Urinary Erythrocyte-Derived miRNAs: Emerging Role in IgA Nephropathy

Duan, Zhi-Yu; Cai, Guangyan; Li, Jijun; Bu, Rongfa; Chen, Xiangmei

doi:10.1159/000481970

Cited by 12 publications

(12 citation statements)

References 59 publications

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“…The more prevalent miRNA present in the urinary sediment of IgAN patients with hematuria were mainly derived from urinary erythrocytes, such as miR-25-3p, miR-144-3p, and miR-486-5p [54]. That implies that miRNA delivered by hematuria could act over renal parenchymal cells, changing their gene expression, and could be involved in the pathogenesis and evolution of kidney disease [55]. In other words, the presence of specific miRNA in the sediment could be a marker of the activity of hematuric disease, and may be a useful diagnostic tool.…”

Section: Hematuria and Renal Damage: Cause Or Consequence?mentioning

confidence: 99%

Glomerular Hematuria: Cause or Consequence of Renal Inflammation?

Moreno

Sevillano

Gutiérrez

et al. 2019

IJMS

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Glomerular hematuria is a cardinal symptom of renal disease. Glomerular hematuria may be classified as microhematuria or macrohematuria according to the number of red blood cells in urine. Recent evidence suggests a pathological role of persistent glomerular microhematuria in the progression of renal disease. Moreover, gross hematuria, or macrohematuria, promotes acute kidney injury (AKI), with subsequent impairment of renal function in a high proportion of patients. In this pathological context, hemoglobin, heme, or iron released from red blood cells in the urinary space may cause direct tubular cell injury, oxidative stress, pro-inflammatory cytokine production, and further monocyte/macrophage recruitment. The aim of this manuscript is to review the role of glomerular hematuria in kidney injury, the role of inflammation as cause and consequence of glomerular hematuria, and to discuss novel therapies to combat hematuria.

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Section: Hematuria and Renal Damage: Cause Or Consequence?mentioning

confidence: 99%

Glomerular Hematuria: Cause or Consequence of Renal Inflammation?

Moreno

Sevillano

Gutiérrez

et al. 2019

IJMS

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“…Therefore, more attention should be directed toward understanding RBC miRNAs. It has been reported that RBC miRNAs not only inhibit the reproduction of Plasmodium falciparum in patients with sickle cell anemia but are also associated with the development of bodily disorders (Lamonte et al, 2012 ; Duan et al, 2016 , 2017 ; Walzer and Chi, 2017 ; Wu et al, 2017 ). In this study, we hypothesized that high-altitude hypoxic environments likely impact RBC miRNA expression levels.…”

Section: Introductionmentioning

confidence: 99%

Different Erythrocyte MicroRNA Profiles in Low- and High-Altitude Individuals

Sun

Fan

et al. 2018

Front. Physiol.

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Background: The number of red blood cells (RBCs) increases significantly in response to high-altitude hypoxic environments, and the RBC microRNA (miRNA) expression pattern is similar to that in whole blood. Studies have shown that miRNA in plasma can act as a circulating hypoxia-associated marker, but the effect of a high-altitude hypoxic environment on RBC-derived miRNAs has not yet been reported.Methods: Blood samples were collected from 20 Han Chinese individuals residing at 500 m (Sichuan Han), 10 migrant Han Chinese citizens residing at 3,658 m (Tibet Han) and 12 native Tibetans, and RBC indices measurements and miRNA sequencing analyses were performed for the three sample groups. The levels of some markedly altered miRNAs at high altitude were subsequently measured from 5 randomly selected samples of each group by real-time PCR. Bioinformatic analyses was performed to determine the potential target genes of selected hypoxia-associated miRNAs.Results: Marked changes of several RBC indices were observed among the Tibet Han population, the Tibetan population and the Sichuan Han population. A total of 516 miRNAs derived from RBCs were initially identified by miRNA sequencing in the three sample groups. Compared with the Sichuan Han population, 49 miRNAs were differentially expressed in the Tibet Han population (17 upregulated and 32 downregulated). 12 upregulated and 21 downregulated miRNAs were observed in the Tibetan population compared with the Sichuan Han population. A total of 40 RBC miRNAs were differentially expressed in the Tibetan population (15 upregulated and 25 downregulated) compared with the Tibet Han population. Two significantly altered miRNAs with the highest expression levels (miRNA-144-5p and miR-30b-5p) were selected for real-time PCR analysis, and the results were consistent with those of miRNA sequencing. Furthermore, bioinformatic analyses showed that some potential target genes of miR-144-5p and miR-30b-5p are involved in the erythroid- hypoxia-, and nitric oxide (NO)-related signaling pathways in response to hypoxia.Conclusion: Our findings provide clear evidence, for the first time, that a high-altitude hypoxic environment significantly affects human RBC miRNA profiles.

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“…Previous studies have proved that miRNAs paly vital roles in the regulation of glomerulonephritis 20,30,31 . Quite a lot of miRNAs have been shown to exert a protective or injury effect on podocytes.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐17‐5p restrains the dysfunction of Ang‐II induced podocytes by suppressing secreted modular calcium‐binding protein 2 via NF‐κB and TGFβ signaling

Yi²,

2021

Environmental Toxicology

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Glomerulonephritis, also known as nephritis syndrome (nephritis for short), is a common kidney disease. Previous research has proved that microRNAs (miRNAs) frequently regulate various diseases including nephritis. Nonetheless, the biological function and molecular mechanism of miR‐17‐5p are unclear in nephritis. In the current study, RT‐qPCR analysis showed that miR‐17‐5p was downregulated in Ang II‐induced podocytes. Also, according to the results from RT‐qPCR analysis, CCK‐8 assay, flow cytometric analysis, western blot analysis, and ELISA miR‐17‐5p elevation alleviated Ang II‐induced podocyte injury. Besides, luciferase reporter assay, western blot and RT‐qPCR analyses revealed that SMOC2 was targeted by miR‐17‐5p in Ang II‐induced podocytes. Additionally, rescue assays demonstrated that overexpressed SMOC2 counteracted the influence of overexpressed miR‐17‐5p on cell injury of Ang II‐induced podocytes. Moreover, our data suggested that miR‐17‐5p‐SMOC2 axis regulated TGFβ and NF‐κB signaling activation in Ang II‐induced podocytes. SMOC2 regulated cell viability, apoptosis and extracellular matrix (ECM) deposition in Ang II‐induced podocytes via TGFβ signaling, and SMOC2 regulated inflammation in Ang II‐induced podocytes through NF‐κB signaling. Overall, our study demonstrated that miRNA‐17‐5p restrained the dysfunction of Ang‐II induced podocytes by suppressing SMOC2 via the NF‐κB and TGFβ signaling.

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Urinary Erythrocyte-Derived miRNAs: Emerging Role in IgA Nephropathy

Cited by 12 publications

References 59 publications

Glomerular Hematuria: Cause or Consequence of Renal Inflammation?

Glomerular Hematuria: Cause or Consequence of Renal Inflammation?

Different Erythrocyte MicroRNA Profiles in Low- and High-Altitude Individuals

MicroRNA‐17‐5p restrains the dysfunction of Ang‐II induced podocytes by suppressing secreted modular calcium‐binding protein 2 via NF‐κB and TGFβ signaling

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