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Bellantuono, I.

Publications and source records attributed to Bellantuono, I..

6 recordsLinked to original sources

Geroprotective interventions preserve trabecular bone during ageing in female mice

Geroprotectors extend lifespan and improve several aspects of healthspan, yet their effects on skeletal ageing remain poorly understood. They hold potential advantages over current bone-targeted osteoporosis therapies, as they may simultaneously improve bone, neuromuscular function, and vision, thereby reducing the risk of falls, the major cause of fractures. Here we examined, for the first time, the long-term effects of rapamycin, acarbose, and 17-estradiol, administered at lifespan-extending doses on trabecular and cortical bone architecture in male and female UM-HET3 mice measured with micro-computed tomography at 12 and 22 months of age. Bayesian modelling analysis reveals that all interventions produced responses in trabecular bone in females at 22 months. These effects were driven mainly by increases in trabecular number, with little evidence for changes in trabecular thickness. In contrast, treatment effects in males were generally negligible. Cortical responses were modest. Moderate increases in cortical area fraction were observed in females treated with rapamycin or 17-estradiol at 22 months, whereas cortical thickness remained largely unchanged, suggesting a geometrical rather than anabolic effect. Interestingly, geroprotectors strongest skeletal responses in females contrasts with the predominantly male-biased lifespan extension reported for acarbose and 17-estradiol, suggesting differential mechanisms mediating lifespan extension and bone structure preservation.

pharmacology and toxicology↗

Fisetin-mediated MYC restoration improves age-associated decline in macrophage function

Immune decline in older adults is associated with increased susceptibility to infection and chronic inflammatory diseases. Macrophages are critical innate immune cells that show reduced capacity for phagocytosis and migration with age. Our previous work shows that reduced levels of MYC and USF1 transcription factors are drivers of macrophage age-related functional decline. Here we show that macrophage-specific Myc overexpression improves macrophage migration and, more importantly, is able to improve physical performance at older age in Drosophila, while lifespan remains unaffected. Treatment of human primary macrophages from older individuals with the geroprotective supplement fisetin reverses the decline in MYC expression and improves phagocytosis of pathogens and cell migration functions towards levels seen in younger individuals. Mechanistically, fisetin acts via MYC, by restoring expression levels of MYC targets in human macrophages that are altered with age. Finally, fisetin feeding in older mice improves motor activity and reduces frailty, as well as restoring primary macrophage function and Myc expression in vitro. These findings reveal that restoration of MYC in macrophage ageing is responsible, at least in part, for improvement in physical performance with age and identify this pathway as a rational target to reverse age-related immune decline. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=185 SRC="FIGDIR/small/731325v1_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@1ab6731org.highwire.dtl.DTLVardef@3d85dorg.highwire.dtl.DTLVardef@71c2b3org.highwire.dtl.DTLVardef@a59bf3_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

A p21-GFP zebrafish model of senescence for rapid testing of senolytics in vivo.

Senescence drives the onset and severity of multiple ageing-associated diseases as well as frailty. As a result, there has been an increased interest in mechanistic studies and in the search for compounds targeting senescent cells, known as senolytics. Mammalian models are commonly used to test senolytics and generate functional and toxicity data at the level of organs and systems, yet this is expensive and time consuming. Zebrafish share high homology in genes associated with human ageing and disease. They can be genetically-modified relatively easily. In larvae, most organs develop within 5 days of fertilisation and are transparent, which allows tracking of fluorescent cells in vivo in real time, testing drug off-target toxicity and assessment of cellular and phenotypic changes. Here, we have generated a transgenic zebrafish line that expresses green fluorescent protein (GFP) under the promoter of a key senescence marker, p21. We show an increase in p21:GFP+ cells in larvae following exposure to ionising radiation and with natural ageing. p21:GFP+ cells display other markers of senescence, including senescence-associated {beta}-galactosidase and IL6. The observed increase in senescent cells following irradiation is associated with a reduction in the thickness of muscle fibres and mobility, two important ageing phenotypes. We also show that quercetin and dasatinib, two senolytics currently in clinical trials, reduce the number of p21:GFP+ cells, in a rapid 5-day assay. This model provides an important tool to study senescence in a living organism, allowing the rapid selection of senolytics before moving to more expensive and time-consuming mammalian systems.

pharmacology and toxicology↗

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↗

Zoledronate extends healthspan and survival via the mevalonate pathway in a FOXO-dependent manner

Increased longevity has not been paralleled by extended healthspan, resulting in more years spent with multiple diseases in older age. As such, interventions to improve healthspan are urgently required. Zoledronate is a nitrogen containing bisphosphonate, which inhibits the farnesyl pyrophosphate synthase (FPPS) enzyme, central to the mevalonate pathway. It is already used clinically to prevent fractures in osteoporotic patients, who have been reported to derive unexpected and unexplained survival benefits. In this study we show that zoledronate has beneficial effects on both lifespan and healthspan using Drosophila as a model. We found that zoledronate extended lifespan, improved climbing activity and reduced intestinal epithelial dysplasia and permeability in aged flies. Mechanistic studies showed that zoledronate conferred resistance to oxidative stress and reduced accumulation of X-ray-induced DNA damage via inhibition of FPPS. Moreover, zoledronate inhibited pAKT in the mTOR pathway and functioned via dFOXO, a molecule associated with increased longevity, downstream of the mevalonate pathway. Taken together, our work indicates that zoledronate, a drug already widely used and dosed only once a year to prevent osteoporosis, modulates important mechanisms of ageing. Its repurposing holds great promise as a treatment to improve healthspan.

pharmacology and toxicology↗

Genome-wide association and functional analyses identify CASC20 and KIF26B as target loci in heterotopic ossification

Heterotopic ossification (HO) is bone formation that occurs after trauma within tissues that do not normally have the property of ossification, resulting in pain and disability. The genetic architecture of HO remains unclear. In the first genome-wide association studies of this disease, we identify the human-only long non-coding RNA-encoding gene CASC20 as a robust, replicating susceptibility locus for HO and KIF26B as a potential severity locus. We find that both CASC20 and KIF26B are expressed in human bone. Both CASC20 and KIF26B expression is upregulated upon BMP2 induced osteogenic differentiation in primary human mesenchymal stem cells, followed by RUNX2 and OSTERIX upregulation and mineralised nodule formation. A CRISPR-Cas9 mediated knockout of Kif26b inhibits BMP2-induced Runx2, Sp7/Osterix, Col1A1, Alp, and Bglap/Osteocalcin expression in a murine myocyte model of osteogenic trans-differentiation, and prevents mineralised nodule formation. These studies provide the first insights into the heritable biology of common, complex HO.

genetics↗