Please use this identifier to cite or link to this item: 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
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