Serum microRNAs are altered in various stages of chronic kidney disease: a preliminary study

Brigant, Benjamin; Metzinger, Laurent; Massy, Ziad A.; McKay, Nathalie; Liabeuf, Sophie; Pelletier, M.; Sallée, Marion; M'Baya-Moutoula, Eléonore; Paul, Pascale; Drueke, Tilman B.; Burtey, Stéphane

doi:10.1093/ckj/sfw060

Cited by 15 publications

(16 citation statements)

References 36 publications

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“…These differences remained significantly different after adjustment by eGFR, indicating that regulation of these miRNAs is independent of kidney function. Our results are in accordance with other authors which have reported that circulating miRNA-126-3p is decreased in ESRD (Fourdinier et al, 2019) and HD patients (Brigant et al, 2017). miRNA-126-3p has an important role in vascular dysfunction, since it enhances endothelial proliferation and endothelization of large vessels, which in turn attenuates atherosclerosis (Davignon and Ganz, 2004;Zernecke et al, 2009;Economou et al, 2015).…”

Section: Discussionsupporting

confidence: 93%

“…Likewise, miRNA-223-3p is implicated in vascular complications that occur during the later stages of CKD (Brigant et al, 2017). Various studies have reported a significantly lower systemic expression of miR-223-3p at later stages of CKD, as well as up-regulation of this miRNA after kidney transplantation (Ulbing et al, 2017;Fourdinier et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Dysregulation of miRNAs has been linked to the pathophysiology of many inflammatory diseases, such as kidney and cardiovascular diseases ( Metzinger-Le Meuth et al, 2019 ; Zhao et al, 2019 ). In vivo studies have reported that the expression of miR-126 is reduced in end stage renal disease and hemodialysis patients ( Dziedzic et al, 2016 ; Brigant et al, 2017 ; Fourdinier et al, 2019 ). miR-126 is endothelial-specific and it is implicated in endothelial dysfunction promoting angiogenesis, endothelial proliferation and inhibiting vascular inflammation ( Hu et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

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Inflammation, Senescence and MicroRNAs in Chronic Kidney Disease

Carmona

Guerrero

Jiménez

et al. 2020

Front. Cell Dev. Biol.

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Background: Patients with chronic kidney disease (CKD) show a chronic microinflammatory state that promotes premature aging of the vascular system. Currently, there is a growth interest in the search of novel biomarkers related to vascular aging to identify CKD patients at risk to develop cardiovascular complications. Methods: Forty-five CKD patients were divided into three groups according to CKDstages [predialysis (CKD4-5), hemodialysis (HD) and kidney transplantation (KT)]. In all these patients, we evaluated the quantitative changes in microRNAs (miRNAs), CD14+C16++ monocytes number, and microvesicles (MV) concentration [both total MV, and monocytes derived MV (CD14+Annexin V+CD16+)]. To understand the molecular mechanism involved in senescence and osteogenic transdifferentation of vascular smooth muscle cells (VSMC), these cells were stimulated with MV isolated from THP-1 monocytes treated with uremic toxins (txMV). Results: A miRNA array was used to investigate serum miRNAs profile in CKD patients. Reduced expression levels of miRNAs-126-3p,-191-5p and-223-3p were observed in CKD4-5 and HD patients as compared to KT. This down-regulation disappeared after KT, even when lower glomerular filtration rates (eGFR) persisted. Moreover, HD patients had higher percentage of proinflammatory monocytes (CD14+CD16++) and MV derived of proinflammatory monocytes (CD14+Annexin V+CD16+) than the other groups. In vitro studies showed increased expression of osteogenic markers (BMP2 and miRNA-223-3p), expression of cyclin D1, β-galactosidase activity and VSMC size in those cells treated with txMV. Conclusion: CKD patients present a specific circulating miRNAs expression profile associated with the microinflammatory state. Furthermore, microvesicles generated by monocytes treated with uremic toxins induce early senescence and osteogenic markers (BMP2 and miRNA-223-3p) in VSMC.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inflammation, Senescence and MicroRNAs in Chronic Kidney Disease

Carmona

Guerrero

Jiménez

et al. 2020

Front. Cell Dev. Biol.

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“…A total of 26 miRNAs including 3 upregulated miRNAs and 23 downregulated miRNAs were found differently expressed in normal rats and rats with CGN (supplement file). Of those differently expressed miRNAs, miR‐145‐5p was especially interesting because it was confirmed to highly express in mesangial cells (Harvey et al, ) and make a difference in inflammatory responses and cell proliferation (Lin et al, ), Brigant et al () found that serum level of miR‐145 was elevated in patients with CKD compared with healthy controls, which was correlated with estimated glomerular filtration rate. However, the mechanism of how miR‐145‐5p regulates CGN remained unclear.…”

Section: Discussionmentioning

confidence: 99%

MiR‐145‐5p inhibits proliferation and inflammatory responses of RMC through regulating AKT/GSK pathway by targeting CXCL16

Luo

et al. 2017

Journal Cellular Physiology

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The main pathological characteristics of chronic glomerulonephritis (CGN) are diffuse mesangial cells proliferation and inflammatory responses. Our previous studies have confirmed that miR-145-5p was abnormally elevated in CGN rats, but its mechanism remains unclear. Therefore, this study aimed to elucidate the mechanism of miR-145-5p in regulation of renal mesangial cells proliferation and inflammatory responses. In vivo study, the cationic bovine serum albumin (C-BSA)-induced CGN rat model was established, and the content of miR-145-5p in renal was examined by qRT-PCR, meanwhile, we also determined the renal function and inflammatory infiltrate. In vitro, the cell proliferation rate, cell cycle and inflammatory changes of rat mesangial cells (RMCs) were measured. Our results suggested that miR-145-5p extended the G0-G1 phase, shortened S phase, inhibited cell proliferation and suppressed inflammatory responses in RMCs. Moreover, miR-145-5p inhibited CXCL16 protein expression through binding the 3'-UTR of CXCL16, suppressed AKT/GSK signaling pathway, and decreased expression of inflammation related mRNAs, such as IL-1α, IL-2, IL-6, and TNF-α mRNAs. Further, locking CXCL16 alleviated inflammatory reactions and down-regulated AKT/GSK pathway in RMCs. Above all, we concluded that miR-145-5p inhibited proliferation and inflammatory responses of RMCs through regulation of AKT/GSK pathway by targeting CXCL16.

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“…Neal et al were the first to use RT-qPCR to show that certain circulating miRNAs are decreased in various stages of CKD [ 15 ]. Relative expression of miRNA-155 and miRNA-223 was increased in the serum of patients with CKD, but decreased in renal transplant recipients [ 16 ], while serum expression of miRNA-125b, miRNA-145, and miRNA-155 was decreased in a cohort of 90 CKD patients at stage 3 and 4 [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Expression of Circulating MicroRNAs Linked to Bone Metabolism in Chronic Kidney Disease-Mineral and Bone Disorder

et al. 2020

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The pathophysiology of chronic kidney disease–mineral and bone disorder (CKD-MBD) is complex and multifactorial. Recent studies have identified a link between microRNAs (miRNAs) and bone loss. In this study, we investigated the expression of miRNAs in CKD-MBD. In this case-control study, we included thirty patients with CKD-MBD (cases) and 30 age- and gender-matched healthy individuals (controls). Bone mineral density (BMD) and trabecular bone score (TBS) evaluation was performed with dual X-ray absorptiometry. The selected panel of miRNAs included: hsa-miRNA-21-5p; hsa-miRNA-23a-3p; hsa-miRNA-24-2-5p; hsa-miRNA-26a-5p; hsa-miRNA-29a-3; hsa-miRNA-124-3p; hsa-miRNA-2861. The majority of cases had low BMD values. The relative expression of miRNA-21-5p was 15 times lower [fold regulation (FR): −14.7 ± 8.1, p = 0.034), miRNA-124-3p, 6 times lower (FR: −5.9 ± 4, p = 0.005), and miRNA-23a-3p, 4 times lower (FR: −3.8 ± 2.0, p = 0.036) in cases compared to controls. MiRNA-23a-3p was significantly and inversely correlated with TBS, adjusted for calcium metabolism and BMD values (beta = −0.221, p = 0.003, 95% CI −0.360, −0,081) in cases. In a receiver operating characteristic (ROC) analysis, expression of miRNA-124-3p demonstrated 78% sensitivity and 83% specificity in identifying CKD patents with osteoporosis. Serum expression of miRNAs related to osteoblasts (miRNA-23a-3p) and osteoclasts (miRNA-21-5p, miRNA-124-3p) is significantly altered in patients with CKD-MBD.

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Serum microRNAs are altered in various stages of chronic kidney disease: a preliminary study

Cited by 15 publications

References 36 publications

Inflammation, Senescence and MicroRNAs in Chronic Kidney Disease

Inflammation, Senescence and MicroRNAs in Chronic Kidney Disease

MiR‐145‐5p inhibits proliferation and inflammatory responses of RMC through regulating AKT/GSK pathway by targeting CXCL16

Expression of Circulating MicroRNAs Linked to Bone Metabolism in Chronic Kidney Disease-Mineral and Bone Disorder

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