Biology subjects

Bardell, D.

Publications and source records attributed to Bardell, D..

2 recordsLinked to original sources

bioRxiv2024

Allogenic platelet-rich plasma and platelet-rich plasma extracellular vesicles alter the proteome of tenocytes in an in vitro equine model of tendon inflammation: A pilot study

BackgroundTendon injuries are common in horses, often resulting in a high risk of reinjury. Hemoderivative therapeutics including platelet-rich plasma (PRP) show promise but outcomes vary due to inconsistent composition. PRP is rich in soluble growth factors and extracellular vesicles (EVs), the latter facilitate cell-to-cell communication by delivering biologically active cargo. This pilot study profiled the proteome of PRP and PRP-derived EVs and examined their effects on an equine tendon inflammatory model in vitro. MethodsPlasma was isolated via double centrifugation and PRP produced using a commercial filtration kit. EVs were isolated from PRP and plasma using differential ultracentrifugation and characterised with the Exoview Tetraspanin assay. Equine tenocytes were stimulated with interleukin 1{beta} and tumor necrosis factor , then treated with PRP or PRP-derived EVs. Proteomic analysis was conducted on cell lysates, PRP and PRP-EVs using data-dependent acquisition liquid chromatography-tandem mass spectrometry and the data analyzed using multivariate and univariate approaches. ResultsPRP contained 575 quantifiable proteins and PRP-derived EVs 209 proteins. When compared to plasma and plasma derived EVs respectively, PRP and PRP-EVs were enriched in proteins associated with cellular waste disposal and inhibition of lipid metabolism. Experimental factors (inflammatory stimulation and/or treatments) significantly affected the abundance of 18 proteins as expressed in equine tenocytes including col1a1 (col1a1) and sequestosome 1, associated with collagen metabolism and nuclear factor kappa B signaling. DiscussionThe findings from this study suggest PRP-derived EVs influence inflammatory tenocytes and may be crucial to the efficacy of PRP.

molecular biology↗

bioRxiv2021

miR-24:Prdx6 interactions regulate oxidative stress and viability of myogenic progenitors during ageing

microRNAs regulate a myriad of physiological processes, including skeletal muscle regeneration and homeostasis. During ageing, changes in muscle fibre microenvironment contribute to the capability of satellite cells to regenerate the muscle in response to injury and loading stressors. In this study, we isolated murine satellite cells and primary myogenic progenitors from mice and humans to demonstrate that the microRNA miR-24-3p and its target peroxiredoxin 6 (Prdx6) play an important role in muscle regeneration during ageing, regulating satellite cell viability and their differentiation potential. Our results show upregulation of miR-24 during early stages of muscle regeneration in vivo in adult mice, suggesting a potential role of miR-24 at the early stages of muscle injury. On contrary, miR-24 was downregulated during regeneration of muscle of old mice. miR-24 was also downregulated, whereas its target gene Prdx6 was upregulated, in satellite cells isolated from old mice. miR-24 consistently regulated viability and myogenic potential of myogenic progenitors from both humans and old mice, suggesting that changes in miR-24 levels during ageing may contribute to defective early stages of muscle regeneration during ageing through affecting satellite cell viability and myogenic potential. This regulation likely occurs via miR-24 counteracting the generation of reactive oxygen species through Prdx6 de-repression in primary myogenic progenitors isolated from humans and old mice. We propose that downregulation of miR-24 in muscle of old mice following injury may be a protective mechanism against elevated ROS levels to maintain satellite cell viability and myogenic potential, acting through Prdx6 upregulation. However, as miR-24 is a regulator of p16 and p21, this downregulation may lead to increased satellite cell senescence, therefore representing an age-related failed compensatory mechanism.

cell biology↗