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草酸钙处理TCMK-1细胞和巨噬细胞通过外泌体相互作用的关键分子和途径的鉴定

The identification of key molecules and pathways in the crosstalk of calcium oxalate-treated TCMK-1 cells and macrophage via exosomes

Nature 等信源发布 2024-09-09 06:20

可切换为仅中文


AbstractThe interplay between crystals and epithelial cells forms the cornerstone of kidney stone development, communication between epithelial cells and macrophages emerging as a pivotal role in this process. We conducted next-generation sequencing on the secreted exosomes of TCMK-1 cells treated with calcium oxalate monohydrate (OX_EXO) or controls (NC_EXO), and on the macrophage cell line RAW264.7 stimulated with OX_EXO or NC_EXO, followed by validation of differentially expressed target proteins and miRNAs through Western blot and PCR.

摘要晶体和上皮细胞之间的相互作用是肾结石发展的基石,上皮细胞和巨噬细胞之间的通讯在这一过程中起着关键作用。我们对用草酸钙一水合物(OX\U-EXO)或对照(NC\U-EXO)处理的TCMK-1细胞的分泌外泌体以及用OX\U-EXO或NC\U-EXO刺激的巨噬细胞系RAW264.7进行了下一代测序,然后通过蛋白质印迹和PCR验证差异表达的靶蛋白和miRNA。

UPSET plots were employed to identify genes co-targeted by exosomal miRNAs. Various bioinformatic analyses were employed to predict potential mechanisms of the dysregulated genes. We integrated sequencing data from the GEO database, and validated findings using clinical patient urine and kidney tissues.

扰乱图用于鉴定外泌体miRNA共靶向的基因。各种生物信息学分析被用来预测失调基因的潜在机制。我们整合了GEO数据库中的测序数据,并使用临床患者尿液和肾脏组织验证了发现。

We identified 665 differentially expressed exosomal miRNAs between OX_EXO and NC_EXO. Among the top 10 down-regulated miRNAs, the most targeted genes were AAK1 and NUFIP2, whereas PLCB1 was significantly targeted among the top 10 up-regulated miRNAs. In clinical specimens, we confirmed the differential expressions of five homologous miRNAs, as well as CNOT3, CNCNA1C, APEX1, and TMEM199.

我们在OX\U EXO和NC\U EXO之间鉴定了665个差异表达的外泌体miRNA。在前10个下调的miRNA中,最靶向的基因是AAK1和NUFIP2,而PLCB1在前10个上调的miRNA中显着靶向。在临床标本中,我们证实了五种同源miRNA以及CNOT3,CNCNA1C,APEX1和TMEM199的差异表达。

In conclusion, treatment of TCMK-1 cells with calcium oxalate significantly alerted the expression profile of exosomal miRNAs, subsequently influencing gene expression in macrophages, thereby modulating the processes of kidney stone formation..

总之,用草酸钙处理TCMK-1细胞可显着提醒外泌体miRNA的表达谱,从而影响巨噬细胞中的基因表达,从而调节肾结石的形成过程。。

IntroductionKidney stones are a common urinary system disorder that is increasingly in prevalence due to dietary, environmental, and lifestyle changes1,2. The development of percutaneous nephrolithotomy and ureteroscopy has significantly enhanced the efficiency and safety of stone treatment and removal3,4.

引言肾结石是一种常见的泌尿系统疾病,由于饮食,环境和生活方式的改变,其患病率越来越高1,2。经皮肾镜取石术和输尿管镜检查的发展显着提高了结石治疗和清除的效率和安全性3,4。

However, kidney stones have a high recurrence rate, with approximately 50% of patients experiencing a recurrent episode within five years5, emphasizing the importance of preventive measures and long-term patient management. Early diagnosis and lifestyle modifications are crucial to prevent calculi formation.Exosomes are extracellular vesicles approximately 30–150 nm in diameter and surrounded by a double lipid membrane.

然而,肾结石的复发率很高,大约50%的患者在五年内复发5,强调了预防措施和长期患者管理的重要性。。外泌体是直径约30-150 nm的细胞外囊泡,被双脂质膜包围。

Exosomes selectively package and deliver a range of bioactive materials such as proteins, RNA, and lipids to target cells6, influencing the behavior and function of the recipient cells. Exosomes are important mediators of intercellular communications and play a key role in a variety of biological processes, such as immune responses and disease progression7.

外泌体选择性地包装并将一系列生物活性物质如蛋白质,RNA和脂质递送至靶细胞6,影响受体细胞的行为和功能。外泌体是细胞间通讯的重要介质,在多种生物过程中发挥关键作用,如免疫反应和疾病进展7。

The production and secretion of exosomes represent important mechanisms of intercellular communication8.Among the types of kidney stones, the primary component of stone is calcium oxalate monohydrate (COM). Stone formation is a complex process, that involves several mechanisms, including crystal supersaturation, crystal-cell adhesion, crystal deposition, growth, and crystal-cell interactions, that contribute to the retention of crystals in the kidney damage9,10.

外泌体的产生和分泌代表了细胞间通讯的重要机制8。在肾结石的类型中,结石的主要成分是草酸钙一水合物(COM)。结石形成是一个复杂的过程,涉及多种机制,包括晶体过饱和,晶体细胞粘附,晶体沉积,生长和晶体细胞相互作用,这些机制有助于晶体在肾脏损伤中的保留9,10。

These crystals subsequently induce cytotoxicity and dysfunction in renal tubular epithelial cells (TECs), which in turn increases crystal formation and adhesion11. MicroRNAs (miRNAs) are short, non-coding RNAs comprised of 20–25 nucleotides .

这些晶体随后在肾小管上皮细胞(TECs)中诱导细胞毒性和功能障碍,进而增加晶体形成和粘附11。微小RNA(miRNA)是由20-25个核苷酸组成的短的非编码RNA。

Data availability

数据可用性

Data is provided within the manuscript or supplementary information files. The datasets used and analyzed in this study are available from the corresponding author on reasonable request.

数据在手稿或补充信息文件中提供。本研究中使用和分析的数据集可根据合理要求从通讯作者处获得。

ReferencesThongprayoon, C., Krambeck, A. E. & Rule, A. D. Determining the true burden of kidney stone disease. Nat. Rev. Nephrol. 16, 736–746 (2020).Article

参考文献Thongprayoon,C.,Krambeck,A.E。和Rule,A.D。确定肾结石疾病的真实负担。自然修订版Nephrol。16736-746(2020)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Peerapen, P. & Thongboonkerd, V. Kidney stone prevention. Adv. Nutr. 14, 555–569 (2023).Article

Peerapen,P。&Thongboonkerd,V。肾结石预防。高级营养师。14555-569(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Ganpule, A. P., Vijayakumar, M., Malpani, A. & Desai, M. R. Percutaneous nephrolithotomy (PCNL) a critical review. Int. J. Surg. 36, 660–664 (2016).Article

Ganpule,A.P.,Vijayakumar,M.,Malpani,A。&Desai,M.R。经皮肾镜取石术(PCNL)一篇批判性评论。《国际外科杂志》36660-664(2016)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Proietti, S., Knoll, T. & Giusti, G. Contemporary ureteroscopic management of renal stones. Int. J. Surg. 36, 681–687 (2016).Article

Proietti,S.,Knoll,T。&Giusti,G。当代输尿管镜治疗肾结石。《国际外科杂志》36681-687(2016)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Wigner, P., Bijak, M. & Saluk-Bijak, J. Probiotics in the prevention of the calcium oxalate urolithiasis. Cells 11, 284 (2022).Article

Wigner,P.,Bijak,M。&Saluk-Bijak,J。益生菌预防草酸钙尿石症。。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zhang, Y., Liu, Y., Liu, H. & Tang, W. H. Exosomes: Biogenesis, biologic function and clinical potential. Cell Biosci. 9, 19 (2019).Article

Zhang,Y.,Liu,Y.,Liu,H。&Tang,W.H。外泌体:生物发生,生物学功能和临床潜力。细胞生物科学。9,19(2019)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Gurunathan, S., Kang, M.-H. & Kim, J.-H. A comprehensive review on factors influences biogenesis, functions, therapeutic and clinical implications of exosomes. Int. J. Nanomed. 16, 1281–1312 (2021).Article

Gurunathan,S.,Kang,M.-H。&Kim,J.-H。关于影响外泌体的生物发生,功能,治疗和临床意义的因素的全面综述。内景J.Nanomed。161281-1312(2021)。文章

Google Scholar

谷歌学者

Al-Madhagi, H. The landscape of exosomes biogenesis to clinical applications. Int. J. Nanomed. 19, 3657–3675 (2024).Article

Al-Madhagi,H。外泌体生物发生在临床应用中的前景。内景J.Nanomed。193657–3675(2024)。文章

Google Scholar

谷歌学者

Evan, A. P., Worcester, E. M., Coe, F. L., Williams, J. & Lingeman, J. E. Mechanisms of human kidney stone formation. Urolithiasis 43(Suppl 1), 19–32 (2015).Article

Evan,A.P.,Worcester,E.M.,Coe,F.L.,Williams,J。&Lingeman,J.E。人类肾结石形成的机制。尿石症43(补充1),19-32(2015)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Chung, H.-J. The role of Randall plaques on kidney stone formation. Transl. Androl. Urol. 3, 251–254 (2014).PubMed

Chung,H.-J。Randall斑块在肾结石形成中的作用。翻译。安德洛尔。乌洛尔。。PubMed出版社

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Thongboonkerd, V. Proteomics of crystal-cell interactions: A model for kidney stone research. Cells 8, 1076 (2019).Article

Thongboonkerd,V。晶体细胞相互作用的蛋白质组学:肾结石研究的模型。细胞81076(2019)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Quinn, J. J. & Chang, H. Y. Unique features of long non-coding RNA biogenesis and function. Nat. Rev. Genet. 17, 47–62 (2016).Article

Quinn,J。J。和Chang,H。Y。长非编码RNA生物发生和功能的独特特征。Genet自然Rev。17,47-62(2016)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Taguchi, K. et al. M1/M2-macrophage phenotypes regulate renal calcium oxalate crystal development. Sci. Rep. 6, 35167 (2016).Article

Taguchi,K。等人。M1/M2巨噬细胞表型调节肾草酸钙晶体的发育。科学。代表635167(2016)。文章

ADS

广告

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jia, Y. et al. Extracellular vesicles from albumin-induced tubular epithelial cells promote the M1 macrophage phenotype by targeting klotho. Mol. Ther. 27, 1452–1466 (2019).Article

Jia,Y。等人。来自白蛋白诱导的肾小管上皮细胞的细胞外囊泡通过靶向klotho促进M1巨噬细胞表型。摩尔热。271452-1466(2019)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Lv, L.-L. et al. Exosomal miRNA-19b-3p of tubular epithelial cells promotes M1 macrophage activation in kidney injury. Cell Death Differ. 27, 210–226 (2020).Article

Lv,L.-L.等人。肾小管上皮细胞的外泌体miRNA-19b-3p在肾损伤中促进M1巨噬细胞活化。细胞死亡不同。27210-226(2020)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Kanehisa, M. & Goto, S. KEGG: Kyoto encyclopedia of genes and genomes. Nucleic Acids Res. 28, 27–30 (2000).Article

Kanehisa,M。&Goto,S。KEGG:京都基因与基因组百科全书。核酸研究28,27-30(2000)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Kanehisa, M. Toward understanding the origin and evolution of cellular organisms. Protein Sci. 28, 1947–1951 (2019).Article

Kanehisa,M。了解细胞生物的起源和进化。蛋白质科学。281947-1951(2019)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Kanehisa, M., Furumichi, M., Sato, Y., Kawashima, M. & Ishiguro-Watanabe, M. KEGG for taxonomy-based analysis of pathways and genomes. Nucleic Acids Res. 51, D587–D592 (2023).Article

Kanehisa,M.,Furumichi,M.,Sato,Y.,Kawashima,M。&Ishiguro Watanabe,M。KEGG用于基于分类学的途径和基因组分析。。文章

PubMed

PubMed

Google Scholar

谷歌学者

Alexander, R. T., Fuster, D. G. & Dimke, H. Mechanisms underlying calcium nephrolithiasis. Annu. Rev. Physiol. 84, 559–583 (2022).Article

Alexander,R.T.,Fuster,D.G。&Dimke,H。钙肾结石的潜在机制。年。生理学评论。84559-583(2022)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Arya, S. B., Collie, S. P. & Parent, C. A. The ins-and-outs of exosome biogenesis, secretion, and internalization. Trends Cell Biol. 34, 90–108 (2024).Article

Arya,S.B.,Collie,S.P。和Parent,C.A。外来体生物发生,分泌和内化的来龙去脉。趋势细胞生物学。34,90-108(2024)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Su, X. et al. Ambra1 in exosomes secreted by HK-2 cells damaged by supersaturated oxalate induce mitophagy and autophagy-ferroptosis in normal HK-2 cells to participate in the occurrence of kidney stones. Biochim. Biophys. Acta 1871, 119604 (2024).Article

。生物化学。生物物理。Acta 187119604(2024)。文章

Google Scholar

谷歌学者

He, J. et al. Renal macrophages monitor and remove particles from urine to prevent tubule obstruction. Immunity 57, 106–123 (2024).Article

He,J。等人。肾巨噬细胞监测并去除尿液中的颗粒,以防止肾小管阻塞。免疫力57106-123(2024)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Taguchi, K., Okada, A., Unno, R., Hamamoto, S. & Yasui, T. Macrophage function in calcium oxalate kidney stone formation: A systematic review of literature. Front. Immunol. 12, 673690 (2021).Article

Taguchi,K.,Okada,A.,Unno,R.,Hamamoto,S。&Yasui,T。巨噬细胞在草酸钙肾结石形成中的功能:文献的系统综述。正面。免疫。12673690(2021年)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Liu, J.-L. et al. Epsin1-mediated exosomal sorting of Dll4 modulates the tubular-macrophage crosstalk in diabetic nephropathy. Mol. Ther. 31, 1451–1467 (2023).Article

Liu,J.-L.等人。Epsin1介导的Dll4外泌体分选调节糖尿病肾病中的肾小管巨噬细胞串扰。摩尔热。311451-1467(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Singhto, N., Kanlaya, R., Nilnumkhum, A. & Thongboonkerd, V. Roles of macrophage exosomes in immune response to calcium oxalate monohydrate crystals. Front. Immunol. 9, 316 (2018).Article

Singhto,N.,Kanlaya,R.,Nilnumkhum,A。&Thongboonkerd,V。巨噬细胞外泌体在对草酸钙一水合物晶体的免疫应答中的作用。正面。免疫。9316(2018)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Shyong, Y.-J., Chang, K.-C. & Lin, F.-H. Calcium phosphate particles stimulate exosome secretion from phagocytes for the enhancement of drug delivery. Colloids Surf. B 171, 391–397 (2018).Article

Shyong,Y.-J.,Chang,K.-C.&Lin,F.-H。磷酸钙颗粒刺激吞噬细胞的外泌体分泌以增强药物递送。胶体冲浪B 171391-397(2018)。文章

Google Scholar

谷歌学者

Krützfeldt, J. Strategies to use microRNAs as therapeutic targets. Best Pract. Res. Clin. Endocrinol. Metab. 30, 551–561 (2016).Article

Krützfeldt,J。使用microRNA作为治疗靶标的策略。最佳实践。临床研究。内分泌。代谢。30551-561(2016)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Djuranovic, S., Nahvi, A. & Green, R. miRNA-mediated gene silencing by translational repression followed by mRNA deadenylation and decay. Science 336, 237–240 (2012).Article

Djuranovic,S.,Nahvi,A。&Green,R。miRNA通过翻译抑制介导的基因沉默,然后是mRNA去腺苷酸化和衰变。科学336237-240(2012)。文章

ADS

广告

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Cohen, C. et al. WNT-dependent interaction between inflammatory fibroblasts and FOLR2+ macrophages promotes fibrosis in chronic kidney disease. Nat. Commun. 15, 743 (2024).Article

。国家公社。15743(2024)。文章

ADS

广告

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

He, D. et al. The Wnt11 signaling pathway in potential cellular EMT and osteochondral differentiation progression in nephrolithiasis formation. Int. J. Mol. Sci. 16, 16313–16329 (2015).Article

He,D。等人。肾结石形成中潜在细胞EMT和骨软骨分化进程中的Wnt11信号通路。Int.J.Mol.Sci。1616313–16329(2015)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Unno, R. et al. Deregulated MTOR (mechanistic target of rapamycin kinase) is responsible for autophagy defects exacerbating kidney stone development. Autophagy 16, 709–723 (2020).Article

Unno,R。等人。失调的MTOR(雷帕霉素激酶的机制靶标)是导致自噬缺陷加剧肾结石发展的原因。自噬16709-723(2020)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Yuan, H. et al. The protective role of corilagin on renal calcium oxalate crystal-induced oxidative stress, inflammatory response, and apoptosis via PPAR-γ and PI3K/Akt pathway in rats. Biotechnol. Appl. Biochem. 68, 1323–1331 (2021).PubMed

袁,H。等。科里拉金通过PPAR-γ和PI3K/Akt途径对大鼠肾草酸钙晶体诱导的氧化应激,炎症反应和细胞凋亡的保护作用。生物技术。。生物化学。681323-1331(2021)。PubMed出版社

Google Scholar

谷歌学者

Rao, P. et al. Promotion of β-catenin/forkhead box protein O signaling mediates epithelial repair in kidney injury. Am. J. Pathol. 191, 993–1009 (2021).Article

。美国J.Pathol。191993-1009(2021)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Huang, L. et al. Loss of nephric augmenter of liver regeneration facilitates acute kidney injury via ACSL4-mediated ferroptosis. J. Cell Mol. Med. 28, e18076 (2024).Article

Huang,L。等人。肝再生肾增强因子的丧失通过ACSL4介导的铁浓化促进急性肾损伤。J、 细胞分子医学28,e18076(2024)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Li, Y. et al. LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family. Mol. Med. 27, 143 (2021).Article

Li,Y。等人。LncRNA-ATB通过海绵状miR-200家族参与草酸钙晶体诱导的肾损伤的调节。分子医学27143(2021)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Li, R. et al. Novel drug delivery systems and disease models for pulmonary fibrosis. J. Control Release 348, 95–114 (2022).Article

Li,R。等人。新型药物输送系统和肺纤维化疾病模型。J、 控制版本348,95-114(2022)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Tampe, D. & Zeisberg, M. Potential approaches to reverse or repair renal fibrosis. Nat. Rev. Nephrol. 10, 226–237 (2014).Article

Tampe,D。&Zeisberg,M。逆转或修复肾纤维化的潜在方法。自然修订版Nephrol。10226-237(2014)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Guo, M. et al. Syndecan-1 shedding destroys epithelial adherens junctions through STAT3 after renal ischemia/reperfusion injury. iScience 26, 108211 (2023).Article

Guo,M。等人。Syndecan-1脱落在肾缺血/再灌注损伤后通过STAT3破坏上皮粘附连接。iScience 26108211(2023)。文章

ADS

广告

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Xun, Y. et al. Role of Nox4 in high calcium-induced renal oxidative stress damage and crystal deposition. Antioxid. Redox Signal. 36, 15–38 (2022).Article

Xun,Y.等人。Nox4在高钙诱导的肾脏氧化应激损伤和晶体沉积中的作用。抗氧化剂。氧化还原信号。36,15-38(2022)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Song, B.-F. et al. Overexpression of sirtuin 1 attenuates calcium oxalate-induced kidney injury by promoting macrophage polarization. Int. Immunopharmacol. 121, 110398 (2023).Article

Song,B.-F.等人。sirtuin 1的过表达通过促进巨噬细胞极化来减轻草酸钙诱导的肾损伤。国际免疫药理学。121110398(2023)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Lian, J. et al. Extracellular vesicle-transmitted miR-671-5p alleviates lung inflammation and injury by regulating the AAK1/NF-κB axis. Mol. Ther. 31, 1365–1382 (2023).Article

Lian,J。等人。细胞外囊泡传递的miR-671-5p通过调节AAK1/NF-κB轴减轻肺部炎症和损伤。摩尔热。311365-1382(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Song, Q. et al. FKBP5 deficiency attenuates calcium oxalate kidney stone formation by suppressing cell-crystal adhesion, apoptosis and macrophage M1 polarization via inhibition of NF-κB signaling. Cell Mol. Life Sci. 80, 301 (2023).Article

Song,Q。等人。FKBP5缺乏症通过抑制NF-κB信号传导抑制细胞晶体粘附,细胞凋亡和巨噬细胞M1极化,从而减弱草酸钙肾结石的形成。细胞分子生命科学。80301(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jia, J. et al. Membrane Atg8ylation, stress granule formation, and MTOR regulation during lysosomal damage. Autophagy 19, 1893–1895 (2023).Article

Jia,J。等人。溶酶体损伤过程中的膜ATG8化,应激颗粒形成和MTOR调节。。文章

PubMed

PubMed

Google Scholar

谷歌学者

Song, T.-J. et al. Effect of SNHG11/miR-7–5p/PLCB1 axis on acute pancreatitis through inhibiting p38MAPK pathway. Cells 12, 65 (2022).Article

Song,T.-J.等人。SNHG11/miR-7-5p/PLCB1轴通过抑制p38MAPK途径对急性胰腺炎的影响。细胞12,65(2022)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Peckert-Maier, K. et al. CD83 expressed by macrophages is an important immune checkpoint molecule for the resolution of inflammation. Front. Immunol. 14, 1085742 (2023).Article

巨噬细胞表达的CD83是解决炎症的重要免疫检查点分子。正面。免疫。141085742(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Liu, W. et al. Exosomal microRNA-342-5p secreted from adipose-derived mesenchymal stem cells mitigates acute kidney injury in sepsis mice by inhibiting TLR9. Biol. Proced. Online 25, 10 (2023).Article

Liu,W。等人。脂肪间充质干细胞分泌的外泌体microRNA-342-5p通过抑制TLR9减轻脓毒症小鼠的急性肾损伤。生物学过程。在线25,10(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Liu, B. et al. The RNase MCPIP3 promotes skin inflammation by orchestrating myeloid cytokine response. Nat. Commun. 12, 4105 (2021).Article

Liu,B。等人。RNase MCPIP3通过协调髓样细胞因子反应来促进皮肤炎症。国家公社。。文章

ADS

广告

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zhu, M., Jin, T., Wu, D., Zhang, S. & Wang, A. Transcriptomics analysis revealed key genes associated with macrophage autophagolysosome in male ApoE-/- mice aortic atherosclerosis. J. Inflamm. Res. 16, 5125–5144 (2023).Article

。J、 发炎。第165125-5144号决议(2023年)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Verstraelen, P. et al. Serum amyloid A3 fuels a feed-forward inflammatory response to the bacterial amyloid curli in the enteric nervous system. Cell Mol. Gastroenterol. Hepatol. 18, 89–104 (2024).Article

Verstraelen,P。等人。血清淀粉样蛋白A3促进肠道神经系统中细菌淀粉样蛋白卷曲的前馈炎症反应。细胞分子胃肠道。肝病。18,89-104(2024)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zhang, M. et al. IL-27 disturbs lipid metabolism and restrains mitochondrial activity to inhibit γδ T17 cell-mediated skin inflammation. Cell Death Dis. 15, 491 (2024).Article

IL-27干扰脂质代谢并抑制线粒体活性以抑制γδT17细胞介导的皮肤炎症。细胞死亡Dis。15491(2024)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Maruyama, K. et al. The antioxidant and DNA-repair enzyme apurinic/apyrimidinic endonuclease 1 limits the development of tubulointerstitial fibrosis partly by modulating the immune system. Sci. Rep. 9, 7823 (2019).Article

Maruyama,K。等人。抗氧化剂和DNA修复酶嘌呤/嘧啶核酸内切酶1部分通过调节免疫系统来限制肾小管间质纤维化的发展。科学。代表97823(2019)。文章

ADS

广告

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jansen, J. C. et al. TMEM199 deficiency is a disorder of golgi homeostasis characterized by elevated aminotransferases, alkaline phosphatase, and cholesterol and abnormal glycosylation. Am. J. Hum. Genet. 98, 322–330 (2016).Article

Jansen,J.C.等人,TMEM199缺乏症是一种高尔基体内平衡障碍,其特征是氨基转移酶,碱性磷酸酶和胆固醇升高以及糖基化异常。上午J。嗯。Genet。98322-330(2016)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Larsen, L. E. et al. Defective lipid droplet-lysosome interaction causes fatty liver disease as evidenced by human mutations in TMEM199 and CCDC115. Cell Mol. Gastroenterol. Hepatol. 13, 583–597 (2022).Article

Larsen,L.E.等人。有缺陷的脂滴-溶酶体相互作用会导致脂肪肝,TMEM199和CCDC115中的人类突变证明了这一点。细胞分子胃肠道。肝病。13583-597(2022)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Dusabimana, T. et al. GOLPH3 promotes endotoxemia-induced liver and kidney injury through Golgi stress-mediated apoptosis and inflammatory response. Cell Death Dis. 14, 458 (2023).Article

Dusabimana,T。等人。GOLPH3通过高尔基体应激介导的细胞凋亡和炎症反应促进内毒素血症诱导的肝脏和肾脏损伤。细胞死亡Dis。14458(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Johnson, D. L., Kumar, R., Kakhniashvili, D., Pfeffer, L. M. & Laribee, R. N. Ccr4-Not ubiquitin ligase signaling regulates ribosomal protein homeostasis and inhibits 40S ribosomal autophagy. J. Biol. Chem. 60, 107582 (2024).Article

Johnson,D.L.,Kumar,R.,Kakhniashvili,D.,Pfeffer,L.M。&Laribee,R.N。Ccr4 Not泛素连接酶信号调节核糖体蛋白质稳态并抑制40S核糖体自噬。J、 生物。。60107582(2024)。文章

Google Scholar

谷歌学者

Kessi, M. et al. Disruption of mitochondrial and lysosomal functions by human CACNA1C variants expressed in HEK 293 and CHO cells. Front. Mol. Neurosci. 16, 1209760 (2023).Article

Kessi,M.等人。HEK 293和CHO细胞中表达的人CACNA1C变体对线粒体和溶酶体功能的破坏。正面。分子神经科学。161209760(2023)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zhao, S. et al. Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys. Theranostics 11, 8660–8673 (2021).Article

Zhao,S。等人。来自肾小管细胞的外泌体miR-21通过靶向阻塞肾脏中的PTEN激活成纤维细胞,从而促进肾纤维化。Theranostics 118660-8673(2021)。文章

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zhu, S. et al. Urine-derived exosomes and their role in modulating uroepithelial cells to prevent hypospadias. Int. Immunopharmacol. 132, 111828 (2024).Article

Zhu,S.等人。尿源性外泌体及其在调节尿路上皮细胞以预防尿道下裂中的作用。国际免疫药理学。132111828(2024)。文章

PubMed

PubMed

Google Scholar

谷歌学者

Download referencesAcknowledgementsWe thank Bullet Edits Limited for the linguistic editing and proofreading of the manuscript.FundingThis work was supported by National Natural Science Foundation of China (82170775, and 82100806).Author informationAuthor notesThese authors contributed equally: Yushi Sun, Bojun Li and Xiangjun Zhou.Authors and AffiliationsDepartment of Urology, Renmin Hospital of Wuhan University, No.238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei, People’s Republic of ChinaYushi Sun, Bojun Li, Xiangjun Zhou, Ting Rao & Fan ChengAuthorsYushi SunView author publicationsYou can also search for this author in.

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PubMed Google ScholarBojun LiView author publicationsYou can also search for this author in

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PubMed Google ScholarContributionsConceptualization, Yushi Sun and Bojun Li; Formal analysis, Yushi Sun and Bojun Li; Funding acquisition, Fan Cheng; Methodology, Bojun Li; Supervision, Rao Ting and Fan Cheng; Validation, Yushi Sun, Bojun Li and Xiangjun Zhou; Visualization, Yushi Sun; Writing—original draft, Yushi Sun, Bojun Li and Fan Cheng; Writing—review & editing, Yushi Sun, Bojun Li, Xiangjun Zhou and Fan Cheng.Corresponding authorsCorrespondence to.

PubMed谷歌学术贡献概念化,孙玉石和李伯军;;资金收购,范成;方法论,李伯军;监督,饶婷和范成;验证,孙玉石,李伯军和周向军;可视化,孙玉石;撰写原稿,孙玉石,李伯军和范成;写作评论与编辑,孙玉石,李伯军,周向军,范成。通讯作者通讯。

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Competing interests

相互竞争的利益

The authors declare no competing interests.

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Ethical approval

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The clinical specimen collection (approval number: WDRY2021-KS047) was approved by the Ethics Committee of the Renmin Hospital of Wuhan University. Confirms that all experiments were performed in accordance with relevant named guidelines and regulations. Confirms that informed consent was obtained from all participants and/or their legal guardians..

临床标本采集(批准号:WDRY2021-KS047)经武汉大学人民医院伦理委员会批准。确认所有实验均按照相关命名指南和法规进行。确认已获得所有参与者和/或其法定监护人的知情同意。。

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Reprints and permissionsAbout this articleCite this articleSun, Y., Li, B., Zhou, X. et al. The identification of key molecules and pathways in the crosstalk of calcium oxalate-treated TCMK-1 cells and macrophage via exosomes.

转载和许可本文引用本文Sun,Y.,Li,B.,Zhou,X。等人通过外泌体鉴定草酸钙处理的TCMK-1细胞和巨噬细胞串扰中的关键分子和途径。

Sci Rep 14, 20949 (2024). https://doi.org/10.1038/s41598-024-71755-yDownload citationReceived: 17 May 2024Accepted: 30 August 2024Published: 09 September 2024DOI: https://doi.org/10.1038/s41598-024-71755-yShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

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KeywordsExosomesMiRNAMacrophageBiomarkers in kidney stonesTranscriptomics of kidney stones

关键词肾结石中的sosomesmiRNamacrophagebiomarkers肾结石的描述组学

Subjects

主题

BiomarkersImmunologyMolecular medicineNephrologySequencingUrology

生物标志物免疫分子医学肾脏测序生物学

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