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1-Deoxy-D-xylulose-5-phosphate synthase (DXS) is the first key enzyme in the MEP responsible for monoterpene synthesis. To reveal its regulatory effect on floral scents of lily, LiDXS2 was cloned from Oriental Lily 'Sorbonne'; the protein location was determined using subcellular localisation; and the expression pattern in different flowering stages and tissues was probed by fluorescence quantitative PCR. The plant expression vector was constructed to transform Arabidopsis thaliana, and the transgenic plants were characterised. The results showed that the LiDXS2 ORF area was 2142 bp and encoded a total of 713 amino acids. Analysis of homologous sequences showed that it contains two highly conserved regions, WDVGHQ and IAEQHA, which were closely related to Ginkgo DXS2 protein and Periwinkle DXS protein. Subcellular localisation showed that the LiDXS2 gene of Lilium 'Sorbonne' was localised in chloroplasts. In different flowering stages, the expression patterns of LiDXS2 were basically the same as the TranScriptome sequencing results, and the overall trend was initially increasing and then decreasing. In different floral organ tissues, the expression level of LiDXS2 was significantly higher in petals than other tissues, and almost no expression was observed in anthers. In A. thaliana transformed by LiDXS2, the transgenic lines showed an increased plant height and early flowering phenotype, and the expression of volatile synthesis genes for key structures downstream of DXS in the MEP pathway was upregulated compared with controls. Collectively, these results suggest that LiDXS2 may play an important role in regulating Lilium 'Sorbonne' monoterpene synthesis and its floral flavour release. [ABSTRACT FROM AUTHOR]

Vitamin D was found to regulate inflammatory response and angiogenesis, which were often impaired in diabetic wound healing. This study aimed to investigate the effects of 1,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] on diabetic wound healing both in vivo and in vitro. Diabetes was induced by high-fat diet combined with streptozotocin. After four weeks of establishing diabetic mouse model, full-thickness excisional wounds were created on their dorsal skin. Then 1,25(OH) 2 D 3 was administered via intraperitoneal injection for 14 consecutive days. Human umbilical vein endothelial cells (HUVECs) were cultured with normal glucose, high glucose, high glucose plus 1,25(OH) 2 D 3. Cell proliferation, migration, tube formation, and expression levels of relevant pathway components were measured. Intervention with 1,25(OH) 2 D 3 significantly increased wound closure rates of diabetic mice. During the inflammatory phase, 1,25(OH) 2 D 3 alleviated excessive inflammation and promoted the transition of macrophages from M1 to M2 phenotype. Regarding vascular endothelial function, 1,25(OH) 2 D 3 significantly up-regulated eNOS protein expression and inhibited Vcam-1 mRNA expression in diabetic mice (P < 0.05). As for angiogenesis, 1,25(OH) 2 D 3 markedly increased CD31-positive area, the protein and mRNA expression of VEGF, VEGFR2, PDGF, and PDGFRβ, as well as the mRNA expression of Bfgf and Egfr (P < 0.05). In vitro, 1,25(OH) 2 D 3 restored impaired cell proliferation, migration, and tube formation induced by high-glucose, and up-regulated expression of angiogenesis-related factors. These protective effects might be mediated through PI3K/AKT/HIF-1α pathway. These findings suggested that 1,25(OH) 2 D 3 accelerated diabetic wound healing by modulating inflammation, restoring vascular endothelial dysfunction, and promoting angiogenesis. [Display omitted] • Intervention of 1,25(OH) 2 D 3 significantly accelerated diabetic wound healing. • 1,25(OH) 2 D 3 accelerated diabetic wound healing by modulating inflammation. • 1,25(OH) 2 D 3 accelerated diabetic wound healing through promoting angiogenesis. • The protective effects of 1,25(OH) 2 D 3 might be mediated through PI3K/AKT/HIF-1α pathway. [ABSTRACT FROM AUTHOR]