ArticleBMC nephrology2016
Mesangial cells from patients with IgA nephropathy have increased susceptibility to galactose-deficient IgA1.
Article in BMC nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Acteoside relieves mesangial cell injury by regulating Th22 cell chemotaxis and proliferation in IgA nephropathy.Renal failure · 2018Trial
- Intrinsic renal cells induce lymphocytosis of Th22 cells from IgA nephropathy patients through B7-CTLA-4 and CCL-CCR pathways.Molecular and cellular biochemistry · 2018Trial
- Review
- Integrative bioinformatics analysis unveils hub transcription factors and their interacting drugs in immunoglobulin A nephropathy: Implications for pathogenesis and treatments.Journal, genetic engineering & biotechnology · 2025Article
- O-glycosylation of IgA1 and the pathogenesis of an autoimmune disease IgA nephropathy.Glycobiology · 2024Review
- Emerging Biochemical and Immunologic Mechanisms in the Pathogenesis of IgA Nephropathy.Seminars in nephrology · 2024Review
- Cytokines and Production of AberrantlyJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- New Insights into the Treatment of Glomerular Diseases: When Mechanisms Become Vivid.International journal of molecular sciences · 2022Review
- Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation.Frontiers in cell and developmental biology · 2022Review
- The Glomerulus According to the Mesangium.Frontiers in medicine · 2021Review
- TLR7 in B cells promotes renal inflammation and Gd-IgA1 synthesis in IgA nephropathy.JCI insight · 2020Article
- [Expression and significance of follicular helper T cells and galactose-deficient IgA1 in children with Henoch-Schönlein purpura].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020Article
- Quantitative analysis of protein crotonylation identifies its association with immunoglobulin A nephropathy.Molecular medicine reports · 2020Article
- Integrated bioinformatics analysis reveals novel hub genes closely associated with pathological mechanisms of immunoglobulin A nephropathy.Experimental and therapeutic medicine · 2019Article
- From expression footprints to causal pathways: contextualizing large signaling networks with CARNIVAL.NPJ systems biology and applications · 2019Article
- MicroRNAs: a new avenue to understand, investigate and treat immunoglobulin A nephropathy?Clinical kidney journal · 2018Article
- Transcriptomic and Proteomic Profiling Provides Insight into Mesangial Cell Function in IgA Nephropathy.Journal of the American Society of Nephrology : JASN · 2017Article
- Serial Galactose-Deficient IgA1 Levels in Children with IgA Nephropathy and Healthy Controls.International journal of nephrology · 2017Article
- Mesangioproliferative Kidney Diseases and Platelet-Derived Growth Factor-Mediated AXL Phosphorylation.Kidney medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIgA nephropathy (IgAN) is the most common glomerulonephritis in the world, affecting close to a million people. Circulating galactose-deficient IgA (gd-IgA), present in patients with IgAN, form immune complex deposits in the glomerular mesangium causing local proliferation and matrix expansion. Intriguing though, individuals having gd-IgA deposits in the kidneys do not necessarily have signs of glomerular disease. Recurrence of IgAN only occurs in less than half of transplanted patients with IgAN, indicating that gd-IgA is not the only factor driving the disease. We hypothesize that, in addition to IgA complexes, patients with IgAN possess a subtype of mesangial cells highly susceptible to gd-IgA induced cell proliferation.
methodsTo test the hypothesis, we designed a technique to culture primary mesangial cells from renal biopsies obtained from IgAN patients and controls. The cell response to gd-IgA treatment was then measured both on gene and protein level and the proliferation rate of the cells in response to PDGF was investigated.
resultsWhen treated with gd-IgA, mesangial cells from patients with IgAN express and release more PDGF compared to controls. In addition, the mesangial cells from patients with IgAN were more responsive to treatment with PDGF resulting in an increased proliferation rate of the cells compared to control. Mesangial cells cultured from patients with IgAN expressed and released more IL-6 than controls and had a higher expression of matrix genes. Both mesangial cells derived from patients with IgAN and controls increased their expressed TGFβ1 and CCL5 when treated with gd-IgA.
conclusionWe conclude that mesangial cells derived from IgAN patients have a mesangioproliferative phenotype with increased reactivity to IgA and that these cellular intrinsic properties may be important for the development of IgA nephropathy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.