Quantitative analysis of the molecular sliding mechanisms in native tendon collagen — time-resolved dynamic studies using synchrotron radiation

A constitutive model for vascular tissue that integrates fibril, fiber and continuum levels with application to the isotropic and passive properties of the infrarenal aorta

“…The close packing and the cross-linking of collagen fibrils defines a virtually inextensible fiber, such that the strain within collagen fibrils is always much smaller than the macroscopic strain in collagenous tissue (Folkhard et al, 1987a;Folkhard et al, 1987b;Fratzl et al, 1998). This has been confirmed by recent experimental data, which suggests that sliding between collagen fibers (inter-fiber sliding) and between collagen fibrils (as it is captured by the present model) plays a significant role in tendon deformation (Gupta et al, 2010).…”

Molecular assessment of the elastic properties of collagen-like homotrimer sequences

“…As stated in the introduction, three possible mechanisms are involved in molecular stretching at the molecular level: molecular elongation, the increase in the distance between the C and N terminals of two consecutive molecules along the fibril axis, and a relative slippage of lateral adjoining molecules (Mosler et al 1985;Folkhard et al 1987;Sasaki and Odajma 1996;Puxkandl 2002). The present study focused on the molecular elongation mechanism, which was considered the primary and most effective mechanism in collagen fibril stretching (Sasaki and Odajima 1996), whereas the other two mechanisms were not taken into consideration.…”

“…At the fibril level, the most probable alternative process is the fibril sliding, and it is mediated by proteoglycans (Scott 1988 and1992;Raspanti et al 1997Raspanti et al , 2000Raspanti et al , 2002Redaelli et al 2003). At the molecular level, three possible mechanisms are recognized: molecular elongation, the increase of the gap zones between consecutive molecules along the fibril axis and the relative slippage of lateral adjoining molecules (Mosler et al 1985;Folkhard et al 1987;Sasaki and Odajma 1996;Puxkandl 2002). The first mechanism is likely to be the main actor, contributing up to 80% of fibril elongation (Sasaki and Odajima 1996); the other two mechanisms are probably mediated by intermolecular links.…”

Supramolecular Nanofibrillar Polymer Hydrogels

“…The toe region (defined as the region between zero strain and the intersection of linear fit and strain axis) corresponds to the straightening of crimps in the fibrils due to the flexibility of the fibers and the presence of nonhelical telomeric regions on the molecular level [63]. In the linear region, an increase in the Young's modulus of the gel is associated with stretching the collagen triple helices and with sliding of the collagen molecules past each other [54,64]. At even higher strain, disruption of the fibrillar structure results in failure of the gel.…”