ArticlePediatric nephrology (Berlin, Germany)2011
Plasma from a case of recurrent idiopathic FSGS perturbs non-muscle myosin IIA (MYH9 protein) in human podocytes.
Article in Pediatric nephrology (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Past and future in vitro and in vivo approaches toward circulating factors and biomarkers in idiopathic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Review
- Advances in focal segmental glomerulosclerosis research: genetic causes to non-coding RNAs.Molecular biology reports · 2025Review
- Investigating the role of gut microbiota in diabetic nephropathy through plasma proteome mediated analysis.Scientific reports · 2025Article
- Proteomics of Plasma and Plasma-Treated Podocytes: Application to Focal and Segmental Glomerulosclerosis.International journal of molecular sciences · 2023Article
- A non-muscle myosin heavy chain 9 genetic variant is associated with graft failure following kidney transplantation.Kidney research and clinical practice · 2023Article
- Use of genomic and functional analysis to characterize patients with steroid-resistant nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2018Article
- The Role of Palladin in Podocytes.Journal of the American Society of Nephrology : JASN · 2018Article
- Changes in podocyte TRPC channels evoked by plasma and sera from patients with recurrent FSGS and by putative glomerular permeability factors.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Article
- TNFα pathway blockade ameliorates toxic effects of FSGS plasma on podocyte cytoskeleton and β3 integrin activation.Pediatric nephrology (Berlin, Germany) · 2012Article
- Nonfunction of the ECT2 gene may cause renal tubulointerstitial injury leading to focal segmental glomerulosclerosis.Clinical and experimental nephrology · 2012Article
- Glomerular MYH9 expression is reduced by HIV-1.AIDS (London, England) · 2012Article
- Non-muscle myosins and the podocyte.Clinical kidney journal · 2012Article
- Recurrent focal segmental glomerulosclerosis: a discrete clinical entity.International journal of nephrology · 2012Article
- Post-Transplant Recurrence of Focal Segmental Glomerulosclerosis: Circulating Factors, Molecular Biomarkers, and Treatments.Kidney diseases (Basel, Switzerland)Article
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8 authors at 1 institution in 1 country.
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Abstract
The MYH9 gene encodes a non-muscle myosin IIA heavy chain (NMMHC-IIA) expressed in podocytes. Heterozygous MYH9 mutations cause a set of overlapping syndromes characterized by variable degrees of deafness, morphologic abnormalities of platelets and focal segmental glomerulosclerosis (FSGS) with progressive renal dysfunction. Similar glomerular lesions are seen in a variety of nephropathies, including an idiopathic form of FSGS in children which recurs in renal allografts, implying a circulating factor that affects glomerular podocyte biology. It is unknown whether NMMHC-IIA is perturbed in the idiopathic form of FSGS. We describe a pediatric patient with typical idiopathic FSGS, in whom proteinuria recurred within hours of deceased donor renal transplantation but who responded to plasmapheresis. We demonstrate in vitro that plasmapheresis effluent from our patient rapidly decreased cultured podocyte levels of the phosphorylated myosin light chain (MLC) that mediates NMMHC-IIA binding to actin and induced dispersion of NMMHC-IIA from its usual position along actin stress fibers. FSGS plasma also caused dispersion of slit diaphragm proteins (nephrin and podocin) and vinculin-positive focal adhesion complexes. Our observations suggest that the putative circulating factor in idiopathic FSGS disrupts normal NMMHC-IIA function in podocytes and might contribute to the pathogenesis of recurrent FSGS in other children.
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