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Updated: Mar 31, 2026
Quantitative Real-Time PCR Evaluation of microRNA Expressions in Mouse Kidney with Unilateral Ureteral Obstruction
Published on: August 27, 2020
Comprehensive lnc-RNAs expression profiles in uremic cardiomyopathy before and after renal transplantation
Xiaoxia Song1, Sijia Zhao1, Pin Sun1
1Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Insights
This study identified key long non-coding RNAs (lncRNAs) in blood exosomes of patients with uremic cardiomyopathy (UCM) before and after kidney transplantation. Lnc-LINC02194 shows potential as a therapeutic target for UCM.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Genomics
Background:
- Chronic kidney disease (CKD) elevates cardiovascular risks, leading to uremic cardiomyopathy (UCM) characterized by myocardial structural and functional changes.
- Renal transplantation can reverse UCM, but the underlying molecular mechanisms, particularly involving exosome-mediated communication, are not fully understood.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their regulatory roles in cardiac disease pathogenesis.
Purpose of the Study:
- To investigate the expression profiles of exosome-derived lncRNAs in UCM patients pre- and post-kidney transplantation.
- To identify specific lncRNAs involved in UCM pathogenesis and explore their regulatory networks.
- To discover potential therapeutic targets for UCM based on lncRNA expression patterns.
Main Methods:
- High-throughput RNA sequencing was employed to identify differentially expressed lncRNAs in UCM patients.
- Bioinformatic analyses, including lncRNA-mRNA interaction networks and pathway enrichment (GO, KEGG), were performed.
- Quantitative reverse transcription PCR (RT-qPCR) was used for validation of key lncRNA candidates.
Main Results:
- Gene sequencing identified 769 dysregulated lncRNAs (440 downregulated, 329 upregulated) in UCM patients.
- Computational analysis suggested involvement of p53 and FoxO signaling pathways in UCM.
- Three potential UCM-associated lncRNAs were identified, with RT-qPCR confirming differential expression of lnc-LINC02194, lnc-MYOSLID-AS1, and lnc-LINC01229.
Conclusions:
- lncRNA expression in blood exosomes significantly correlates with UCM progression, both before and after renal transplantation.
- lnc-LINC02194 emerges as a potential therapeutic target for uremic cardiomyopathy.
- Exosomal lncRNAs represent promising biomarkers and therapeutic targets for managing UCM.
Background:
Chronic kidney disease (CKD) significantly contributes to increased cardiovascular morbidity and mortality. CKD-induced cardiac remodeling, clinically termed uremic cardiomyopathy (UCM), manifests as morphological and physiological alterations in the myocardium. While renal transplantation is known to mitigate uremia's effects on myocardial remodeling, improve cardiac function, and reverse damage, its underlying biological mechanism remains unclear. Exosomes mediate inter-organ communication, with their nucleic acid components serving as key regulatory molecules. Emerging evidence indicates long non-coding RNAs (lncRNAs) critically participate in cardiac disease mechanisms.
Objective:
This study aimed to analyze the expression profile of blood exosome-derived lncRNAs in UCM patients before and after transplantation to explore lncRNA expression patterns, regulatory mechanisms, and identify key lncRNAs involved in UCM pathogenesis.
Patients And Methods:
Our study utilized high-throughput RNA sequencing to identify differentially expressed long non-coding RNAs (lncRNAs) in patients with uremic cardiomyopathy (UCM) before and after kidney transplantation. We analyzed the differential expression of lncRNAs from multiple perspectives, including expression profiles, lncRNA-mRNA interaction networks, and enriched GO and KEGG pathways, followed by validation through RT-qPCR.
Results:
Gene sequencing revealed 769 dysregulated lncRNAs [440 downregulated, 329 upregulated; log2(fold change) > 2.0, p < 0.05]. Computational biological analysis implicated p53 and FoxO signaling pathways in UCM pathogenesis. Differential lncRNA-mRNA interaction networks identified three potential UCM-associated genes: lnc-LOC105379080, lnc-LOC101927608, and lnc-LOC105369947. RT-qPCR validation confirmed significant upregulation of lnc-LINC02194 (p = 0.0003), and lnc-MYOSLID-AS1 (p = 0.0030), and significant downregulation of lnc-LINC01229 (p = 0.0052).
Conclusion:
LncRNAs show significant correlation with UCM progression before and after renal transplantation. Lnc-LINC02194 may represent a candidate therapeutic target for UCM.
