bioRxiv Science⌕ Search

Biology subjects

Fertala, A.

Publications and source records attributed to Fertala, A..

2 recordsLinked to original sources

Development of a Humanized Anti-Fibrotic Antibody Targeting Extracellular Collagen Assembly to Reduce Post-Traumatic Scarring

BackgroundExcessive accumulation of fibrillar collagen causes pathological scarring and fibrosis. A promising anti-fibrotic strategy targets the extracellular assembly of collagen fibrils rather than intracellular synthesis pathways. We previously developed a chimeric monoclonal antibody targeting the C-terminal telopeptide of the 2(I) chain of human collagen I that effectively disrupts fibrillogenesis. This study details the engineering of a humanized antibody variant optimized for therapeutic application, augmented with a collagen-binding peptide (CBP) to enhance targeted retention in fibrotic tissues. MethodsA humanized ACA was engineered by in silico homology modeling, complementarity-determining region grafting, and sequence optimization to eliminate chemical liabilities. Variants were expressed in mammalian cells and evaluated for binding kinetics and specificity. To improve spatial localization, the CBP was fused to the antibody. The lead variant was assessed for in vitro cytotoxicity, matrix retention, and in vivo efficacy using a rabbit model of post-traumatic knee arthrofibrosis. ResultsThe humanized ACA variants maintained high specificity and affinity for the 2Ct target domain. Fusing the CBP to the C-terminus of the light chain (C-cbpACA) successfully enhanced matrix retention without compromising target engagement or causing cellular toxicity. In the rabbit arthrofibrosis model, intra-articular C-cbpACA delivery significantly reduced flexion contracture and decreased total collagen deposition in the joint capsule compared to untreated controls. ConclusionWe successfully engineered a clinically viable, humanized, and matrix-targeted anti-fibrotic antibody that specifically inhibited extracellular collagen assembly and exhibited enhanced localization within fibrotic tissues. This construct represents a promising therapeutic strategy for mitigating pathological scarring and improving post-traumatic functional outcomes.

pathology↗

Naproxen impairs load-induced bone formation, reduces bone toughness, and delays stress fracture repair in mice

Debilitating stress fractures are surprisingly common in physically active individuals, including athletes, military recruits, and dancers. These individuals are overrepresented in the 30 million daily users of non-steroidal anti-inflammatory drugs (NSAIDs). We hypothesized that regular use of NSAIDs would predispose habitually loaded bones to stress fracture and delay the repair of these injuries. To test this hypothesis, adult mice were subjected to six bouts of axial forelimb compression over two weeks. Aspirin, naproxen, or vehicle was administered 24 hours before loading. Naproxen-treated mice had diminished load-induced bone formation as well as a significant loss in toughness in non-loaded bone, which were not observed in aspirin-treated mice. Furthermore, there were no differences in RANKL/OPG ratio or cortical bone parameters. Picrosirius red staining and second harmonic generation imaging revealed that alterations in bone collagen fibril size and organization were driving the loss of toughness in naproxen-treated mice. Separately, adult mice were subjected to an ulnar stress fracture generated by a single bout of fatigue loading, with NSAIDs provided 24 hours before injury. Both aspirin-treated and naproxen-treated mice had normal forelimb use in the week after injury, whereas control mice favored the injured forelimb until day 7. However, woven bone volume was only significantly impaired by naproxen. Both NSAIDs were found to significantly inhibit Cox2 and Ngf expression following stress fracture, but only naproxen significantly affected serum PGE2 concentration. Overall, our results suggest that naproxen, but not aspirin, may increase the risk of stress fracture and extend the healing time of these injuries, warranting further clinical evaluation for patients at risk for fatigue injuries.

bioengineering↗