缺氧通过HIF-1α/NF-κB通路诱导肾小管上皮细胞C3aR表达（英文）
发布时间：2024-02-18 07:33
C3aR是补体C3a的受体.在肾脏,已发现C3aR表达于包括肾小管上皮细胞在内的多种细胞.在特定的病理情况下,C3aR表达上调并参与多种肾脏疾病的病理过程,但有关C3aR在肾脏细胞中的表达调控机制仍不清楚.小管间质缺氧是肾脏疾病中的一种常见现象,也是一种重要致病因素.为了探讨缺氧对C3aR的表达调控作用,本文利用体外缺氧模型,对模型条件下C3aR在肾小管上皮细胞中的表达变化情况进行了分析,同时检测了HIF-1α和NF-κB的表达变化及活化情况,以及HIF-1α和NF-κB抑制剂对C3aR的表达影响情况.结果发现缺氧可诱导C3aR mRNA及蛋白质水平的表达上调、HIF-1α和NF-κB的核转移.HIF-1α和NF-κB抑制剂可阻断缺氧对C3aR的诱导作用,且HIF-1α抑制剂可抑制NF-κB的核转移.这些结果说明缺氧可通过HIF-1α/NF-κB通路诱导肾小管上皮细胞C3aR的表达.考虑到C3aR活化可促进肾小管的损伤,我们推测C3aR通路可能参与了缺氧和NF-κB诱导的肾小管损伤过程,可能是防治缺氧和NF-κB诱导肾组织损伤的一个新靶标.
【文章页数】：8 页
【文章目录】：
1 Materials and methods
1.1 Cell culture and experimental design
1.2 RT-PCR
1.3 Immunofluorescence
1.4 Western blotting
1.5 Statistical analysis
2 Results
2.1 Hypoxia induced C3a R expression in HK-2cells
2.2 Hypoxia induced translocation of HIF-1αand NF-κB into nucleus
2.3 HIF-1αinhibitor attenuated the upregulation of C3a R and translocation of NF-κB induced by hypoxia
2.4 The upregulation of C3a R in hypoxia condition was attenuated by NF-κB inhibitor
3 Discussion
本文编号：3902146
【文章页数】：8 页
【文章目录】：
1 Materials and methods
1.1 Cell culture and experimental design
1.2 RT-PCR
1.3 Immunofluorescence
1.4 Western blotting
1.5 Statistical analysis
2 Results
2.1 Hypoxia induced C3a R expression in HK-2cells
2.2 Hypoxia induced translocation of HIF-1αand NF-κB into nucleus
2.3 HIF-1αinhibitor attenuated the upregulation of C3a R and translocation of NF-κB induced by hypoxia
2.4 The upregulation of C3a R in hypoxia condition was attenuated by NF-κB inhibitor
3 Discussion
本文编号：3902146
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