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Experimental cell research 24건

  1. [해외논문]   Msi2 plays a carcinogenic role in esophageal squamous cell carcinoma via regulation of the Wnt/β-catenin and Hedgehog signaling pathways   SCI SCIE

    Li, Zhiwei (Correspondence to: Department of Thoracic Surgery, Zhoukou Central Hospital, No. 26 Renmin East Road, Chuanhui District, Zhoukou 466000, Henan Province, China.) , Jin, Hui , Mao, Guozhang , Wu, Liuguang , Guo, Qingwei
    Experimental cell research v.361 no.1 ,pp. 170 - 177 , 2017 , 0014-4827 ,

    초록

    Abstract Msi2 has been widely reported to be upregulated and strongly associated with fast progress and poor prognosis in many cancers. However, the expression and role of Msi2 in esophageal squamous cell carcinoma (ESCC) remain unknown. In this study, we found that Msi2 was upregulated in ESCC clinical samples, and was significantly associated with tumor size, differentiation status, and lymph node metastasis in ESCC patients. Multivariate Cox regression analysis showed that Msi2 was an independent predictor for disease-free survival (DFS) and overall survival (OS). Moreover, knockdown of Msi2 impaired ESCC cell proliferation, epithelial-mesenchymal transition (EMT) and migration, while overexpression of Msi2 promoted ESCC cell proliferation, EMT and migration in vitro. Animal experiments also confirmed that Msi2 promoted ESCC cell proliferation in vivo . Mechanistically, Msi2 promoted ESCC cell proliferation, EMT and migration via regulation of the Wnt/β-catenin and Hedgehog (Hh) signaling pathways. Taken together, our study suggested that Msi2 could serve as a candidate for diagnosis and prognosis and as a potential therapeutic target in ESCC. Highlights Msi2 is upregulated in ESCC tissues and cell lines. Msi2 is associated with tumor progression and poor prognosis of ESCC patients. Msi2 promotes ESCC cell proliferation, EMT and migration. Msi2 functions by regulating the Wnt/β-catenin and Hh signaling pathways.

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  2. [해외논문]   The viability of primary hepatocytes is maintained under a low cysteine-glutathione redox state with a marked elevation in ophthalmic acid production   SCI SCIE

    Lee, Jaeyong (Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Japan ) , Kang, Eun Sil (Sanghuh College of Life Sciences, Konkuk University, Republic of Korea ) , Kobayashi, Sho (Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Japan ) , Homma, Takujiro (Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Japan ) , Sato, Hideyo (Laboratory of Biochemistry and Molecular Biology, Department of Medical Technology, Faculty of Medicine, Niigata University, Japan ) , Seo, Han Geuk (Sanghuh College of Life Sciences, Konkuk University, Republic of Korea ) , Fujii, Junichi (Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Japan)
    Experimental cell research v.361 no.1 ,pp. 178 - 191 , 2017 , 0014-4827 ,

    초록

    Abstract Extracellular cystine, the oxidized form of cysteine (Cys), is taken up by cells via the cystine transporter xCT. xCT is not expressed in the liver but is induced in primary hepatocytes under conventional cultured conditions. However, compared to wild-type hepatocytes those from the xCT-knockout mouse showed no evidence of an abnormality and the levels of both Cys and glutathione (GSH) remained unchanged. The levels of ophthalmic acid (OPT), which is produced as an alternative compound by the GSH-synthesizing pathway, became increased during the culturing of hepatocytes. It therefore appears that, in primary hepatocytes, Cys is provided by systems other than xCT, most likely via the transsulfuration pathway, but the levels that are produced are not sufficient. We also employed mouse hepatoma-derived Hepa1-6 cells, which constitutively express xCT. When Hepa 1-6 cells were cultivated in Cys-free media, the levels of intracellular Cys and GSH were decreased, compared to cells cultured in conventional media, leading to cell death accompanied by an increase in the levels of reactive oxygen species and lipid peroxidation products with characteristics similar to ferroptosis. While OPT levels were increased by only to a limited extent in Hepa 1-6 cells, primary hepatocytes cultured in Cys- and Met-free media showed a marked elevation in OPT, reaching levels nearly equivalent to the GSH levels when the cells were cultured in conventional media. Thus, OPT may become a marker for Cys insufficiency and might be used to predict pathological conditions of cells with elevated oxidative stress. Highlights xCT is induced in primary mouse hepatocytes under culture conditions. xCT-KO hepatocytes contained normal levels of cysteine and glutathione (GSH). Primary hepatocytes were viable in cysteine- and methionine-free media. Ophthalmic acid levels were equivalent to those of GSH in hepatocytes. Graphical abstract Differential cysteine-supply systems between the primary mouse hepatocytes and Hepa 1-6 cells under conventional or Cys/Met-free culture. Met; Methionine, Hcy; Homocysteine, Cst; Cystathionine, Cys; Cysteine, Thr; Threonine, Glu; Glutamate, 2OB; 2-Oxo-butyric acid, 2AB; 2-Amino-butyric acid, GSH; Glutathione, OPT; Ophthalmic acid, γGCS; γ-Glutamylcysteine synthetase, GS; Glutathione synthetase; NAAT; neutral amino acid transporter [DISPLAY OMISSION]

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  3. [해외논문]   Up-regulation of caveolin-1 by DJ-1 attenuates rat pulmonary arterial hypertension by inhibiting TGFβ/Smad signaling pathway   SCI SCIE

    Gao, Weiwei (Department of Respiratory Medicine) , Shao, Runxia (The Second Affiliated Hospital of Zhengzhou University, ZhengZhou 450014, Henan, China ) , Zhang, Xiaoping (Department of Respiratory Medicine) , Liu, Daijian (The Second Affiliated Hospital of Zhengzhou University, ZhengZhou 450014, Henan, China ) , Liu, Ying (Department of Respiratory Medicine) , Fa, Xian'en (The Second Affiliated Hospital of Zhengzhou University, ZhengZhou 450014, Henan, China )
    Experimental cell research v.361 no.1 ,pp. 192 - 198 , 2017 , 0014-4827 ,

    초록

    Abstract Pulmonary arterial hypertension (PAH), characterized by excessive proliferation and apoptosis resistance of pulmonary artery smooth muscle cells (PASMCs), is closely associated with the imbalance in vasoactive mediators and massive remodeling of pulmonary vasculature. DJ-1/park7, a multifunctional protein, plays a critical defense role in several cytobiological activity, such as transcriptional regulation, anti-oxidative stress and tumor formation. In this study, we investigated the effects of DJ-1 on hypoxia-induced PAH model rats and PASMCs, as well as its possible molecular mechanism. First, the low expressions of DJ-1 and caveolin-1 (Cav-1) were synchronously detected in lung tissue of PAH model rats and hypoxia-induced PASMCs by Western blot. Then, the DJ-1 wild type (WT) or Knock out (KO) rats were exposed to chronic hypoxia to mimic a hypoxic PAH condition. The protein level of Cav-1 was markedly decreased in the tissue of DJ-1 KO rats, and additionally lower in tissue of the hypoxia group than that in the normoxia group for DJ-1 WT and KO rats. In vivo , hemodynamic data showed that the pulmonary arterial pressure (mPAP), right ventricle systolic pressure (RVSP) and pulmonary arterial systolic pressure (PASP), as well as the weight of the right ventricle/left ventricle plus septum (RV/LV+S) ratio of PAH model rats were higher in the DJ-1 KO group than those in the DJ-1 WT group. Moreover, knockout of DJ-1 also results in the phenotype switch from contractile to synthetic PASMC, which is reflected by reduced calponin and SM22α expressions. In vitro, DJ-1 overexpression reversed hypoxia-induced elevation of PASMC cell proliferation, migration and Ca 2+ concentration, which were not obviously observed in Cav-1 shRNA (sh-Cav-1) and DJ-1 co-transfected cells. Then the increased levels of calponin and SM22α were detected in the DJ-1 group; similarly those levels were not changed in the DJ-1+sh-Cav-1 group. Finally, the expression of TGFβ1, p-Smad2 and p-Smad3 were obviously decreased in the ad-DJ-1 group, however those were all elevated in the DJ-1 and sh-Cav-1 co-transfected groups. In conclusion, these results indicate that DJ-1 may alleviate hypoxia-induced PASMCs injury by Cav-1 through inhibiting the TGFβ/Smad signaling pathway. Highlights Knockout of DJ-1-aggravated hypoxic pulmonary arterial hypertension of rats. Overexpression of DJ-1 alleviated PASMs injury induced by hypoxia. DJ-1 alleviated hypoxia-induced PASMCs injury via Cav-1 by inhibiting TGFβ/Smad.

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  4. [해외논문]   Corrigendum to “MicroRNA-140-5p attenuated oxidative stress in Cisplatin induced acute kidney injury by activating Nrf2/ARE pathway through a Keap1-independent mechanism” [Exp. Cell Res. (2017) 292–302]   SCI SCIE

    Liao, Weitang (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Fu, Zongjie (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Zou, Yanfang (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Wen, Dan (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Ma, Hongkun (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Zhou, Fangfang (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Chen, Yongxi (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Zhang, Mingjun (Research Center for Experimental Medicine of Ruijin Hospital, Shanghai, China ) , Zhang, Wen (Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China)
    Experimental cell research v.361 no.1 ,pp. 199 - 199 , 2017 , 0014-4827 ,

    초록

    Abstract Pulmonary arterial hypertension (PAH), characterized by excessive proliferation and apoptosis resistance of pulmonary artery smooth muscle cells (PASMCs), is closely associated with the imbalance in vasoactive mediators and massive remodeling of pulmonary vasculature. DJ-1/park7, a multifunctional protein, plays a critical defense role in several cytobiological activity, such as transcriptional regulation, anti-oxidative stress and tumor formation. In this study, we investigated the effects of DJ-1 on hypoxia-induced PAH model rats and PASMCs, as well as its possible molecular mechanism. First, the low expressions of DJ-1 and caveolin-1 (Cav-1) were synchronously detected in lung tissue of PAH model rats and hypoxia-induced PASMCs by Western blot. Then, the DJ-1 wild type (WT) or Knock out (KO) rats were exposed to chronic hypoxia to mimic a hypoxic PAH condition. The protein level of Cav-1 was markedly decreased in the tissue of DJ-1 KO rats, and additionally lower in tissue of the hypoxia group than that in the normoxia group for DJ-1 WT and KO rats. In vivo , hemodynamic data showed that the pulmonary arterial pressure (mPAP), right ventricle systolic pressure (RVSP) and pulmonary arterial systolic pressure (PASP), as well as the weight of the right ventricle/left ventricle plus septum (RV/LV+S) ratio of PAH model rats were higher in the DJ-1 KO group than those in the DJ-1 WT group. Moreover, knockout of DJ-1 also results in the phenotype switch from contractile to synthetic PASMC, which is reflected by reduced calponin and SM22α expressions. In vitro, DJ-1 overexpression reversed hypoxia-induced elevation of PASMC cell proliferation, migration and Ca 2+ concentration, which were not obviously observed in Cav-1 shRNA (sh-Cav-1) and DJ-1 co-transfected cells. Then the increased levels of calponin and SM22α were detected in the DJ-1 group; similarly those levels were not changed in the DJ-1+sh-Cav-1 group. Finally, the expression of TGFβ1, p-Smad2 and p-Smad3 were obviously decreased in the ad-DJ-1 group, however those were all elevated in the DJ-1 and sh-Cav-1 co-transfected groups. In conclusion, these results indicate that DJ-1 may alleviate hypoxia-induced PASMCs injury by Cav-1 through inhibiting the TGFβ/Smad signaling pathway. Highlights Knockout of DJ-1-aggravated hypoxic pulmonary arterial hypertension of rats. Overexpression of DJ-1 alleviated PASMs injury induced by hypoxia. DJ-1 alleviated hypoxia-induced PASMCs injury via Cav-1 by inhibiting TGFβ/Smad.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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