AI Article Synopsis
- Collagen XI is essential for various tissues like cartilage and tendons, contributing to the process of forming fibrils and maintaining mechanical properties.
- The study examined the mechanical response of tendons and ligaments in mice lacking collagen XI (Col11a1ΔTen/ΔTen) compared to wild type mice, showing significant reductions in area, maximum load, stiffness, and modulus in the affected tendons and ligaments.
- Findings indicate that the influence of collagen XI on tendon properties is specific to the type of tendon and its location, suggesting a link to joint hypermobility observed in conditions like type II Stickler's Syndrome.
Article Abstract
Collagen XI is ubiquitous in tissues such as joint cartilage, cancellous bone, muscles, and tendons and is an important contributor during a crucial part in fibrillogenesis. The COL11A1 gene encodes one of three alpha chains of collagen XI. The present study elucidates the role of collagen XI in the establishment of mechanical properties of tendons and ligaments. We investigated the mechanical response of three tendons and one ligament tissues from wild type and a targeted mouse model null for collagen XI: Achilles tendon (ACH), the flexor digitorum longus tendon (FDL), the supraspinatus tendon (SST), and the anterior cruciate ligament (ACL). Area was substantially lower in Col11a1ΔTen/ΔTen ACH, FDL, and SST. Maximum load and maximum stress were significantly lower in Col11a1ΔTen/ΔTen ACH and FDL. Stiffness was lower in Col11a1ΔTen/ΔTen ACH, FDL, and SST. Modulus was reduced in Col11a1ΔTen/ΔTen FDL and SST (both insertion site and midsubstance). Collagen fiber distributions were more aligned under load in both wild type group and Col11a1ΔTen/ΔTen groups. Results also revealed that the effect of collagen XI knockout on collagen fiber realignment is tendon-dependent and location-dependent (insertion versus midsubstance). In summary, this study clearly shows that the regulatory role of collagen XI on tendon and ligament is tissue specific and that joint hypermobility in type II Stickler's Syndrome may in part be due to suboptimal mechanical response of the soft tissues surrounding joints.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11500803 | PMC |
| http://dx.doi.org/10.1115/1.4066570 | DOI Listing |
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