华支睾吸虫外泌体源Csi-miR-125a致肝纤维化作用及其机制

doi:10.12140/j.issn.1000-7423.2025.02.008

中国寄生虫学与寄生虫病杂志 ›› 2025, Vol. 43 ›› Issue (2): 198-204.doi: 10.12140/j.issn.1000-7423.2025.02.008

华支睾吸虫外泌体源Csi-miR-125a致肝纤维化作用及其机制

吴银娟¹^,²()(), 易雪晴¹, 李美玉¹^,², 徐安远¹, 武奥迅¹, 钟籽丰¹, 李学荣¹^,^*()()

1 中山大学中山医学院寄生虫学教研室，中山大学教育部热带病防治研究重点实验室，广东省媒介生物防控工程技术研究中心，广东广州 510080
2 中山大学中山医学院基础医学实验教学中心，广东广州 510080

收稿日期:2024-08-18 修回日期:2024-11-28 出版日期:2025-04-30 发布日期:2025-04-27
通讯作者: * 李学荣（ORCID：0000-0002-5518-1617），男，博士，教授，从事病原生物感染与免疫研究。E-mail：xuerong2@mail.sysu.edu.cn
作者简介:吴银娟（ORCID：0000-0002-2404-2358），女，博士，主要从事病原生物学研究。E-mail：wuyinjuan@mail.sysu.edu.cn
基金资助:
国家重点研发计划(2021YFC2300800);国家重点研发计划(2021YFC2300801);广东省自然科学基金(2022A1515012560);广东省自然科学基金(2023A1515010955);广东省自然科学基金(2025A1515012017)

Effect and mechanism of Csi-miR-125a induced liver fibrosis in the exosomes of Clonorchis sinensis

WU Yinjuan¹^,²()(), YI Xueqing¹, LI Meiyu¹^,², XU Anyuan¹, WU Aoxun¹, ZHONG Zifeng¹, LI Xuerong¹^,^*()()

1 Department of Parasitology, Zhongshan School of Medicine, Sun Yat-sen University; Key Laboratory for Tropical Diseases Control, Ministry of Education, Sun Yat-sen University; Provincial Engineering Technology Research Center for Biological Vector Control, Guangzhou 510080, Guangdong, China
2 Basic Medical Experimental Teaching Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, Guangdong, China

Received:2024-08-18 Revised:2024-11-28 Online:2025-04-30 Published:2025-04-27
Contact: * E-mail：xuerong2@mail.sysu.edu.cn
Supported by:
National Key Research and Development Program of China(2021YFC2300800);National Key Research and Development Program of China(2021YFC2300801);Guangdong Natural Science Foundation(2022A1515012560);Guangdong Natural Science Foundation(2023A1515010955);Guangdong Natural Science Foundation(2025A1515012017)

摘要/Abstract

摘要：

目的探究华支睾吸虫外泌体中关键miRNA分子在肝纤维化中的作用，以期为华支睾吸虫致肝纤维化的机制提供新的线索。方法从阳性家猫肝脏剖取华支睾吸虫成虫，体外培养，从排泄/分泌产物中提取外泌体，透射电子显微镜观察并对粒径分布进行鉴定。提取外泌体总RNA并测序，miRDeep2软件预测miRNA，与miRBase数据库中序列进行比对，测算比较每个miRNA的表达量并筛选。使用miRanda、miRDB、PITA软件分别对选定miRNA进行靶基因预测分析，topGO、clusterProfiler软件分别对靶基因的基因本体和信号通路进行富集分析。分别用浓度为5、10、20 μg/ml外泌体与肝星状细胞（HSC）共培养24、48 h，设置空白对照组；终浓度为50 nmol/L的选定miRNA（Csi-miR-125a）转染HSC 48 h，设置阴性对照组，均采用细胞计数试剂盒（CCK-8）检测各组HSC增殖情况。使用小鼠抗人β-actin、兔抗人α-平滑肌肌动蛋白（α-SMA）、兔抗人Ⅲ型胶原、兔抗人微管相关蛋白1A/1B-轻链3（LC3）、兔抗人p62、兔抗人细胞外信号调节激酶（ERK）、兔抗人p-ERK抗体（1∶1 000）作为一抗，辣根过氧化物酶（HRP）标记的山羊抗小鼠或抗兔IgG（1∶10 000）作为二抗，蛋白质免疫印迹（Western blotting）检测HSC的活化相关蛋白α-SMA、Ⅲ型胶原，自噬相关蛋白LC3、p62的表达水平及信号通路相关ERK蛋白磷酸化水平。结果华支睾吸虫外泌体呈小泡状，具有磷脂双分子层结构，粒径分布主峰值为72 nm，分布范围主要为30~150 nm。外泌体中含有多种miRNA，选择表达量次高且与已知miRNA序列相似度高的Csi-miR-125a进行后续研究。Csi-miR-125a存在301个靶基因预测位点重合，主要富集在细胞质、胞浆等细胞组件，参与蛋白结合、离子结合等分子功能，涉及生物调节、系统发育、神经系统发育等生物过程；靶基因信号通路大多富集于Hedgehog信号通路、细胞外基质-受体互作的相关通路、NOD样受体信号通路等。CCK-8法检测结果表明，外泌体浓度为10 μg/ml、孵育24 h时A₄₅₀达最高，为1.707；Csi-miR-125a共孵育组A₄₅₀为1.122，高于阴性对照组（0.492）。Western blotting检测结果显示，阴性对照组及Csi-miR-125a组的α-SMA条带灰度值分别为0.588和0.904（t = 10.560，P < 0.01）；Ⅲ型胶原条带灰度值分别为0.783和0.997（t = 6.483，P < 0.05）。阴性对照组和Csi-miR-125a组LC3Ⅱ/LC3Ⅰ条带灰度比值分别为1.093和2.215（t = 5.206，P < 0.05），p62条带灰度值分别为0.537和1.369（t = 13.100，P < 0.01），p-ERK/ERK条带灰度比值分别为0.791和1.037（t = 5.067，P < 0.05）。结论华支睾吸虫外泌体中miRNA种类丰富多样，且涉及多种细胞功能和多条信号通路。Csi-miR-125a可能通过阻断HSC自噬流和激活ERK信号通路促进HSC增殖活化从而在肝纤维化的发生中发挥一定的作用。

关键词: 华支睾吸虫, 肝纤维化, 外泌体, Csi-miR-125a, ERK信号通路

Abstract:

Objective To examine the role of hub miRNAs from Clonorchis sinensis exosomes in hepatic fibrosis, so as to provide new insights into deciphering the mechanisms underlying hepatic fibrosis induced by C. sinensis. Methods Adult worms of C. sinensis was collected from liver specimens of a domestic cat infected with C. sinensis, cultured in vitro, and excretory/secretory products were collected, centrifuged and filtered. Exosomes were extracted and observed under a transmission electron microscope, and their particle size distribution was analyzed. Total RNA was extracted from exosomes, and sequenced, and miRNA was predicted using the miRDeep2 software. The miRNA sequences were aligned with those in the miRBase database, and the expression of each miRNA was quantified and screened. The target genes of selected miRNAs were predicted using the miRanda, miRDB, and PITA software, and the Gene Ontology (GO) and signaling pathways of target genes were subjected to enrichment analyses using the topGO and clusterProfiler software. Hepatic stellate cells (HSCs) were incubated with exosomes at concentrations of 5, 10, and 20 μg/ml for 24 and 48 h, and a blank control group was assigned. HSCs were transfected with a selected miRNA (Csi-miR-125a) at a final concentration of 50 nmol/L for 48 h, and a negative control group was assigned. The proliferation of HSCs was measured using the cell counting kit-8 (CCK-8) assay, and the expression of HSC activation-related protein α-smooth muscle actin (α-SMA) and type Ⅲ collagen, autophagy-related proteins microtubule associated protein 1A/1B light chain 3 (LC3) and p62, and the phosphorylation of the signaling pathway-related extracellular signal regulated kinase (ERK) protein was determined using Western blotting with mouse anti-human β-actin, rabbit anti-human α-SMA, rabbit anti-human type Ⅲ collagen, rabbit an-human LC3, rabbit anti-human p62, rabbit anti-human ERK, and rabbit anti-human p-ERK primary antibodies (1∶1 000 dilution), and the secondary horseradish peroxidase (HRP) conjugated goat anti-mouse or anti-rabbit IgG antibody (1∶1 000 dilution). Results The C. sinensis exosomes appeared a small vesicular shape with a phospholipid bilayer structure, and the main peak particle size was 72 nm (range, 30 to 150 nm). The C. sinensis exosomes contained multiple miRNAs, and Csi-miR-125a, which had the second highest expression and a high similarity to known miRNA sequences, was selected for subsequent experiment. Csi-miR-125a had overlapping of 301 predicted sites of target genes, and these target genes were significantly enriched in cellular components such as cytoplasm, involved in molecular functions of protein binding and ion binding, and biological processes of biological regulation, systematic development, and nervous system development, and significantly enriched in Hedgehog signaling pathways, extracellular matrix- receptor interaction related pathways, and NOD like receptor signaling pathways. The CCK-8 assay measured the highest A₄₅₀ value (1.707) at an exosome concentration of 10 μg/ml for 24 h incubation, and the A₄₅₀ value was higher in the Csi-miR-125a co-culture group (1.122) than in the negative control group (0.492). Western blotting determined that the grayscale values of the α-SMA bands were 0.588 and 0.904 in the negative control group and the Csi-miR-125a group (t = 10.560, P < 0.01), and the grayscale values of type Ⅲ collagen bands were 0.783 and 0.997 in the negative control group and the Csi-miR-125a group (t = 6.483, P < 0.05).The grayscale ratios of LC3 Ⅱ/LC3 Ⅰ bands were 1.093 and 2.215 in the negative control group and the Csi-miR-125a group (t = 5.206, P < 0.05), and the grayscale values of p62 bands were 0.537 and 1.369 in the negative control group and the Csi-miR-125a group (t = 13.100, P < 0.01), while the grayscale ratios of pERK/ERK bands were 0.791 and 1.037 in the negative control group and the Csi-miR-125a group, respectively (t = 5.067, P < 0.05). Conclusion There are diverse miRNAs in C. sinensis exosomes, which are involved in multiple cellular functions and signaling pathways. Csi-miR-125a may contribute to hepatic fibrosis through blocking the autophagic flux of HSCs and activating the ERK signaling pathway to promote HSCs proliferation and activation.

Key words: Clonorchis sinensis, Hepatic fibrosis, Exosomes, Csi-miR-125a, ERK signaling pathway

中图分类号:

R383.22

吴银娟, 易雪晴, 李美玉, 徐安远, 武奥迅, 钟籽丰, 李学荣. 华支睾吸虫外泌体源Csi-miR-125a致肝纤维化作用及其机制[J]. 中国寄生虫学与寄生虫病杂志, 2025, 43(2): 198-204.

WU Yinjuan, YI Xueqing, LI Meiyu, XU Anyuan, WU Aoxun, ZHONG Zifeng, LI Xuerong. Effect and mechanism of Csi-miR-125a induced liver fibrosis in the exosomes of Clonorchis sinensis[J]. Chinese Journal of Parasitology and Parasitic Diseases, 2025, 43(2): 198-204.

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参考文献 42

[1]	诸欣平, 苏川. 人体寄生虫学[M]. 9版. 北京: 人民卫生出版社, 2018: 93-97.
	Zhu XP, Su C. Human parasitology[M]. 9th ed. Beijing: People’s Medical Publishing House, 2018: 93-97. (in Chinese)
[2]	陈颖丹, 周长海, 朱慧慧, 等. 2015年全国人体重点寄生虫病现状调查分析[J]. 中国寄生虫学与寄生虫病杂志, 2020, 38(1): 5-16. doi: 10.12140/j.issn.1000-7423.2020.01.002
	Chen YD, Zhou CH, Zhu HH, et al. National survey on the current status of important human parasitic diseases in China in 2015[J]. Chin J Parasitol Parasit Dis, 2020, 38(1): 5-16. (in Chinese)
[3]	Qian MB, Utzinger J, Keiser J, et al. Clonorchiasis[J]. Lancet, 2016, 387(10020): 800-810.
[4]	Tang ZL, Huang Y, Yu XB. Current status and perspectives of Clonorchis sinensis and clonorchiasis: Epidemiology, pathogenesis, omics, prevention and control[J]. Infect Dis Poverty, 2016, 5: 71.
[5]	Pellicoro A, Ramachandran P, Iredale JP, et al. Liver fibrosis and repair: Immune regulation of wound healing in a solid organ[J]. Nat Rev Immunol, 2014, 14(3): 181-194. doi: 10.1038/nri3623 pmid: 24566915
[6]	Tsuchida T, Friedman SL. Mechanisms of hepatic stellate cell activation[J]. Nat Rev Gastroenterol Hepatol, 2017, 14(7): 397-411. doi: 10.1038/nrgastro.2017.38 pmid: 28487545
[7]	邹学华, 陈良贵, 何丽洁, 等. 华枝睾吸虫病4 679例临床分析[J]. 中国热带医学, 2004, 4(2): 227-228.
	Zou XH, Chen LG, He LJ, et al. Clinical analysis of 4 679 clonorchiasis patients[J]. China Trop Med, 2004, 4(2): 227-228. (in Chinese)
[8]	王兆为, 余珂, 王武, 等. 162例肝吸虫病临床分析[J]. 中国热带医学, 2014, 14(11): 1384-1385, 1390.
	Wang ZW, Yu K, Wang W, et al. Clinical analysis of 162 clonorchiasis cases[J]. China Trop Med, 2014, 14(11): 1384-1385, 1390. (in Chinese)
[9]	Yan C, Wang L, Li B, et al. The expression dynamics of transforming growth factor-β/Smad signaling in the liver fibrosis experimentally caused by Clonorchis sinensis[J]. ParasitVectors, 2015, 8: 70.
[10]	Wang Y, Gong P, Zhang X, et al. TLR3 activation by Clonorchis sinensis infection alleviates the fluke-induced liver fibrosis[J]. PLoS Negl Trop Dis, 2023, 17(5): e0011325.
[11]	Kalluri R, McAndrews KM. The role of extracellular vesicles in cancer[J]. Cell, 2023, 186(8): 1610-1626. doi: 10.1016/j.cell.2023.03.010 pmid: 37059067
[12]	Kalluri R, LeBleu VS. The biology, function, and biomedical applications of exosomes[J]. Science, 2020, 367(6478): eaau6977.
[13]	Valadi H, Ekström K, Bossios A, et al. Exosome-mediated transfer of mRNAs and microRNAs is a novel mechanism of genetic exchange between cells[J]. Nat Cell Biol, 2007, 9(6): 654-659. doi: 10.1038/ncb1596 pmid: 17486113
[14]	Hu XJ, Ge QL, Zhang YT, et al. A review of the effect of exosomes from different cells on liver fibrosis[J]. Biomed Pharmacother, 2023, 161: 114415.
[15]	Chen L, Yao X, Yao H, et al. Exosomal miR-103-3p from LPS-activated THP-1 macrophage contributes to the activation of hepatic stellate cells[J]. FASEB J, 2020, 34(4): 5178-5192. doi: 10.1096/fj.201902307RRR pmid: 32061112
[16]	Chen L, Huang Y, Duan Z, et al. Exosomal miR-500 derived from lipopolysaccharide-treated macrophage accelerates liver fibrosis by suppressing MFN2[J]. Front Cell Dev Biol, 2021, 9: 716209.
[17]	Wang LF, Liao Y, Yang RB, et al. Sja-miR-71a in schistosome egg-derived extracellular vesicles suppresses liver fibrosis caused by schistosomiasis via targeting semaphorin 4D[J]. J Extracell Vesicles, 2020, 9(1): 1785738.
[18]	Wang Y, Gong W, Zhou H, et al. A novel miRNA from egg-derived exosomes of Schistosoma japonicum promotes liver fibrosis in murine schistosomiasis[J]. Front Immunol, 2022, 13: 860807.
[19]	梁翠莎, 陈剑煌, 徐鸣阳, 等. 家猫华支睾吸虫感染状况与肝胆管病变观察[J]. 热带医学杂志, 2021, 21(12): 1509-1511, 1538, 1641.
	Liang CS, Chen JH, Xu MY, et al. Clonorchis sinensis infection situation and hepatobiliary duct lesion observation in domestic cats[J]. J Trop Med, 2021, 21(12): 1509-1511, 1538, 1641. (in Chinese)
[20]	Coppola N, Potenza N, Pisaturo M, et al. Liver microRNA hsa-miR-125a-5p in HBV chronic infection: Correlation with HBV replication and disease progression[J]. PLoS One, 2013, 8(7): e65336.
[21]	Isaac R, Reis FCG, Ying W, et al. Exosomes as mediators of intercellular crosstalk in metabolism[J]. Cell Metab, 2021, 33(9): 1744-1762. doi: 10.1016/j.cmet.2021.08.006 pmid: 34496230
[22]	Chen L, Chen R, Kemper S, et al. Therapeutic effects of serum extracellular vesicles in liver fibrosis[J]. J Extracell Vesicles, 2018, 7(1): 1461505.
[23]	Potenza N, Russo A. Biogenesis, evolution and functional targets of microRNA-125a[J]. Mol Genet Genom, 2013, 288(9): 381-389.
[24]	林德照, 郑建建, 林镯, 等. 血浆miR-125a-5p在肝纤维化患者中的表达及意义[J]. 中国卫生检验杂志, 2014, 24(3): 380-382.
	Lin DZ, Zheng JJ, Lin Z, et al. miR-125a-5p expression and its clinical significance in liver fibrosis patients[J]. Chin J Health Lab Technol, 2014, 24(3): 380-382. (in Chinese)
[25]	Chang Y, Han JA, Kang SM, et al. Clinical impact of serum exosomal microRNA in liver fibrosis[J]. PLoS One, 2021, 16(9): e0255672.
[26]	Cao S, Wang D, Wu Y, et al. Mmu-miRNA-342-3p promotes hepatic stellate cell activation and hepatic fibrosis induced by Echinococcus multilocularis infection via targeting Zbtb7a[J]. PLoS Negl Trop Dis, 2023, 17(7): e0011520.
[27]	You K, Li SY, Gong J, et al. microRNA-125b promotes hepatic stellate cell activation and liver fibrosis by activating RhoA signaling[J]. Mol Ther Nucleic Acids, 2018, 12: 57-66.
[28]	Tao L, Yang GY, Sun TT, et al. Capsaicin receptor TRPV1 maintains quiescence of hepatic stellate cells in the liver via recruitment of SARM1[J]. J Hepatol, 2023, 78(4): 805-819.
[29]	Zhou BS, Zeng S, Li L, et al. Angiogenic factor with G patch and FHA domains 1 (Aggf1) regulates liver fibrosis by modulating TGF-β signaling[J]. Biochim Biophys Acta BBA Mol Basis Dis, 2016, 1862(6): 1203-1213.
[30]	Xuan J, Zhu DM, Cheng ZY, et al. Crocin inhibits the activation of mouse hepatic stellate cells via the lnc-LFAR1/MTF-1/GDNF pathway[J]. Cell Cycle, 2020, 19(24): 3480-3490. doi: 10.1080/15384101.2020.1848064 pmid: 33295246
[31]	Wang XH, Ai LY, Xu QQ, et al. A20 attenuates liver fibrosis in NAFLD and inhibits inflammation responses[J]. Inflammation, 2017, 40(3): 840-848. doi: 10.1007/s10753-017-0528-2 pmid: 28251449
[32]	O’Brien J, Hayder H, Zayed Y, et al. Overview of microRNA biogenesis, mechanisms of actions, and circulation[J]. Front Endocrinol (Lausanne), 2018, 9: 402.
[33]	Foglia B, Cannito S, Bocca C, et al. ERK pathway in activated, myofibroblast-like, hepatic stellate cells: A critical signaling crossroad sustaining liver fibrosis[J]. Int J Mol Sci, 2019, 20(11): E2700.
[34]	Ni MM, Wang YR, Wu WW, et al. Novel insights on notch signaling pathways in liver fibrosis[J]. Eur J Pharmacol, 2018, 826: 66-74.
[35]	Nishikawa K, Osawa Y, Kimura K. Wnt/β-catenin signaling as a potential target for the treatment of liver cirrhosis using antifibrotic drugs[J]. Int J Mol Sci, 2018, 19(10): E3103.
[36]	Chen Y, Zhao C, Liu X, et al. Plumbagin ameliorates liver fibrosis via a ROS-mediated NF-кB signaling pathway in vitro and in vivo[J]. Biomed Pharmacother, 2019, 116: 108923.
[37]	Loos B, Engelbrecht AM, Lockshin RA, et al. The variability of autophagy and cell death susceptibility[J]. Autophagy, 2013, 9(9): 1270-1285. doi: 10.4161/auto.25560 pmid: 23846383
[38]	Le TV, Phan-Thi HT, Huynh-Thi MX, et al. Autophagy inhibitor chloroquine downmodulates hepatic stellate cell activation and liver damage in bile-duct-ligated mice[J]. Cells, 2023, 12(7): 1025.
[39]	Lucantoni F, Martínez-Cerezuela A, Gruevska A, et al. Understanding the implication of autophagy in the activation of hepatic stellate cells in liver fibrosis: Are we there yet?[J]. J Pathol, 2021, 254(3): 216-228.
[40]	Kim KM, Han CY, Kim JY, et al. Gα12 overexpression induced by miR-16 dysregulation contributes to liver fibrosis by promoting autophagy in hepatic stellate cells[J]. J Hepatol, 2018, 68(3): 493-504.
[41]	Wang H, Liu Y, Wang D, et al. The upstream pathway of mTOR-mediated autophagy in liver diseases[J]. Cells, 2019, 8(12): E1597.
[42]	Seo HY, Lee SH, Han E, et al. Increased levels of phosphorylated ERK induce CTGF expression in autophagy-deficient mouse hepatocytes[J]. Cells, 2022, 11(17): 2704.

华支睾吸虫外泌体源Csi-miR-125a致肝纤维化作用及其机制

Effect and mechanism of Csi-miR-125a induced liver fibrosis in the exosomes of Clonorchis sinensis

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[7]	柴应植, 陈华良, 余可根, 张轩, 王笑笑, 张家祺, 徐文婕, 阮卫. 2013—2022年浙江省华支睾吸虫感染监测结果分析[J]. 中国寄生虫学与寄生虫病杂志, 2024, 42(4): 469-474.
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[9]	刘柳, 张静, 李健科, 张浩, 张凤玉. 华支睾吸虫体内神经递质5-羟色胺的分布[J]. 中国寄生虫学与寄生虫病杂志, 2024, 42(1): 78-82.
[10]	赵磊, 李佳, 莫刚, 李醇, 黄国洋, 彭小红. 华支睾吸虫感染对小鼠肝纤维化和免疫调节功能的影响[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(6): 760-765.
[11]	李晓芹, 赖雅诗, 陈豫, 吕嘉慧, 韦帅, 张立林, 何姗姗, 石云良, 李艳文. 华支睾吸虫囊蚴脱囊的超微结构观察[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(5): 601-608.
[12]	徐银, 刘婷, 徐慧, 曾小军, 兰炜明, 龚志红, 戴坤教, 邱婷婷, 郝先, 谢曙英. PCR-CRISPR/Cas12a华支睾吸虫囊蚴检测方法的建立和应用[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(4): 421-426.
[13]	蔡长煌, 张芝平, 卓鸣莺, 郭理平, 傅志辉, 刘亦若. 基于虫卵内转录间隔区2序列分析诊断麝猫后睾吸虫和华支睾吸虫感染[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(4): 427-433.
[14]	李天星, 张家明, 徐晨曦, 王子戈, 郭晶洁, 李姗. 基于网络药理学探讨复方鳖甲软肝片治疗华支睾吸虫感染所致肝纤维化的机制[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(4): 510-515.
[15]	王可艺, 舒黄芳, 方悦怡, 曾庆生, 宋铁. 2016—2020年广东省华支睾吸虫病高流行地区人群感染监测分析[J]. 中国寄生虫学与寄生虫病杂志, 2022, 40(5): 629-634.