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Lind, D. R. G.

Publications and source records attributed to Lind, D. R. G..

2 recordsLinked to original sources

Deep behavioral phenotyping tracks functional recovery following tibia fracture in mice

IntroductionAn estimated 178 million fractures occur worldwide each year, with lower limb fractures in particular showing a high incidence of poor healing, and these often lead to reduced mobility and chronic pain. Bone healing and the ability to bear weight are closely tied to the mechanical stability of the fracture site. Although fracture stabilization is a well-established factor modulating the rate and extent of bone repair, there is a notable gap in non-destructive technologies that can rapidly and objectively quantify functional recovery in preclinical settings. We consider this to be a significant limiting factor in translational studies directed at improving fracture healing. Here, we describe a novel behavioral phenotyping approach that enables rapid quantification of post-fracture weightbearing and kinematic metrics in freely behaving mice. Our goal is to identify and characterize metrics most indicative of fracture-induced behavioral impairment and to use these metrics to quantify how functional recovery is altered in mice with pin stabilized versus non-stabilized fractures. We also use this approach to explore whether sex is a significant contributor to functional recovery. MethodsMale and female adult C57BL6/J received a mid-shaft tibial fracture that was either left unstabilized or fixed with an intramedullary pin. Non-fractured naive mice served as controls. Behavioral recordings of freely moving mice were acquired prior to fracture and then throughout the time course of healing, from 5 to 35 days post fracture (DPF). To track mice and analyze changes in paw pressure and kinematic behaviors after fracture, we then applied a novel machine learning-enabled behavioral phenotyping analysis. ResultsIn this study, we demonstrate that severity of the behavioral phenotype is more significant in mice with unstabilized fractures when compared to mice with pin-stabilized fractures. Pin stabilization generally allowed increased weightbearing and produced smaller changes in kinematic metrics. Interestingly, we observed only minor sex specific differences in fracture-induced behavioral impairments and recovery. Our analysis also revealed that functional recovery is more complex than is a set of individual parameters viewed in isolation. In fact, unique behavioral parameters identified different time windows for functional recovery. Therefore, we developed a comprehensive, unified graph theoretic metric of fracture recovery that encompasses all behavioral parameters quantified. Using this unified metric, we confirmed the increased severity of the fracture phenotype in unstabilized versus pin stabilized mice and identified a clear time window of functional recovery, for both fracture groups. DiscussionOur findings demonstrate how this novel comprehensive behavioral phenotyping approach, which combines machine learning and graph theory, makes it possible to rapidly quantify longitudinal changes in mice after fracture. This approach enables us to determine functional recovery patterns based on a unified behavioral metric of healing. Our data and methodology form a foundation for future mechanistic experiments focused on understanding biological or mechanical variables that influence functional healing and will also enable more rapid testing of various strategies to accelerate bone healing.

animal behavior and cognition↗

Murine Progeria Model Exhibits Delayed Fracture Healing with Dysregulated Local Immune Response

ABSTRACTO_ST_ABSBackgroundC_ST_ABSBone fracture is one of the most globally prevalent injuries, with an estimated 189 million bone fractures occurring annually. Delayed union or nonunion occurs in up to 15% of fractures and involves the interruption or complete failure of bone continuity following fracture. Preclinical testing is essential to support the translation of novel strategies to promote improved fracture repair treatment, but there is a paucity of small animal models that recapitulate clinical attributes associated with delayed fracture healing. This study explores whether the Zmpste24-/- (Z24-/-) knockout mouse model of Hutchinson-Gilford progeria syndrome presents with delayed fracture healing. Leveraging the previously characterized Z24-/- phenotype of genomic instability, epigenetic changes, and fragility, we hypothesize that these underlying alterations will lead to significantly delayed fracture healing relative to age-matched wild type (WT) controls. MethodsWT and Z24-/- mice received intramedullary fixed tibia fractures at [~]12 weeks of age. Mice were sacrificed throughout the time course of repair for the collection of organs that would provide information regarding the local (fracture callus, bone marrow, inguinal lymph nodes) versus peripheral (peripheral blood, contralateral tibia, abdominal organs) tissue microenvironments. Analyses of these specimens include histomorphometry, CT, mechanical strength testing, protein quantification, gene expression analysis, flow cytometry for cellular senescence, and immunophenotyping. ResultsZ24-/- mice demonstrated a significantly delayed rate of healing compared to WT mice with consistently smaller fracture calli containing higher proportion of cartilage and less bone after injury. Cellular senescence and pro-inflammatory cytokines were elevated in the Z24-/- mice before and after fracture. These mice further presented with a dysregulated immune system, exhibiting generally decreased lymphopoiesis and increased myelopoiesis locally in the bone marrow, with more naive and less memory T cell but greater myeloid activation systemically in the peripheral blood. Surprisingly, the ipsilateral lymph nodes had increased T cell activation and other pro-inflammatory NK and myeloid cells, suggesting that elevated myeloid abundance and activation contributes to an injury-specific hyperactivation of T cells. ConclusionTaken together, these data establish the Z24-/- progeria mouse as a model of delayed fracture healing that exhibits decreased bone in the fracture callus, with weaker overall bone quality, immune dysregulation, and increased cellular senescence. Based on this mechanism for delayed healing, we propose this Z24-/- progeria mouse model could be useful in testing novel therapeutics that could address delayed healing. The Translational Potential of this ArticleThis study employs a novel animal model for delayed fracture healing that researchers can use to screen fracture healing therapeutics to address the globally prevalent issue of aberrant fracture healing.

molecular biology↗