Yang Bin, Cao Pingli, Bao Guoqing, Wu Ming, Chen Weihong, Wu Shuangyan, Luo Ding, Bi Pinduan
Department of Hepatobiliary Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Heliyon. 2024 Aug 22;10(17):e36679. doi: 10.1016/j.heliyon.2024.e36679. eCollection 2024 Sep 15.
miRNA has been implicated in regulating cholesterol homeostasis, a critical factor in gallstone formation. Here, we focused on elucidating the role of miR-146a in this pathological process.
C57BL/6 mice were fed with lithogenic diet (LD) and injected with miR-146 antagomir (anta-146) via the tail vein for various weeks. The gallbladders and liver tissues were collected for cholesterol crystal imaging, gallstone mass quantification, and molecular analysis. Levels of cholesterol, bile salt, phospholipids, and metabolic parameters in serum and bile were assessed by ELISA. A 3' UTR reporter gene assay was used to verify the direct target genes for miR-146. The relative expression of metabolism genes was analyzed by quantitative real-time PCR and immunoblotting.
miR-146a-5p expression was reduced in mice and clinical samples with gallstones. Anta-146 treatment effectively prevented LD-induced gallstone formation in mice without hepatic and cholecystic damage. The mice treated with anta-146 exhibited beneficial alterations in bile cholesterol and bile acids and lipid levels in the blood. A key biliary cholesterol transporter-Megalin was identified as a direct target of miR-146. Anta-146 administration upregulated megalin expression, thereby ameliorating impaired gallbladder cholesterol absorption associated with the LXR-megalin/cubilin pathway.
The data demonstrates that miR-146 modulates gallbladder cholesterol absorption by targeting megalin, and prevents the pathogenesis of cholesterol gallstones.
微小RNA(miRNA)已被证明参与调节胆固醇稳态,而胆固醇稳态是胆结石形成的关键因素。在此,我们着重阐明miR-146a在这一病理过程中的作用。
给C57BL/6小鼠喂食致石性饮食(LD),并通过尾静脉注射miR-146拮抗剂(anta-146),持续数周。收集胆囊和肝脏组织用于胆固醇晶体成像、胆结石质量定量分析及分子分析。采用酶联免疫吸附测定(ELISA)评估血清和胆汁中胆固醇、胆盐、磷脂及代谢参数的水平。运用3'非翻译区(UTR)报告基因检测法验证miR-146的直接靶基因。通过定量实时聚合酶链反应(PCR)和免疫印迹法分析代谢基因的相对表达。
在患有胆结石的小鼠和临床样本中,miR-146a-5p表达降低。Anta-146治疗有效预防了LD诱导的小鼠胆结石形成,且未造成肝脏和胆囊损伤。接受anta-146治疗的小鼠胆汁胆固醇、胆汁酸及血液脂质水平出现有益变化。一种关键的胆汁胆固醇转运蛋白——巨膜蛋白被确定为miR-146的直接靶标。给予anta-146上调了巨膜蛋白的表达,从而改善了与肝X受体(LXR)-巨膜蛋白/立方蛋白途径相关的胆囊胆固醇吸收受损情况。
数据表明,miR-146通过靶向巨膜蛋白调节胆囊胆固醇吸收,并预防胆固醇性胆结石的发病机制。