ArticlePloS one2013
Synergistic effect of mesangial cell-induced CXCL1 and TGF-β1 in promoting podocyte loss in IgA nephropathy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Acteoside relieves mesangial cell injury by regulating Th22 cell chemotaxis and proliferation in IgA nephropathy.Renal failure · 2018Trial
- Complement factor H supplementation rather than complete C3 knockout provides therapeutic benefits in IgA nephropathy.Molecular biomedicine · 2026Article
- Mesenchymal stem cells: a potential therapeutic strategy for IgA nephropathy.Frontiers in pharmacology · 2026Review
- Dual Role of Factor H-Related Protein 1 in IgA Nephropathy Kidney Injury.Kidney international reports · 2026Article
- The intelligent podocyte: sensing and responding to a complex microenvironment.Nature reviews. Nephrology · 2025Review
- Replication kinetics of pathogenic Eurasian orthohantaviruses in human mesangial cells.Virology journal · 2024Article
- The successful use of rituximab in IgA nephropathy patients with podocytopathy: a case series.Clinical kidney journal · 2024Article
- Role of abnormal glycosylated IgA1 and interstitial transformation of glomerular endothelial cells in the development and progression of IgA nephropathy.Italian journal of pediatrics · 2023Article
- Chemokine (C-C motif) receptor 2 is associated with the pathological grade and inflammatory response in IgAN children.BMC nephrology · 2022Article
- Renal deposition and clearance of recombinant poly-IgA complexes in a model of IgA nephropathy.The Journal of pathology · 2021Article
- Monozygotic Twins Discordant for Immunoglobulin A Nephropathy Display Differences in DNA Methylation and Gene Expression.Kidney diseases (Basel, Switzerland) · 2021Article
- The Glomerulus According to the Mesangium.Frontiers in medicine · 2021Review
- Immune Characteristics of IgA Nephropathy With Minimal Change Disease.Frontiers in pharmacology · 2021Article
- Huangkui Capsule in Combination with Leflunomide Improves Immunoglobulin A Nephropathy by Inhibiting the TGF-β1/Smad3 Signaling Pathway.Clinics (Sao Paulo, Brazil) · 2021Article
- The implications of focal segmental glomerulosclerosis in children with IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2020Review
- The soluble VEGF receptor sFlt-1 contributes to endothelial dysfunction in IgA nephropathy.PloS one · 2020Article
- The Role of Immune Modulation in Pathogenesis of IgA Nephropathy.Frontiers in medicine · 2020Review
- Triptolide protects podocytes via autophagy in immunoglobulin A nephropathy.Experimental and therapeutic medicine · 2018Article
- TREM-1 Contributes to Inflammation in IgA Nephropathy.Kidney diseases (Basel, Switzerland) · 2018Article
- Pathogenic role of glycan-specific IgG antibodies in IgA nephropathy.BMC nephrology · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocyte loss has been reported to relate to disease severity and progression in IgA nephropathy (IgAN). However, the underlying mechanism for its role in IgAN remain unclear. Recent evidence has shown that IgA1 complexes from patients with IgAN could activate mesangial cells to induce soluble mediator excretion, and further injure podocytes through mesangial-podocytic cross-talk. In the present study, we explored the underlying mechanism of mesangial cell-induced podocyte loss in IgAN. We found that IgA1 complexes from IgAN patients significantly up-regulated the expression of CXCL1 and TGF-β1 in mesangial cells compared with healthy controls. Significantly higher urinary levels of CXCL1 and TGF-β1 were also observed in patients with IgAN compared to healthy controls. Moreover, IgAN patients with higher urinary CXCL1 and TGF-β1 presented with severe clinical and pathological manifestations, including higher 24-hour urine protein excretion, lower eGFR and higher cresentic glomeruli proportion. Further in vitro experiments showed that increased podocyte death and reduced podocyte adhesion were induced by mesangial cell conditional medium from IgAN (IgAN-HMCM), as well as rhCXCL1 together with rhTGF-β1. In addition, the over-expression of CXCR2, the receptor for CXCL1, by podocytes was induced by IgAN-HMCM and rhTGF-β1, but not by rhCXCL1. Furthermore, the effect of increased podocyte death and reduced podocyte adhesion induced by IgAN-HMCM and rhCXCL1 and rhTGF-β1 was rescued partially by a blocking antibody against CXCR2. Moreover, we observed the expression of CXCR2 in urine exfoliated podocytes in IgAN patients. Our present study implied that IgA1 complexes from IgAN patients could up-regulate the secretion of CXCL1 and TGF-β1 in mesangial cells. Additionally, the synergistic effect of CXCL1 and TGF-β1 further induced podocyte death and adhesion dysfunction in podocytes via CXCR2. This might be a potential mechanism for podocyte loss observed in IgAN.
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