Magnesium promotes vascularized osseointegration in diabetic states
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ABSTRACT:
PROVIDER: PRJNA989125 | ENA |
REPOSITORIES: ENA
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Project description:The poor osseointegration of dental implants in diabetic patients has become a long-standing clinical problem. Magnesium has been proved to promote bone healing under normal conditions. Here, we elucidate the mechanism by which Mg2+ promotes vascularized osseointegration in diabetic status. We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised, with significantly decreased angiogenesis. We then developed Mg-coating implants with hydrothermal synthesis. These implants sucessfully improved the vascularization and osseointegration in diabetic status. Mechanically, Mg2+ promoted the degradation of Kelch-like ECH associated protein 1 (Keap1) and the nucleation of nuclear factor erythroid 2-related factor 2 (Nrf2) by up-regulating the expression of sestrin 2 (SESN2) in endothelial cells, thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia. Altogether, our data proved that Mg2+ promoted vascularized osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.
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Project description:Martian regolith (unconsolidated surface material) is a potential medium for plant growth in bioregenerative life support systems during manned missions on Mars. However, hydrated magnesium sulfate mineral levels in the regolith of Mars can reach as high as 10 wt%, and would be expected to be highly inhibitory to plant growth. A global approach was used to identify novel genes with potential to enhance tolerance to high MgSO4 stress. The early Arabidopsis root transcriptome response to elevated concentrations of magnesium sulfate was characterized in col-0, and also between col-0 and the mutant line cax1-1 – a mutant relatively tolerant of high levels of MgSO4•7H2O in soil solution. After 3 weeks of growth under hydroponic conditions, Arabidopsis thaliana col-0 roots were exposed to a basic nutrient solution (0.25 g/L MES, 1/16x MS, pH 5.7) with an additional 2.08 mM magnesium sulfate (total Ca:Mg ratio = 1:15) for 45 min., 90 min., or 180 min., while a col-0 control set was exposed to the basic nutrient solution without additional magnesium sulfate for 45 minutes. Arabidopsis thaliana cax1-1 roots were exposed to the basic nutrient solution with additional magnesium sulfate for 180 min. only. Four replicate containers were harvested for the control and each of the treatment sets, resulting in a total of 20 samples. Gene expression of the col-0 sets exposed to magnesium sulfate treatment for 45 min., 90 min., or 180 min. was compared to gene expression of the col-0 control set. Gene expression of the cax1-1 set exposed to magnesium sulfate treatment for 180 min. was compared to gene expression of the col-0 set exposed to magnesium sulfate treatment for 180 minutes.
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Project description:Impaired healing of diabetic wounds causes significant morbidity and mortality. This study aimed to identify novel mechanisms of diabetic wound healing defects and test a therapeutic intervention using diabetic mouse and pig models. We found Smad7 transgene expression in mouse epidermis promoting wound healing in diabetic db/db mice, with reductions in obesity and blood glucose. To isolate effects of Smad7 on wounds, we created a Smad7-based biologic (Tat-PYC-Smad7) that penetrates wound cells. Topical application of Tat-PYC-Smad7 to diabetic pig and mouse wounds accelerated healing compared to controls. RNAseq analysis of mouse wound samples showed reduced TGFβ/NFκB signaling, leading to faster re-epithelialization and better extracellular matrix remodeling. Tat-PYC-Smad7 also attenuated neutrophil degranulation and NETosis by blocking histone 3 citrullination and inhibiting myeloperoxidase activities. Our study reveals that Tat-PYC-Smad7 promotes diabetic wound healing by targeting keratinocytes and neutrophils, providing insight into cellular mechanisms of diabetic wound healing defects targetable by Smad7-based therapy.
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Project description:Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level. Micro-molar concentrations of magnesium in culture solution has been shown to ameliorate Al toxicity in soybean and other leguminous species. Different theories have been proposed to explain the chemical mechanisms of how the two ions interact to neutralize the toxic effect of aluminum in the plant root system. To understand the molecular mechanisms of the phenomenon at the gene expression level in soybean, we undertook a comparative transcriptome analysis in Al-tolerant and Al-sensitive genotypes treated with aluminum alone or aluminum plus magnesium using DNA microarrays. The results revealed magnesium enhances Al-tolerance level in the Al-tolerant genotype by down-regulating genes commonly induced in response to Al toxicity. We hypothesized that the magnesium-mediated alleviation of Al toxicity in the Al-tolerant genotype emanates from reduction in energy expenditure of gene expression induced in response to Al stress. Conversely, magnesium appears to ameliorate Al toxicity in the sensitive genotype by dual mechanisms of increasing the expression level of several genes involved in Al-tolerance and decreasing the expression level of most genes. Keywords: Soybean, aluminum toxicity, magnesium, transcriptome
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