There is evidence that space flight condition-induced biological damage is associated with increased oxidative stress and extracellular matrix (ECM) remodeling. To explore possible mechanisms, changes in gene expression profiles implicated in oxidative stress and in ECM remodeling in mouse skin were examined after space flight. The metabolic effects of space flight in skin tissues were also characterized. Space Shuttle Atlantis (STS-135) was launched at the Kennedy Space Center on a 13-day mission. Female C57BL/6 mice were flown in the STS-135 using animal enclosure modules (AEMs). Within 3-5 h after landing, the mice were euthanized and skin samples were harvested for gene array analysis and metabolic biochemical assays. Many genes responsible for regulating production and metabolism of reactive oxygen species (ROS) were significantly (p < 0.05) altered in the flight group, with fold changes >1.5 compared to AEM control. For ECM profile, several genes encoding matrix and metalloproteinases involved in ECM remodeling were significantly up-/down-regulated following space flight. To characterize the metabolic effects of space flight, global biochemical profiles were evaluated. Of 332 named biochemicals, 19 differed significantly (p < 0.05) between space flight skin samples and AEM ground controls, with 12 up-regulated and 7 down-regulated including altered amino acid, carbohydrate metabolism, cell signaling, and transmethylation pathways. Collectively, the data demonstrated that space flight condition leads to a shift in biological and metabolic homeostasis as the consequence of increased regulation in cellular antioxidants, ROS production, and tissue remodeling. This indicates that astronauts may be at increased risk for pathophysiologic damage or carcinogenesis in cutaneous tissue.

Biomaterial-based tissue engineering strategies hold great promise for osteochondral tissue repair. Yet significant challenges remain in joining highly dissimilar materials to achieve a biomimetic, mechanically robust design for repairing interfaces between soft tissue and bone. This study sought to improve interfacial properties and function in a bilayer, multi-phase hydrogel interpenetrated with a fibrous collagen scaffold. ‘Soft’ 10% (w/w) and ‘stiff’ 30% (w/w) PEGDM was formed into mono- or bilayer hydrogels possessing a sharp diffusional interface. Hydrogels were evaluated as single- (hydrogel only) or multi-phase (hydrogel+fibrous scaffold penetrating throughout the stiff layer and extending >500μm into the soft layer). Including a fibrous scaffold into both soft and stiff single-phase hydrogels significantly increased tangent modulus and toughness and decreased lateral expansion under compressive loading. In multi-phase hydrogels, finite element simulations predict substantially reduced stress and strain gradients across the soft—stiff hydrogel interface. When combining two low moduli constituent material, composites theory poorly predicts the observed, large modulus increases. These results suggest material structure associated with the fibrous scaffold penetrating within the PEG hydrogel as the major contributor to improved properties and function – the hydrogel bore compressive loads and the 3D fibrous scaffold was loaded in tension thus resisting lateral expansion.

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Aging is a complex biological process with many factors1. Regulation of a single ion such as phosphorus (Pi) can change with age. Pi takes part in cell signaling, energy metabolism and nucleic acid synthesis2. It is systemically regulated by the intestine and kidney3. Pi regulation declines with age3 and in diseases like diabetes mellitus and chronic renal disease. Disruption of Pi regulation can lead to disease in skeletal and cardiac systems, as well as further renal issues4. Since 85% of Pi is stored in the skeleton5, we focused on aging bone where the effects of systemic Pi dysfunction are apparent3. Mice aged 12, 80, and more than 100 weeks were euthanized. Femurs were harvested for gene expression analysis of Pi transporters, cytokines, and inflammatory markers. Fold‐changes in expression were determined using 2−ΔΔCτ method. The difference between age groups was analyzed using one way ANOVA. The results show that Pi homeostasis is not efficient with older age. Expression of Pi transporters and bone health markers both change with age. Understanding the link between chronic diseases and bone health is vital to the aging population for future management and prevention.

Rapid bone loss during spaceflight is a well-established and continuing medical issue for astronauts. It has been reported that astronauts have displayed bone loss at rates of up to 2.7%/month in weight-bearing bones, or about 6 times that of post-menopausal women [1]. Rodent models have provided a means to further our understanding of the effects of microgravity on bone quality, both from studies in which rodents have flown aboard space missions and those in which weightlessness is simulated on earth through musculoskeletal unloading [2]. Such studies have the potential to not only further our understanding of the cause of decreased bone integrity in space, but also provide an accelerated model for the study of osteo-degenerative diseases affecting the general public, leading to improved treatment methods for both spaceflight and age or illness related osteoporosis.