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- 저자 : Guiming Chen (검색결과 3 건)
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Chen Liang,Liu Yuting,Wang Zheyu,Zhang Leiyang,Xu Yi,Li Yinan,Zhang Lan,Wang Guiming,Yang Shuofei,Xue Guanhua 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Neutrophil extracellular traps (NETs) play an important role in abdominal aortic aneurysm (AAA) formation; however, the underlying molecular mechanisms remain unclear. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) may exert therapeutic effects on AAA through their immunomodulatory and regenerative abilities. This study aimed to examine the role and mechanism of MSC-EVs in regulating the development of NET-mediated AAA. Excessive release of NETs was observed in patients with AAA, and the levels of NET components were associated with the clinical outcomes of the patients. Datasets from the Gene Expression Omnibus database were analyzed and revealed that the PI3K/AKT pathway and ferroptosis were strongly associated with NETosis during AAA formation. Further experiments verified that NETs promoted AAA formation by inducing ferroptosis in smooth muscle cells (SMCs) by inhibiting the PI3K/AKT pathway. The PI3K agonist 740 Y-P, the ferroptosis inhibitor ferrostatin-1, and Padi4 deficiency significantly prevented AAA formation. MSC-EVs attenuated AAA formation by reducing NET release in an angiotensin II-induced AAA mouse model. In vitro experiments revealed that MSC-EVs reduced the release of NETs by shifting NETosis to apoptosis. Our study indicates an important role for NET-induced SMC ferroptosis in AAA formation and provides several potential targets for AAA treatment
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Jiao, Lin,Chen, Ye,Kohama, Yoshimitsu,Graf, David,Bauer, E. D.,Singleton, John,Zhu, Jian-Xin,Weng, Zongfa,Pang, Guiming,Shang, Tian,Zhang, Jinglei,Lee, Han-Oh,Park, Tuson,Jaime, Marcelo,Thompson, J. D National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.3
<P><B>Significance</B></P><P>Conventional, thermally driven continuous phase transitions are described by universal critical behavior that is independent of microscopic details of a specific material. An analogous description is lacking for phase transitions that are driven at absolute zero temperature by a nonthermal control parameter. Classification of quantum-driven phase transitions is a fundamental but open problem that arises in diverse contexts and multiple classes of materials. Here we report the first observation, to our knowledge, of a sharp Fermi surface reconstruction while applying a strong magnetic field to suppress an antiferromagnetic transition to zero temperature. These experiments demonstrate that direct measurements of the Fermi surface can distinguish theoretically proposed models of quantum criticality and point to a universal description of quantum phase transitions.</P><P>Conventional, thermally driven continuous phase transitions are described by universal critical behavior that is independent of the specific microscopic details of a material. However, many current studies focus on materials that exhibit quantum-driven continuous phase transitions (quantum critical points, or QCPs) at absolute zero temperature. The classification of such QCPs and the question of whether they show universal behavior remain open issues. Here we report measurements of heat capacity and de Haas–van Alphen (dHvA) oscillations at low temperatures across a field-induced antiferromagnetic QCP (<I>B</I><SUB>c0</SUB> ≈ 50 T) in the heavy-fermion metal CeRhIn<SUB>5</SUB>. A sharp, magnetic-field-induced change in Fermi surface is detected both in the dHvA effect and Hall resistivity at [Formula] ≈ 30 T, well inside the antiferromagnetic phase. Comparisons with band-structure calculations and properties of isostructural CeCoIn<SUB>5</SUB> suggest that the Fermi-surface change at [Formula] is associated with a localized-to-itinerant transition of the Ce-4<I>f</I> electrons in CeRhIn<SUB>5</SUB>. Taken in conjunction with pressure experiments, our results demonstrate that at least two distinct classes of QCP are observable in CeRhIn<SUB>5</SUB>, a significant step toward the derivation of a universal phase diagram for QCPs.</P>
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Yun Li,Jinping Liu,Rong Luo,Yong You,Guiming Chen 한국생물공학회 2022 Biotechnology and Bioprocess Engineering Vol.27 No.4
Gefitinib has been widely used as a firstgeneration epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for non-small-cell lung cancer (NSCLC) patients with EGFR mutation. In this study, we explored the key molecules responsible for acquired Gefitinib resistance in NSCLC cells. 3-(4,5-Dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide assay was performed to analyze the Gefitinib resistance and proliferation ability of NSCLC cells. Cell proliferation was also assessed by colony formation assay. Flow cytometry was performed to analyze cell apoptosis. Wound healing assay and transwell invasion assay were performed to the migration and invasion abilities of NSCLC cells, respectively. The target relationship between microRNA-409-3p (miR-409-3p) and circular RNA mannosidase alpha class 1A member 2 (circ- MAN1A2) or twist family bHLH transcription factor 1 (TWIST1) was verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. Circ-MAN1A2 level was markedly elevated in Gefitinib-resistant NSCLC cell lines and tissues. Circ-MAN1A2 interference sensitized Gefitinib-resistant NSCLC cells to Gefitinib. Furthermore, circ-MAN1A2 interference suppressed the proliferation, migration and invasion and promoted the apoptosis of Gefitinib-resistant NSCLC cells. Circ-MAN1A2 overexpression negatively regulated miR-409-3p level by directly binding to it. miR-409-3p silencing partly counteracted circ-MAN1A2 silencing-mediated anti-tumor effects in Gefitinib-resistant NSCLC cells. TWIST1 was a target of miR-409-3p, and miR-409-3p overexpression-induced antitumor effects in Gefitinib-resistant NSCLC cells were partly reversed by TWIST1 overexpression. Circ-MAN1A2 silencing aggravated Gefitinib-mediated inhibition of tumor growth in vivo. In conclusion, circ-MAN1A2 facilitated the acquired resistance of Gefitinib and other malignant behaviors of NSCLC cells through mediating miR-409-3p/ TWIST1 axis.
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