Determination of the elastic modulus of native collagen fibrils via radial indentation

Heim, August J.; Matthews, William G.; Koob, Thomas J.

doi:10.1063/1.2367660

Cited by 124 publications

(93 citation statements)

References 23 publications

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“…Indentation tests on fibrils using scanned force microscopy provided substantial insight into the qualitative and to a lesser extent the quantitative mechanical behaviour of individual fibrils [23][24][25]. Any attempt at quantitative interpretation of the measurements requires, in addition to knowledge of the size and shape of the tip of the indenter, determination of the contact area throughout the loading.…”

Section: Introductionmentioning

confidence: 99%

Tension tests on mammalian collagen fibrils

2016

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A brief overview of isolated collagen fibril mechanics testing is followed by presentation of the first results testing fibrils isolated from load-bearing mammalian tendons using a microelectromechanical systems platform. The in vitro modulus (326 ± 112 MPa) and fracture stress (71 ± 23 MPa) are shown to be lower than previously measured on fibrils extracted from sea cucumber dermis and tested with the same technique. Scanning electron microscope images show the fibrils can fail with a mechanism that involves circumferential rupture, whereas the core of the fibril stays at least partially intact.

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Section: Introductionmentioning

confidence: 99%

Tension tests on mammalian collagen fibrils

2016

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“…At the fibrillar level, direct mechanical measurements have only recently become possible by atomic force microscopy (AFM) and microelectromechanical systems (MEMS). The mechanical properties of single collagen fibrils have been measured using AFM-based tensile [7][8][9][10], nanoindentation [11][12][13][14][15][16][17][18][19], and bending [20][21][22] tests, and MEMS-based tensile [23][24][25] tests.…”

Section: Introductionmentioning

confidence: 99%

Tensile Strength of Single Collagen Fibrils Isolated from Tendons

Yamamoto¹

2017

EJB

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Abstract:Tensile failure properties of single collagen fibrils were determined using our original tensile test method. Fibrils were directly isolated from the fascicles of mouse tail tendons. Both the ends of each fibril were wound onto the tips of two microneedles several times using micromanipulators. The fibril and tips were immersed in physiological saline solution. Then, the fibril was stretched to failure by moving the one microneedle. During tensile testing, the fibril was firmly attached to the tips of the microneedles, and broken between the tips with no slippage observed. The diameter of tested 10 fibrils was 410±60 nm (Mean±S.D.). The stress-strain curves of these fibrils were almost linear. Their tensile strength and failure strain were 100±32 MPa and 34±11%, respectively. These values were approximately 480 and 190% of those of the fascicles with the diameter of 81±12 µm, respectively.

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“…The fine-balanced interplay between all these elements is massively disturbed in conditions of heart fibrosis and pathological remodelling. The principal ECM component in the heart is fibrillar collagen type I [72], which provides tensile strength by virtue of its extraordinary mechanical property with an extension modulus of several GPa [76,77]. Other fibrillar collagens in the myocardium are types III and V. The fibrillar collagens are produced by cardiac fibroblasts and kept in homeostasis by balancing synthesis with degradation mediated by matrix metalloproteinases (MMPs) [78].…”

Section: Composition and Function Of The Ecm In The Heartmentioning

confidence: 99%

The Stressful Life of Cardiac Myofibroblasts

Zimina

Hinz

2015

Cardiac Fibrosis and Heart Failure: Cause or Effect?

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The ability of cardiac fibroblasts to sense and control the mechanical properties of the extracellular matrix is essential to adapt the heart tissue to mechanical load, such as in conditions of hypertension and to repair injuries after myocardial infarct. Aberrant mechanosensing and/or persistent stress results in the chronic activation of cardiac fibroblasts and other progenitors into myofibroblasts. Myofibroblasts drive the development of fibrosis by excessive collagen secretion and contraction of the neo-matrix into scar tissue. Stiff fibrotic tissue impairs heart distensibility, pumping and valve function, contributes to diastolic and systolic dysfunction, and affects myocardial electrical transmission, leading to arrhythmia and ultimately heart failure. To explore novel therapeutic strategies that specifically target the myofibroblasts in heart fibrosis, we here elaborate on the common factors that control myofibroblast activation from different precursor cells in the heart. At least two factors are pivotal for myofibroblast activation and function: mechanical stress, manifested in disease as a stiff extracellular matrix, and active TGF-β1. Because of uncontrollable side effects, global TGF-β1 inhibition has failed in clinical trials to treat fibrosis but preventing TGF-β1 activation in a myofibroblastspecific manner has promising perspectives.

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Determination of the elastic modulus of native collagen fibrils via radial indentation

Cited by 124 publications

References 23 publications

Tension tests on mammalian collagen fibrils

Tension tests on mammalian collagen fibrils

Tensile Strength of Single Collagen Fibrils Isolated from Tendons

The Stressful Life of Cardiac Myofibroblasts

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