…”

Section: Discussionsupporting

confidence: 85%

“…The cardiac ECM itself is a dynamic entity composed of basement membrane adhesion proteins such as fibronectin, collagen type IV, laminin, and proteoglycans (17), which serve as a crucial interface between myocytes and structural ECM proteins like collagen types I and III (1), all of which continuously remodel during cardiac development. Furthermore, the levels of collagen type I and III rapidly increase in neonatal rat myocardium after birth (10), along with myocyte hypertrophic changes (48), resulting in a dramatic increase in passive elastic modulus (26). These changes in tissue composition and biophysical properties can alter the myofibrillar architecture and myocyte function (48).…”

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confidence: 99%

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Cardiac myocyte remodeling mediated by N-cadherin-dependent mechanosensing

Chopra

Tabdanov

Patel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

126

184

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Chopra A, Tabdanov E, Patel H, Janmey PA, Kresh JY. Cardiac myocyte remodeling mediated by N-cadherin-dependent mechanosensing. Am J Physiol Heart Circ Physiol 300: H1252-H1266, 2011. First published January 21, 2011 doi:10.1152 doi:10. /ajpheart.00515.2010 adhesions are crucial in maintaining the structural and functional integrity of cardiac cells. Little is known about the mechanosensitivity and mechanotransduction of cell-to-cell interactions. Most studies of cardiac mechanotransduction and myofibrillogenesis have focused on cell-extracellular matrix (ECM)-specific interactions. This study assesses the direct role of intercellular adhesion, specifically that of N-cadherin-mediated mechanotransduction, on the morphology and internal organization of neonatal ventricular cardiac myocytes. The results show that cadherin-mediated cell attachments are capable of eliciting a cytoskeletal network response similar to that of integrinmediated force response and transmission, affecting myofibrillar organization, myocyte shape, and cortical stiffness. Traction forces mediated by N-cadherin were shown to be comparable to those sustained by ECM. The directional changes in predicted traction forces as a function of imposed loads (gel stiffness) provide the added evidence that N-cadherin is a mechanoresponsive adhesion receptor. Strikingly, the mechanical sensitivity response (gain) in terms of the measured cell-spread area as a function of imposed load (adhesive substrate rigidity) was consistently higher for N-cadherin-coated surfaces compared with ECM protein-coated surfaces. In addition, the cytoskeletal architecture of myocytes on an N-cadherin adhesive microenvironment was characteristically different from that on an ECM environment, suggesting that the two mechanotransductive cell adhesion systems may play both independent and complementary roles in myocyte cytoskeletal spatial organization. These results indicate that cell-to-cell-mediated force perception and transmission are involved in the organization and development of cardiac structure and function.cell-to-cell interaction; myofibrillogenesis; extracellular matrix; cell biomechanics NUMEROUS STUDIES IN CELL MECHANOBIOLOGY have shown that the stiffness of the material on which or within which cells grow has sizeable, specific effects on cell morphology, cytoskeletal structure, motility, differentiation, and proliferation (16,39,43,50,62). Mechanical cues, which can act together with or in opposition to chemical stimuli, are potentially associated with pathological conditions that occur in cancer, fibrotic disease, abnormal wound healing, and cardiac remodeling. The mechanical microenvironment of the cell in vivo is defined by its attachment to the extracellular matrix (ECM) and to other cells via forces generated and transmitted across cell-to-cell junctions constituting a network assembly of cells. Nearly all studies of cell mechanobiology in vitro have focused on the attachment of subconfluent cells to ECM ligands such as fibronectin, collagen, and laminin. ...

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Section: Discussionsupporting

confidence: 85%

mentioning

confidence: 99%

Cardiac myocyte remodeling mediated by N-cadherin-dependent mechanosensing

Chopra

Tabdanov

Patel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

126

184

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“…Furthermore, EA mesh is reduced even further to values as low as 0.01 N/m, upon noncoplanar buckling of interconnects, as in SI Appendix. These values are exceptionally small compared with cardiac tissue, which has EA cardiac = 76 N/m and EI cardiac = 23 μN-m for 1.9-mm-thick ventricular walls (36) and an elastic modulus of E heart = 40 kPa (37). By comparison with previously reported active cardiac and neural mapping sheets [bending stiffness 31 N-m (6)], the web devices presented in this study are 5 orders of magnitude softer and comparable to passive devices used on the brain (34).The most favorable epidermal electronics had values of EA = 4.2 N/m and EI = 0.3 nN-m (35).…”

Section: Resultsmentioning

confidence: 95%

“…The experimental parameters are p air = 1.0 atm, w x × w y = 560 × 290 μm 2 , L unit = 1.0 mm, and ν = 0.45 (37). Literature reports suggest that μ ∼ 1.6 with certain values that are an order of magnitude smaller (42).…”

Section: Resultsmentioning

confidence: 99%

Electronic sensor and actuator webs for large-area complex geometry cardiac mapping and therapy

Kim

Ghaffari

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

221

167

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Curved surfaces, complex geometries, and time-dynamic deformations of the heart create challenges in establishing intimate, nonconstraining interfaces between cardiac structures and medical devices or surgical tools, particularly over large areas. We constructed large area designs for diagnostic and therapeutic stretchable sensor and actuator webs that conformally wrap the epicardium, establishing robust contact without sutures, mechanical fixtures, tapes, or surgical adhesives. These multifunctional web devices exploit open, mesh layouts and mount on thin, bio-resorbable sheets of silk to facilitate handling in a way that yields, after dissolution, exceptionally low mechanical moduli and thicknesses. In vivo studies in rabbit and pig animal models demonstrate the effectiveness of these device webs for measuring and spatially mapping temperature, electrophysiological signals, strain, and physical contact in sheet and balloon-based systems that also have the potential to deliver energy to perform localized tissue ablation.flexible electronics | semiconductor nanomaterials | stretchable electronics | implantable biomedical devices | cardiac electrophysiology C ardiac arrhythmias occur in all component structures and 3D regions of the heart, resulting in significant challenges in diagnosis and treatment of precise anatomic targets (1). Many common arrhythmias, including atrial fibrillation and ventricular tachycardia, originate in endocardial substrates and then propagate in the transverse direction to affect epicardial regions (1, 2). Characterizing arrhythmogenic activity at specific regions of the heart is thus critical for establishing the basis for definitive therapies such as cardiac ablation (3). Advanced tools that offer sufficient spatial resolution (<1 mm) and intimate mechanical coupling with myocardial tissue, but without undue constraints on natural motions, would therefore be of great clinical importance (4-6). To date, cardiac ablation procedures have largely relied on point ablation catheters deployed in the endocardial space (1, 5, 7-9). Although successful in the treatment of simple arrhythmias originating in and around the pulmonary veins, these devices are poorly suited for treating complex arrhythmias, such as persistent atrial fibrillation (10-13), that arise from various sites inside the left atrium. Other classes of devices have demonstrated the utility of spatiotemporal voltage mapping using various modes of operation, including noninvasive surface mapping designs (14, 15), epicardial voltage-mapping "socks" (16-20), and endocardial contact and noncontact catheters, with densities approaching 64 electrodes (21-31). These solutions all exploit arrays of passive metal wirebased electrodes integrated on wearable vests and socks (14-20) or catheter systems (21-26) for mapping of complex arrhythmias. Building such mesh structures requires manual assembly and is only possible because the individual wires are millimeter scale in diameter and thus sufficiently large to be threaded to form a mesh.Fo...

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“…The cardiac cells are subjected to mechanical forces from early development and they are very sensitive to the surrounding cardiac tissue. In the study of Jacot et al [11] the mechanobiology of cardiomyocyte development was investigated. The effect of direct stretching, electrically induced beating and substrate stiffening was analyzed.…”

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confidence: 99%