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        MiR-1297 and MiR-26a-5p Inhibit Cell Progression of Keratinocytes in Cholesteatoma Depending on the Regulation of BMI1

        Xiaodan Zhu,Fanglei Ye,Shaojuan Hao,Qiuning Yu,Yang Wang,Weihua Lou,Kun Zhao,Hongmin Li 한국생물공학회 2022 Biotechnology and Bioprocess Engineering Vol.27 No.1

        Cholesteatoma is a pathologically benign but clinically destructive middle ear disease characterized by hyperproliferative keratinocytes. B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) has been reported to be upregulated in cholesteatoma tissues. This study aimed to explore the biological role and underlying mechanisms of BMI1 in the progression of cholesteatoma. The expression levels of microRNA (miR)-1297, miR-26a- 5p, and BMI1 in cholesteatoma tissues and cells were examined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Functional experiments were performed by CCK-8 assay for cell proliferation viability, 5-ethynyl-2'deoxyuridine (EdU) incorporation assay for DNA biosynthesis, colony formation assay for cloning forming ability analysis, transwell assay and wound healing assay for cell metastasis, flow cytometry for cell cycle distribution and cell apoptosis. The protein expression of apoptosis-associated proteins was investigated by western blot. Dual-luciferase reporter assay was conducted to verify the interaction between miR-1297 or miR-26a-5p and BMI1. BMI1 was highly expressed in cholesteatoma tumor tissues. Functional analyses showed that BMI1 knockdown could inhibit the proliferation, colony formation, migration, invasion, cell cycle progression and promoted the apoptosis of keratinocytes. Mechanically, BMI1 was a target of miR-1297 and miR-26a-5p. Moreover, the rescue experiments presented that BMI1 addition could abolish the suppressive effects of miR-1297 or miR-26a-5p overexpression on cell malignant behaviors in keratinocytes. BMI1 could exert an oncogenic role in the malignant development of cholesteatoma through serving as the targets of miR-1297 and miR-26a-5p, which might provide novel strategies for cholesteatoma treatment.

      • KCI등재

        Characteristics and mechanism of Pb(II) adsorption/desorption on GO/ r-GO under sulfide-reducing conditions

        Jianfeng Zhang,Xiaodan Xie,Cheng Liang,Weihuang Zhu,Xiaoguang Meng 한국공업화학회 2019 Journal of Industrial and Engineering Chemistry Vol.73 No.-

        Compared with graphene oxide (GO), r-GO (the reduced form) has a lower adsorption capacity for heavymetal ions and, therefore, generates concern over the release of adsorbed contaminants when GOadsorbent is discharged into a reducing environment. This study reveals that the maximum adsorptioncapacity of Pb(II) on GO and r-GO was 937.65 and 92.99 mg g 1 respectively. GO was reduced to r-GO bysulfide, causing 2.59–6.46% of the adsorbed Pb(II) to be released and was stably dispersed as a Pb(II)-oxidative debris (OD) complex. Our results provide valuable information about heavy metaltransportation in environments containing GO under different redox conditions.

      • Highly stretchable polymer semiconductor films through the nanoconfinement effect

        Xu, Jie,Wang, Sihong,Wang, Ging-Ji Nathan,Zhu, Chenxin,Luo, Shaochuan,Jin, Lihua,Gu, Xiaodan,Chen, Shucheng,Feig, Vivian R.,To, John W. F.,Rondeau-Gagné,, Simon,Park, Joonsuk,Schroeder, Bob C.,L American Association for the Advancement of Scienc 2017 Science Vol.355 No.6320

        <P>Soft and conformable wearable electronics require stretchable semiconductors, but existing ones typically sacrifice charge transport mobility to achieve stretchability. We explore a concept based on the nanoconfinement of polymers to substantially improve the stretchability of polymer semiconductors, without affecting charge transport mobility. The increased polymer chain dynamics under nanoconfinement significantly reduces the modulus of the conjugated polymer and largely delays the onset of crack formation under strain. As a result, our fabricated semiconducting film can be stretched up to 100% strain without affecting mobility, retaining values comparable to that of amorphous silicon. The fully stretchable transistors exhibit high biaxial stretchability with minimal change in on current even when poked with a sharp object. We demonstrate a skinlike finger-wearable driver for a light-emitting diode.</P>

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        Ginsenoside Rg3 ameliorates myocardial glucose metabolism and insulin resistance via activating the AMPK signaling pathway

        Jingyu Ni,Zhihao Liu,Miaomiao Jiang,Lan Li,Jie Deng,Xiaodan Wang,Jing Su,Yan Zhu,Feng He,Jingyuan Mao,Xiumei Gao,Guanwei Fan 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.2

        Background: Ginsenoside Rg3 is one of the main active ingredients in ginseng. Here, we aimed to confirm its protective effect on the heart function in transverse aortic coarctation (TAC)-induced heart failure mice and explore the potential molecular mechanisms involved. Methods: The effects of ginsenoside Rg3 on heart and mitochondrial function were investigated by treating TAC-induced heart failure in mice. The mechanism of ginsenoside Rg3 for improving heart and mitochondrial function in mice with heart failure was predicted through integrative analysis of the proteome and plasma metabolome. Glucose uptake and myocardial insulin sensitivity were evaluated using micro-positron emission tomography. The effect of ginsenoside Rg3 on myocardial insulin sensitivity was clarified by combining in vivo animal experiments and in vitro cell experiments. Results: Treatment of TAC-induced mouse models with ginsenoside Rg3 significantly improved heart function and protected mitochondrial structure and function. Fusion of metabolomics, proteomics, and targeted metabolomics data showed that Rg3 regulated the glycolysis process, and Rg3 not only regulated glucose uptake but also improve myocardial insulin resistance. The molecular mechanism of ginsenoside Rg3 regulation of glucose metabolism was determined by exploring the interaction pathways of AMPK, insulin resistance, and glucose metabolism. The effect of ginsenoside Rg3 on the promotion of glucose uptake in IR-H9c2 cells by AMPK activation was dependent on the insulin signaling pathway. Conclusions: Ginsenoside Rg3 modulates glucose metabolism and significantly ameliorates insulin resistance through activation of the AMPK pathway.

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