التفاصيل البيبلوغرافية
| العنوان: |
泛醌氧化还原酶铁硫蛋白 4 通过影响线粒体功能参与肺炎衣原体感染诱导的血管平滑肌细胞焦亡 (Chinese) |
| العنوان البديل: |
Ubiquinone oxidoreductase iron-sulfur protein 4 participates in vascular smooth muscle cell pyroptosis induced by Chlamydia pneumoniae infection through affecting mitochondrial function. (English) |
| المؤلفون: |
张雨珂, 赵茜, 张利军, 王蓓蓓, 苗国琳, 张琪, 张丽莙 |
| المصدر: |
Chinese Journal of Arteriosclerosis; Jul2023, Vol. 31 Issue 7, p573-580, 8p |
| مصطلحات موضوعية: |
VASCULAR smooth muscle, IRON-sulfur proteins, LACTATE dehydrogenase, GENE expression, OXIDATIVE phosphorylation |
| الملخص (بالإنجليزية): |
Aim To explore the pyroptosis of vascular smooth muscle cell (VSMC) induced by Chlamydia pneumoniae (C. pn) infection and its possible mechanisms. Methods Primary rat VSMC were cultured by explant method. After the model of VSMC infected with C. pn was established, the changes in morphology of VSMC were observed under an inverted phase microscope, the lactic dehydrogenase (LDH) content was detected by the kit, and the expression levels of GSDMD and Caspase-1 were determined by Western blot, the changes in mitochondrial oxidative phosphorylation and the expression of complex-related proteins were measured by quantitative proteomic analysis by tandem mass tag technology and gene ontology. Results Compared with the control group, bubble-like vesicles were found outside the membrane of VSMC after C. pn infection under an inverted phase microscope. After C. pn infection of VSMC for 36 h and 48 h, LDH content increased by 38. 92% and 79. 54% (P <0. 001), respectively, and the expression of pyropotosisrelated protein GSDMD increased by 1. 74 times and 1. 67 times (P<0. 001). After C. pn infection of VSMC for 48 h, the expression(pro-Caspase-1) and activity(Caspase-1 p12/p10)of Caspase-1 increased by 2. 69 times and 3. 47 times (P<0. 001), respectively. The mass spectrometry results showed that there were 20 differentially expressed proteins enriched in the oxidative phosphorylation pathway after C. pn infection, and at the same time, ComplexⅠubiquinone oxidoreductase iron-sulfur protein 4 (NDUFS4) decreased significantly. Further Western blot results showed that the expression level of NDUFS4 decreased by 57. 5% and 57% (P<0. 001) after C. pn infection of VSMC for 36 h and 48 h respectively. Conclusion C. pn infection may induce VSMC pyroptosis by affecting mitochondrial function through downregulating NDUFS4 expression. [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): |
[目的] 探究肺炎衣原体(C. pn)感染诱导血管平滑肌细胞(VSMC)焦亡及其可能机制。[ 方法] 组 织贴块法培养大鼠原代VSMC,利用C. pn 感染VSMC 模型,使用倒置相差显微镜观察C. pn 感染后VSMC 形态学的 变化,试剂盒检测C. pn 感染VSMC 后乳酸脱氢酶(LDH)含量变化,Western blot 实验检测GSDMD 和Caspase-1 的表 达,串联质谱标签法定量蛋白质组学实验和GO 富集分析检测线粒体氧化磷酸化和氧化呼吸链Complex 相关蛋白 的变化。[结果] 与对照组相比,倒置相差显微镜下可见C. pn 感染后VSMC 膜外出现气泡状囊泡,C. pn 感染 VSMC 36 h、48 h 后LDH 含量分别增加38. 92%和79. 54%(均P<0. 001),焦亡相关蛋白GSDMD 表达增加1. 74 倍 和1. 67 倍(均P<0. 001);C. pn 感染VSMC 48 h 后Caspase-1 表达(pro-Caspase-1)和活性(Caspase-1 p12/p10)分别 增加2. 69 倍和3. 47 倍(均P<0. 001);质谱结果显示,C. pn 感染VSMC 后有20 种差异表达的蛋白质富集在氧化磷 酸化通路中,同时发现,ComplexⅠ泛醌氧化还原酶铁硫蛋白4(NDUFS4) 下降最为显著。进一步的Western blot 实 验结果显示,C. pn 感染VSMC 36 h、48 h 后NDUFS4 的表达水平分别下降了57. 5%和57%(均P<0. 001)。[结论] C. pn 感染可能通过抑制NDUFS4 表达影响线粒体功能,从而诱导VSMC 焦亡. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
