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- 저자 : Kaidong Liu (검색결과 2 건)
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Kaidong Liu,Runqing Yue,Changchun Yuan,Jinxiang Liu,Lei Zhang,Tao Sun,Yanjun Yang,Shuanggui Tie,Chenjia Shen 한국식물학회 2015 Journal of Plant Biology Vol.58 No.6
Iron deficiency is one of the most serious nutrient limiting factors that affect rice plant growth and photosynthesis. Several phytohormones, including auxin, participate in iron uptake and homeostasis. However, how auxin signaling is involved in iron deficiency-induced inhibition of shoot growth and photosynthetic efficiency is largely unknown. The Nipponbare (NIP) seedlings displayed typical chlorotic symptoms, biomass reduction and photosynthesis depression when subjected to iron deficiency. We measured the soluble Fe content in the shoots under different conditions. The soluble Fe content in the shoots under Fe deficiency was increased by 1-naphthoxyaceticacids (1-NOA) treatment and was decreased by 1-naphthaleneacetic acid (NAA) treatment. Blocking (1-NOA treatment) or enhancement (NAA treatment) of auxin signaling also affects photosynthetic parameters under Fe deficiency conditions. Furthermore, rice microarray data (GSE17245 and GSE39429) were used to analyze the relationship between iron deficiency responses and auxin signaling in shoots. Most iron deficiency response gene expression levels in the shoots increased under exogenous auxin treatment, and most auxin early response gene expression levels responded to iron deficiency. It suggested that there is a crosstalk between iron deficiency signaling and auxin signaling. Our results indicated that iron deciencyinduced growth inhibition and photosynthesis depression were mediated by systemic auxin signaling.
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Kai Dong,Wen-Juan Zhou,Zhong-Hao Liu 대한치주과학회 2023 Journal of Periodontal & Implant Science Vol.53 No.1
Purpose: The purpose of this study was to determine whether metformin (MF) could alleviate the expresssion of reactive oxygen species (ROS) and improve the osteogenic ability of bone marrow mesenchymal stem cells derived from diabetic rats (drBMSCs) in vitro, and to evaluate the effect of MF on the ectopic osteogenesis of drBMSCs in a nude mouse model in vivo. Methods: BMSCs were extracted from normal and diabetic rats. In vitro, a cell viability assay (Cell Counting Kit-8), tests of alkaline phosphatase (ALP) activity, and western blot analysis were first used to determine the cell proliferation and osteogenic differentiation of drBMSCs that were subjected to treatment with different concentrations of MF (0, 50, 100, 200, 500 μM). The cells were then divided into 5 groups: (1) normal rat BMSCs (the BMSCs derived from normal rats group), (2) the drBMSCs group, (3) the drBMSCs + Mito-TEMPO (10 μM, ROS scavenger) group, (4) the drBMSCs + MF (200 μM) group, and (5) the drBMSCs + MF (200 μM) + H2O2 (50 μM, ROS activator) group. Intracellular ROS detection, a senescenceassociated β-galactosidase assay, ALP staining, alizarin red staining, western blotting, and immunofluorescence assays were performed to determine the effects of MF on oxidative stress and osteogenic differentiation in drBMSCs. In vivo, the effect of MF on the ectopic osteogenesis of drBMSCs was evaluated in a nude mouse model. Results: MF effectively reduced ROS levels in drBMSCs. The cell proliferation, ALP activity, mineral deposition, and osteogenic-related protein expression of drBMSCs were demonstrably higher in the MF-treated group than in the non-MF-treated group. H2O2 inhibited the effects of MF. In addition, ectopic osteogenesis was significantly increased in drBMSCs treated with MF. Conclusions: MF promoted the proliferation and osteogenic differentiation of drBMSCs by inhibiting the oxidative stress induced by diabetes and enhenced the ectopic bone formation of drBMSCs in nude mice.
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