ArticlePloS one2013
Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Candidate Genetic Modifiers in Alport Syndrome: A Case Series.Life (Basel, Switzerland) · 2025Article
- Focal segmental glomerulosclerosis and proteinuria associated with Myo1E mutations: novel variants and histological phenotype analysis.Pediatric nephrology (Berlin, Germany) · 2023Article
- Overexpression of Myo1e promotes albumin endocytosis by mouse glomerular podocytes mediated by Dynamin.PeerJ · 2020Article
- Protein phosphatase 2A modulates podocyte maturation and glomerular functional integrity in mice.Cell communication and signaling : CCS · 2019Article
- Review
- FAT1 mutations cause a glomerulotubular nephropathy.Nature communications · 2016Article
- Genetic causes of proteinuria and nephrotic syndrome: impact on podocyte pathobiology.Pediatric nephrology (Berlin, Germany) · 2015Review
- ELAVL1 modulates transcriptome-wide miRNA binding in murine macrophages.Cell reports · 2014Article
- Using zebrafish to study podocyte genesis during kidney development and regeneration.Genesis (New York, N.Y. : 2000) · 2014Review
- Molecular Mechanisms of Podocyte Development Revealed by Zebrafish Kidney Research.Cell & developmental biology · 2014Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPodocytes serve as an important constituent of the glomerular filtration barrier. Recently, we and others identified Myo1e as a key molecular component of the podocyte cytoskeleton.
resultsMyo1e mRNA and protein was expressed in human and mouse kidney sections as determined by Northern blot and reverse transcriptase PCR, and its expression was more evident in podocytes by immunofluorescence. By specific knock-down of MYO1E in zebrafish, the injected larvae exhibited pericardial edema and pronephric cysts, consistent with the appearance of protein in condensed incubation supernate. Furthermore, specific inhibition of Myo1e expression in a conditionally immortalized podocyte cell line induced morphological changes, actin cytoskeleton rearrangement, and dysfunction in cell proliferation, migration, endocytosis, and adhesion with the glomerular basement membrane.
conclusionsOur results revealed that Myo1e is a key component contributing to the functional integrity of podocytes. Its impairment may cause actin cytoskeleton re-organization, alteration of cell shape, and membrane transport, and podocyte drop-out from the glomerular basement membrane, which might eventually lead to an impaired glomerular filtration barrier and proteinuria.
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Registered trials
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