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- 저자 : Luo Chun Xia (검색결과 5 건)
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Yi-Chun Wang,Qiong Chen,Jun-Ming Luo,Jing Nie,Qing-He Meng,Wei Shuai,Han Xie,Jia-Mei Xia,Hui Wang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
The goals of this study were to investigate the role of the Notch1/PDGFRβ/ROCK1 signaling pathway in the pathogenesis of pulmonary fibrosis and to explore the possibility of treating fibrosis by targeting Notch1. Lung tissues from patients with pulmonary fibrosis were examined for the expression of Notch1/PDGFRβ/ROCK1 using RT-qPCR, western blotting, and immunostaining. Cultured mouse lung pericytes were transfected with Notch1-overexpressed vectors or shRNA targeting PDGFRβ/ROCK1 to examine cell behaviors, including proliferation, cell cycle arrest, and differentiation toward myofibroblasts. Finally, a mouse pulmonary fibrosis model was prepared, and a Notch1 inhibitor was administered to observe tissue morphology and pericyte cell behaviors. Human pulmonary fibrotic tissues presented with overexpression of Notch1, PDGFRβ, and ROCK1, in addition to a prominent transition of pericytes into myofibroblasts. In cultured mouse lung pericytes, overexpression of Notch1 led to the accelerated proliferation and differentiation of cells, and it also increased the expression of the PDGFRβ and ROCK1 proteins. The knockdown of PDGFRβ/ROCK1 in pericytes remarkably suppressed pericyte proliferation and differentiation. As further substantiation, the administration of a Notch1 inhibitor in a mouse model of lung fibrosis inhibited the PDGFRβ/ROCK1 pathway, suppressed pericyte proliferation and differentiation, and alleviated the severity of fibrosis. Our results showed that the Notch1 signaling pathway was aberrantly activated in pulmonary fibrosis, and this pathway may facilitate disease progression via mediating pericyte proliferation and differentiation. The inhibition of the Notch1 pathway may provide one promising treatment strategy for pulmonary fibrosis.
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Exogenous p53 Upregulated Modulator of Apoptosis (PUMA) Decreases Growth of Lung Cancer A549 Cells
Liu, Chun-Ju,Zhang, Xia-Li,Luo, Da-Ya,Zhu, Wei-Feng,Wan, Hui-Fang,Yang, Jun-Ping,Yang, Xiao-Jun,Wan, Fu-Sheng Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.2
Purpose: To investigate the influence of exogenous p53 upregulated modulator of apoptosis (PUMA) expression on cell proliferation and apoptosis in human non-small cell lung cancer A549 cells and transplanted tumor cell growth in nude mice. Materials and Methods: A549 cells were divided into the following groups: control, non-carrier (NC), PUMA (transfected with pCEP4-(HA) 2-PUMA plasmid), DDP ($10{\mu}g/mL$ cisplatin treatment) and PUMA+DDP (transfected with pCEP4-(HA)2-PUMA plasmid and $10{\mu}g/mL$ cisplatin treatment). The MTT method was used to detect the cell survival rate. Cell apoptosis rates were measured by flow cytometry, and PUMA, Bax and Bcl-2 protein expression levels were measured by Western blotting. Results: Compared to the control group, the PUMA, DDP and PUMA+DDP groups all had significantly decreased A549 cell proliferation (p<0.01), with the largest reduction in the PUMA+DDP group. Conversely, the apoptosis rates of the three groups were significantly increased (P<0.01), and the PUMA and DDP treatments were synergistic. Moreover, Bax protein levels significantly increased (p<0.01), while Bcl-2 protein levels significantly decreased (p<0.01). Finally, both the volume and the weights of transplanted tumors were significantly reduced (p<0.01), and the inhibition ratio of the PUMA+DDP group was significantly higher than in the single DDP or PUMA groups. Conclusions: Exogenous PUMA effectively inhibited lung cancer A549 cell proliferation and transplanted tumor growth by increasing Bax protein levels and reducing Bcl-2 protein levels.
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Post-fire Bond Behaviors Between Grout and Steel Rebar
Liang-Lin Liu,Chun-Yong Luo,Lu-Xia Ouyang,Zhen-Hua Xia,Wei-Hua Li 한국콘크리트학회 2022 International Journal of Concrete Structures and M Vol.16 No.5
Firstly, according to the theoretical analysis, the force mechanism and failure modes were assured for the bond behavior between grout and steel rebar. Then, a pull-out experiment was exerted to probe the bond behavior developments of specimens after exposed to 500 °C. It is found that the mixed measures of pre-drying and slow elevating rate, i.e., 5 °C/min, inhibits the explosive spalling in grout with compressive strength of 76.7 MPa. In addition, there are two failure modes including the steel rebar fracture and the bond slip failure in the test. Based on the elevated temperature, compressive strength of post-fire grout, diameter of steel rebar and its embedment length, a new expression has been built to calculate the bond strength between grout and steel rebar of post-fire specimens. Furthermore, the finite element simulation is employed to investigate the bond behaviors of pull-out specimens after exposed to elevated temperatures up to 500 °C. The steel rebar fracture is captured firstly in the pull-out test simulation. Moreover, it is found that the peak slips increase and peak loads decrease along with the temperature elevating. Finally, it is proposed that the crucial elevated temperatures of the failure mode change should be 300, 300 and 400 °C for the specimens with embedment lengths of 6, 7 and 8 times diameter of steel rebar with diameter of 16 mm, respectively, which is beneficial for evaluating the fire safety of the existing structure elements.
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Xiang Gao,Wen-Li Ai,Huan Gong,Li-Juan Cui,Bo-Xia Chen,Hong-Yi Luo,Zhong-Chun Zhang,Bao-Sheng Qiu 한국식물생명공학회 2016 Plant biotechnology reports Vol.10 No.2
Transgenic research was preformed by transferring a cyanobacterial (Nostoc flagelliforme) iron superoxide dismutase gene (NfFeSOD) into heavy metal hyperaccumulator Sedum alfredii via Agrobacterium-mediated method. Beyond expectation, NfFeSOD-overexpressing S. alfredii plants exhibited profound impairments, including plant growth retardation, abnormal root architecture, and reduced leaf greenness, photosynthetic efficiency and metal accumulation efficiency. Although transgenic plants appeared physiologically sensitive to high temperature, a higher relative biomass growth was still observed under long-term high temperature and osmotic stresses. Further investigation found that reactive oxygen species (ROS) homeostasis of transgenic plants was significantly affected, being ~50 % reduction of H2O2 level relative to wild-type plants. Gene transcription including ROS responsive genes was overall attenuated in transgenic plants, being more significant at normal temperature than at high temperature. In addition, ascorbate peroxidase (APX) activity was increased nearly twofolds in transgenic plants as compared to wild-type control. It may be inferred that ectopic NfFeSOD overexpression gives rise to a substantial increase of APX activity and leads to a sharp reduction of H2O2 level, thus impairing basal ROS signaling and plant growth. Specific genetic background of S. alfredii may be responsible for this sharp reduction of H2O2 level induced by NfFeSOD overexpression. S. alfredii plant has acclimated to elevated levels of ROS induced by heavy metals in native habitats and should require high ROS levels for basal signaling. We thus suppose that a sustained disturbance of high basal ROS signaling in metal hyperaccumulators may instead incur very sensitive response and thus result in profound growth impairments.
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