Podocyte-derived microparticles in IgA nephropathy

Farzamikia, Negin; Baradaran, Behzad; Mostafavi, Soroush; Ahmadian, Elham; Khatibi, Seyed Mahdi Hosseiniyan; Vahed, Sepideh Zununi; Ardalan, Mohammadreza

doi:10.1016/j.biopha.2021.111891

Cited by 9 publications

(6 citation statements)

References 93 publications

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“…Extracellular vesicles (particles and exosomes) are recognized as biomarkers for many diseases such as lupus nephritis, diabetic nephropathy, preeclampsia, focal segmental glomerulosclerosis, and IgA nephropathy. (Farzamikia et al, 2021). To date, there have been no studies directly comparing the specificity of MP of podocyte origin in detecting these nephropathies.…”

Section: Urinary Podocyte Microparticlesmentioning

confidence: 99%

Urinary biomarkers associated with podocyte injury in lupus nephritis

Guo,

et al. 2024

Front. Pharmacol.

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The most prevalent and devastating form of organ damage in systemic lupus erythematosus (SLE) is lupus nephritis (LN). LN is characterized by glomerular injury, inflammation, cell proliferation, and necrosis, leading to podocyte injury and tubular epithelial cell damage. Assays for urine biomarkers have demonstrated significant promise in the early detection of LN, evaluation of disease activity, and tracking of reaction to therapy. This is because they are non-invasive, allow for frequent monitoring and easy self-collection, transport and storage. Podocyte injury is believed to be a essential factor in LN. The extent and type of podocyte injury could be connected to the severity of proteinuria, making podocyte-derived cellular debris and injury-related urinary proteins potential markers for the diagnosis and monitoring of LN. This article focuses on studies examining urinary biomarkers associated with podocyte injury in LN, offering fresh perspectives on the application of biomarkers in the early detection and management of LN.

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Section: Urinary Podocyte Microparticlesmentioning

confidence: 99%

Urinary biomarkers associated with podocyte injury in lupus nephritis

Guo,

et al. 2024

Front. Pharmacol.

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“…Furthermore, the size of Gd-IgA1-IgG immune complex and polymeric Gd-IgA1 aggregated for their de-glycosylation is large, and these large molecules could not be cleared efficiently from the circulation and, thus, tend to deposit in the renal mesangium to initiate intrarenal inflammation. Clinical studies have revealed that circulatory levels of anti-Gd-IgA1 IgG antibodies correlate with disease severity ( 20 ). Intrarenal inflammation initiated by deposition of Gd-IgA1-containing immune complex affecting mesangial cells, endothelial cells, podocytes, and TECs is shown in Figure 1 .…”

Section: Gd-iga1-containing Immune Complex Depositionmentioning

confidence: 99%

“…The crosstalk between mesangial cells and TECs is mediated by TNF-α, TGF-β1, and MCP-1 ( 6 ). TNF-α from mesangial cells could enhance AT1R expression on TECs in the early phase and then boosts AT2R expression subsequently, after which increased Ang II level from mesangial cells could deteriorate TEC damage by inducing inflammatory response via AT1R through MAPK pathway and inducing TEC apoptosis via AT2R through caspase pathway ( 20 ). Furthermore, Ang II could also upregulate the expression of the mineralocorticoid receptor (MR) by PTECs, and binding of aldosterone to MR on PTECs induces cellular apoptosis through the generation of reactive oxygen species ( 101 ).…”

Section: Tubular Epithelial Cellmentioning

confidence: 99%

Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy

2023

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Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis and the leading cause of kidney failure in the world. The current widely accepted framework for its pathogenesis is the “multi-hit hypothesis.” In this review, we mainly discussed the intrarenal inflammation in IgAN, which is initiated by immune complex deposition with complement molecule activation, by focusing on four main types of cells in nephrons including mesangial cells, endothelial cells, podocytes, and tubular epithelial cells (TECs). Galactose-deficient IgA1 (Gd-IgA1)-containing immune complexes deposit in the mesangium and activate complement molecules and mesangial cells. Activation of mesangial cells by Gd-IgA1 deposition with enhanced cellular proliferation, extracellular matrix (ECM) expansion, and inflammatory response plays a central role in the pathogenesis of IgAN. Regional immune complex deposition and mesangial–endothelial crosstalk result in hyperpermeability of endothelium with loss of endothelial cells and infiltration barrier proteins, and recruitment of inflammatory cells. Podocyte damage is mainly derived from mesangial–podocyte crosstalk, in which tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), renin-angiotensin-aldosterone system (RAAS), and micro-RNAs are the major players in podocyte apoptosis and disorganization of slit diaphragm (SD) related to proteinuria in patients with IgAN. In addition to filtrated proteins into tubulointerstitium and mesangial–tubular crosstalk involved in the injury of TECs, retinoic acid has been discovered innovatively participating in TEC injury.

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“…EVs are released by the majority of cell types and can be found in all biological fluids. Urinary EVs are proper materials to discover candidate biomarkers for the diagnosis of kidney disease [11][12][13] and they can be detected by performing liquid biopsy and reflecting the pattern and severity of renal injury. [14][15][16] According to previous studies, EVs derived from podocytes are present in the urine of patients with different glomerulonephritis (GN) such as diabetic nephropathy, 17,18 lupus nephritis, 19 renal injury in preeclampsia, 20 and renovascular hypertensive disorder.…”

Section: Evaluating Igan-specific Proteins In Urinary Evsmentioning

confidence: 99%

Podocyte-specific proteins in urinary extracellular vesicles of patients with IgA nephropathy: Vasorin and ceruloplasmin

Farzamikia,

Hejazian,

Mostafavi

et al. 2023

Bioimpacts

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Introduction: Urinary extracellular vesicles (uEVs) can be considered biomarkers of kidney diseases. EVs derived from podocytes may reflect podocyte damage in different glomerular diseases. IgA nephropathy (IgAN) is one of the most common forms of glomerulonephritis (GN) characterized by proteinuria and hematuria. This study aimed to analyze the uEVs of IgAN patients to understand the pathophysiological processes of the disease at the protein level. Methods: Patients with GN [biopsy-proven IgAN (n = 16) and membranous glomerulonephritis (MGN, n = 16)], and healthy controls (n = 16) were included in this study. The uEVs were extracted, characterized, and analyzed to evaluate the protein levels of candidate markers of IgAN, including vasorin precursor, aminopeptidase N, and ceruloplasmin by western-blot analysis. Results: Higher levels of both podocytes and EVs-related proteins were observed in the pooled urine samples of GN patients compared to the healthy controls. In IgAN patients, uEV-protein levels of vasorin were statistically lower while levels of ceruloplasmin were significantly higher compared to MGN (P = 0.002, P = 0.06) and healthy controls, respectively (P = 0.020, P= 0.001). Conclusion: Different levels of the studied proteins in uEVs may indicate podocyte injury and represent a direct association with the pathology of IgAN and MGN.

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Podocyte-derived microparticles in IgA nephropathy

Cited by 9 publications

References 93 publications

Urinary biomarkers associated with podocyte injury in lupus nephritis

Urinary biomarkers associated with podocyte injury in lupus nephritis

Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy

Podocyte-specific proteins in urinary extracellular vesicles of patients with IgA nephropathy: Vasorin and ceruloplasmin

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