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https://doi.org/10.1371/journal.pone.0072750
Title: | Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes | Authors: | Mao J. Wang D. Mataleena P. He B. Niu D. Katayama K. Xu X. Ojala J.R.M. Wang W. Shu Q. Du L. Liu A. Pikkarainen T. Patrakka J. Tryggvason K. |
Keywords: | actin antisense oligonucleotide complementary DNA messenger RNA myosin myosin1e nephrin podocin short hairpin RNA synaptopodin unclassified drug vitellogenin actin fluorescein isothiocyanate MYO1E protein, human Myo1e protein, mouse Myo1e protein, zebrafish myosin myosin I transferrin zebrafish protein actin filament animal cell animal tissue Article cardiovascular disease cell adhesion cell culture cell migration cell motility cell proliferation cell shape cell structure congenital nephrotic syndrome controlled study cytoplasm cytoskeleton down regulation embryo endocytosis enzyme linked immunosorbent assay exon fluorescence microscopy gene sequence glomerular filtration barrier glomerulus basement membrane histopathology human human cell human tissue immortalized cell line immunofluorescence incubation time kidney cyst kidney disease kidney failure larva mass spectrometry mouse nonhuman Northern blotting pericarditis phenotype podocyte protein analysis protein expression protein localization proteinuria reverse transcription polymerase chain reaction risk factor RNA splicing supernatant upregulation zebra fish animal cell count cell culture cell migration assay fertilization gene silencing glomerulus metabolism pathology podocyte proteinuria Danio rerio Actins Animals Cell Count Cell Migration Assays Cell Proliferation Cell Shape Cells, Cultured Cytoskeleton Down-Regulation Endocytosis Fertilization Fluorescein-5-isothiocyanate Gene Knockdown Techniques Humans Kidney Diseases Kidney Glomerulus Mice Myosin Type I Myosins Podocytes Proteinuria Transferrin Zebrafish Zebrafish Proteins |
Issue Date: | 2013 | Citation: | Mao J., Wang D., Mataleena P., He B., Niu D., Katayama K., Xu X., Ojala J.R.M., Wang W., Shu Q., Du L., Liu A., Pikkarainen T., Patrakka J., Tryggvason K. (2013). Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes. PLoS ONE 8 (8) : e72750. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0072750 | Rights: | Attribution 4.0 International | Abstract: | Background: Podocytes 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. Results: Myo1e 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. Conclusions: Our 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. © 2013 Mao et al. | Source Title: | PLoS ONE | URI: | https://scholarbank.nus.edu.sg/handle/10635/161275 | ISSN: | 19326203 | DOI: | 10.1371/journal.pone.0072750 | Rights: | Attribution 4.0 International |
Appears in Collections: | Elements Staff Publications |
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