【摘 要】
：
目的：肾内多巴胺系统对维持正常肾功能与血压起重要作用,近期发现多巴胺D2受体(D2R)缺失可激活TGFβ1,导致肾纤维化,但作用通路未明.肾小管上皮细胞凋亡是肾纤维化的重要启动事件.方法：D2R编码基因的单核苷酸多态性(SNPs)在人群中高发,可导致D2R表达与功能下调.本研究利用携带D2R SNP的人肾小管上皮细胞(D2RSNP-RPTC)与未携带D2R SNP的人肾小管上皮细胞(WT-RPTC
【机 构】
：
浙江大学附属第一医院 肾脏病中心 Department of Medicine,School of
【出 处】
：
浙江省生物医学工程学会肾脏病透析移植分会2015年学术年会
论文部分内容阅读
目的：肾内多巴胺系统对维持正常肾功能与血压起重要作用,近期发现多巴胺D2受体(D2R)缺失可激活TGFβ1,导致肾纤维化,但作用通路未明.肾小管上皮细胞凋亡是肾纤维化的重要启动事件.方法：D2R编码基因的单核苷酸多态性(SNPs)在人群中高发,可导致D2R表达与功能下调.本研究利用携带D2R SNP的人肾小管上皮细胞(D2RSNP-RPTC)与未携带D2R SNP的人肾小管上皮细胞(WT-RPTC)对比,研究D2R对细胞凋亡的影响,并观察Wnt3信号通路是否起介导作用.结果：D2R-SNP-RPTC的细胞凋亡率显著高于WT-RPTC(11.00±0.80％vs 2.30±0.40％TUNEL positive cells,P＜0.01).D2R-SNP-RPTC中,Wnt3表达升高,β-catenin磷酸化水平下降,促凋亡因子Bax、FasL表达增加；而向该细胞转染携带DRD2基因的质粒可上调D2R表达,并下调Wnt3、Bax、FasL等表达.在WT-RPTC中,使用RNA干扰下调D2R表达后,Wnt3表达升高,β-catenin磷酸化水平下降,促凋亡因子Bax、FasL表达增加,说明D2R可调控Wnt3/β-catenin信号通路.而在D2R-SNP-RPTC中,使用RNA干扰下调Wnt3表达后,β-catenin磷酸化水平增加,促凋亡因子Bax、FasL表达下降,同时凋亡细胞明显减少(6.52±1.05 vs 12.23±0.92％TUNEL positive cells,P＜0.01),说明Wnt3信号通路可调控RPTC的细胞凋亡水平.结论：D2R可通过调控Wnt3/β-catenin信号通路激活,从而调节肾小管上皮细胞的凋亡水平.
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