Podocyte expression of nonmuscle myosin heavy chain-IIA decreases in idiopathic nephrotic syndrome, especially in focal segmental glomerulosclerosis
Author(s) -
Kenichiro Miura,
Hidetake Kurihara,
Shigeru Horita,
Hiroko Chikamoto,
Motoshi Hattori,
Yutaka Harita,
Haruko Tsurumi,
Yuko Kajiho,
Yoko Sawada,
Satoshi Sasaki,
Takashi Igarashi,
Shinji Kunishima,
Takashi Sekine
Publication year - 2013
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gft350
Subject(s) - podocyte , nephrin , medicine , synaptopodin , focal segmental glomerulosclerosis , glomerulosclerosis , nephrotic syndrome , slit diaphragm , nephrosis , podocin , immunoelectron microscopy , endocrinology , pathology , immunohistochemistry , glomerulonephritis , kidney , proteinuria
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.
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