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Kendra, J. A.

Publications and source records attributed to Kendra, J. A..

2 recordsLinked to original sources

Skeletal Muscle Regeneration is Accelerated Following Injection of Time Release Ion Matrix in Injured Mice

IntroductionSkeletal muscle injury remains a significant cause of disability with limited treatment options. Here we report accelerated skeletal muscle regeneration following injection of an inorganic biomaterial alone, cobalt oxide time-release ion matrix (CoO-TRIM). MethodsThe tibialis anterior (TA) muscle of adult C57BL/6J mice was injured with 70 {micro}L of barium chloride, with uninjured limbs serving as contralateral controls. Following the acute inflammatory phase (3 days post injury, dpi), mice were randomly separated into three groups: untreated controls, 70 {micro}l sterile saline injection alone (vehicle control) or 70 {micro}l CoO-TRIM (5 {micro}g/{micro}l) and evaluated at 8- and 14 dpi. Results14 dpi, injured TA muscles receiving a single injection of CoO-TRIM exhibited greater recovery of maximal force production (means {+/-} SEM: Healthy; TRIM, 31.8 {+/-} 0.6 N/cm3; Untreated, 31.7 {+/-} 0.8 N/cm3; Saline, 31.6 {+/-} 0.8 N/cm3, Injured; TRIM, 31.8 {+/-} 0.8 N/cm3; Untreated, 26.1 {+/-} 1.1 N/cm3, P= <0.01 vs. TRIM Injured; Saline, 26.0 {+/-} 1.3 N/cm3, P= <0.01 vs. TRIM Injured), increased fiber size (Healthy; TRIM, 2466 {+/-} 128 {micro}m2 vs. Untreated, 2351 {+/-} 131 {micro}m2; vs. Saline, 2460 {+/-} 129 {micro}m2, Injured; TRIM, 2179 {+/-} 63 {micro}m2 vs. Untreated, 1525 {+/-} 52 {micro}m2, P= <0.01; vs. Saline, 1470 {+/-} 99 {micro}m2, P= <0.01), and accelerated muscle regeneration (TRIM, 32.7 {+/-} 6.8 eMyHC+ fibers/mm2 vs. Untreated, 91.8 {+/-} 11.8 eMyHC+ fibers/mm2, P= <0.01; vs. Saline, 94.0 {+/-} 9.6 eMyHC+ fibers/mm2, P= <0.01). Vascular endothelial growth factor was elevated 14 dpi (TRIM, 17.3 {+/-} 2.9 pg/mg vs. Untreated, 10.3 {+/-} 1.1 pg/mg, P= 0.04; Saline, 5.5 {+/-} 1.2 pg/mg, P= <0.01), with increased muscle microvascular area (TRIM, 119.9 {+/-} 4.2 {micro}m2/fiber vs. Untreated, 94.9 {+/-} 4.2 {micro}m2/fiber, P= <0.01; Saline, 91.3 {+/-} 4.0 {micro}m2/fiber, P= <0.01) following CoO-TRIM treatment. There were early increases in inflammatory responses 8 dpi in injured TA muscles receiving CoO-TRIM (IL-6; TRIM, 29.1 {+/-} 8.2 pg/ml vs. Untreated, 12.4 {+/-} 1.5 pg/ml, P= 0.02; Saline, 11.7 {+/-} 0.8 pg/mg, P= 0.01), with early resolution of degenerative inflammatory cytokines and elevated regenerative cytokines 14 dpi (IL-10; SEM: TRIM, 2.4 {+/-} 0.1 pg/ml vs. Untreated, 2.1 {+/-} 0.1 pg/ml, P= 0.25; Saline, 2.0 {+/-} 0.1 pg/ml, P= 0.04). No differences were observed in healthy contralateral limbs following treatment with CoO-TRIM compared to healthy control mice at 8- and 14 dpi. DiscussionThis work suggests CoO-TRIM enhances muscle regeneration following injury, possibly through an immune cell-mediated mechanism. Statement of Clinical RelevanceThis is the first report of an injected, inorganic biomaterial alone to accelerate regeneration of injured skeletal muscle with no observed effects on healthy muscle. These findings suggest enhancements to skeletal muscle regeneration following CoO-TRIM treatment may be immune cell mediated with an increased local inflammatory response and subsequent improvements to muscle microvasculature and myogenic regulatory factors.

physiology↗

Characterization of Gait Kinematics and Muscle Function in Becker Muscular Dystrophy Pigs: a pilot study

Vertebrate animal models of Becker muscular dystrophy (BMD) have been developed. Here, we characterized the gait kinematics and muscle function of a naturally occurring BMD pig model of dystrophin insufficiency. BMD pigs tended to have alterations in hip range of motion (ROM): hip (67%, 95% CI -0.64 to 14.12 degrees). While parameters were unaltered in extensor muscles, the dystrophin levels in flexor tibiotarsal joint muscles correlated with fatigue index as well as reduced isometric force (48%, 95% CI -1.86 to -0.61 N-m), and a 33% increase in fatigue index (95% CI -36.25 to 96.71 percent); the extensor muscles had no observable reductions in muscle force, with a 48% increase in fatigue index (95% CI -232.6 to 472.6 percent). Histological analysis of muscle biopsies supported a BMD phenotype in the flexor muscles of BMD pigs, with a 75% (95% CI -55.14 to -15.66 percent) decrease in large and a 43% (95% CI 17.74 to 57.38 percent) increase in small muscle fiber cross-sectional area. Dystrophin protein abundance was 28% less in flexor muscles from BMD pigs (95% CI -49.63 to 11.41 arbitrary units). Together, our model may serve as a clinically relevant model of BMD to assess safety and efficacy of therapeutics.

pathology↗