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Title: Type III collagen is a key regulator of the collagen fibrillar structure and biomechanics of articular cartilage and meniscus
Award ID(s):
1751898
NSF-PAR ID:
10183341
Author(s) / Creator(s):
; ; ; ; ; ; ; ; ; ; ; ;
Date Published:
Journal Name:
Matrix Biology
Volume:
85-86
Issue:
C
ISSN:
0945-053X
Page Range / eLocation ID:
47 to 67
Format(s):
Medium: X
Sponsoring Org:
National Science Foundation
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  2. Abstract

    The objective of this study was to investigate the potential of collagen hybridizing peptides (CHPs), which bind to denatured collagen, to extend the retention time of near‐infrared fluorophores (NIRF) following intra‐articular (IA) injection in rat knee joints. CHPs were synthesized with a NIRF conjugated to the N‐terminus. Male Sprague−Dawley rats were assigned to one of four experimental groups: healthy, CHP; osteoarthritis (OA), CHP; healthy, scrambled‐sequence CHP (sCHP), which has no collagen binding affinity; or OA, sCHP. Animals in the OA groups received an IA injection of monosodium iodoacetate to induce OA. All animals then received the corresponding CHP injection. Animals were imaged repeatedly over 2 weeks using an in vivo fluorescence imaging system. Joint components were isolated and imaged to determine CHP binding distribution. Safranin‐O and Fast Green histological staining was performed to confirm the development of OA. CHPs were found to be retained within the joint following IA injection in both healthy and OA animals for the full study period. In contrast, sCHP signal was negligible by 24−48 h. CHP signal was significantly greater (p < 0.05) in OA joints when compared to healthy joints. At the 2‐week end point, multiple joint components retained CHPs, including cartilage, meniscus, and synovium. CHPs dramatically extended the retention time of NIRFs following IA injection in healthy and OA knee joints by binding to multiple collagenous tissues in the joint. These results support the pursuit of further research to develop CHP based therapeutics for IA treatment of OA.

     
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