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- Title
Podocyte expression of nonmuscle myosin heavy chain-IIA decreases in idiopathic nephrotic syndrome, especially in focal segmental glomerulosclerosis.
- Authors
Miura, Kenichiro; Kurihara, Hidetake; Horita, Shigeru; Chikamoto, Hiroko; Hattori, Motoshi; Harita, Yutaka; Tsurumi, Haruko; Kajiho, Yuko; Sawada, Yoko; Sasaki, Satoshi; Igarashi, Takashi; Kunishima, Shinji; Sekine, Takashi
- Abstract
Background Previous studies have identified significant associations between the development of idiopathic focal segmental glomerulosclerosis (FSGS) and MYH9 encoding nonmuscle myosin heavy chain-IIA (NMMHC-IIA). However, these studies focused only on the linkage of MYH9 polymorphisms and development of FSGS. There have been no reports on pathological changes of NMMHC-IIA in human glomerular diseases. Here we report on the precise localization of NMMHC-IIA in podocytes and changes in NMMHC-IIA expression in pathological states in rats and humans. Methods Immunocytochemical (immunofluorescence and immunoelectron microscopy) studies were performed to determine the precise localization of NMMHC-IIA. Expression levels of NMMHC-IIA were investigated in puromycin aminonucleoside (PAN)-treated rats; and expression levels of NMMHC-IIA and other podocyte-related proteins were investigated in glomeruli of patients with idiopathic FSGS and other heavy proteinuric glomerular diseases. Results NMMHC-IIA was located primarily at the cell body and primary processes of podocytes; this localization is distinct from other podocyte-related molecules causing hereditary FSGS. In PAN-treated rat kidneys, expression levels of NMMHC-IIA in podocytes decreased. Immunohistochemical analysis revealed that expression levels of NMMHC-IIA markedly decreased in idiopathic nephrotic syndrome, especially FSGS, whereas it did not change in other chronic glomerulonephritis showing apparent proteinuria. Changes in NMMHC-IIA expression were observed in glomeruli where expression of nephrin and synaptopodin was maintained. Conclusions Considering previous genome-wide association studies and development of FSGS in patients with MYH9 mutations, the characteristic localization of NMMHC-IIA and the specific decrease in NMMHC-IIA expression in idiopathic nephrotic syndrome, especially FSGS, suggest the important role of NMMHC-IIA in the development of FSGS.
- Subjects
NONMUSCLE myosin; NEPHROTIC syndrome; ESSENTIAL hypertension; FOCAL segmental glomerulosclerosis; GENETIC polymorphisms; IMMUNOHISTOCHEMISTRY
- Publication
Nephrology Dialysis Transplantation, 2013, Vol 28, Issue 12, p2993
- ISSN
0931-0509
- Publication type
Article
- DOI
10.1093/ndt/gft350