Department of Structural Pathology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Cooperative Laboratory of Electron Microscopy, Niigata University, Niigata, Japan.
Cell Tissue Res. 2021 Oct;386(1):117-126. doi: 10.1007/s00441-021-03511-x. Epub 2021 Jul 26.
Fibroblast growth factor 2 (FGF2) augments podocyte injury, which induces glomerulosclerosis, although the mechanisms remain obscure. In this study, we investigated the effects of FGF2 on cultured podocytes with interdigitating cell processes in rats. After 48 h incubation with FGF2 dynamic changes in the shape of primary processes and cell bodies of podocytes resulted in the loss of interdigitation, which was clearly shown by time-lapse photography. FGF2 reduced the gene expressions of constituents of the slit diaphragm, inflections of intercellular junctions positive for nephrin, and the width of the intercellular space. Immunostaining for the proliferation marker Ki-67 was rarely seen and weakly stained in the control without FGF2, whereas intensely stained cells were frequently found in the presence of FGF2. Binucleation and cell division were also observed, although no significant increase in cell number was shown. An in vitro scratch assay revealed that FGF2 enhanced migration of podocytes. These findings show that FGF2 makes podocytes to transition from the quiescent state into the cell cycle and change their morphology due to enhanced motility, and that the culture system in this study is useful for analyzing the pathological changes of podocytes in vivo.
成纤维细胞生长因子 2 (FGF2) 可增强足细胞损伤,进而诱导肾小球硬化,但其具体机制仍不清楚。本研究旨在探讨 FGF2 对大鼠原代具有指状突起的足细胞的影响。孵育 48 小时后,FGF2 可引起足细胞原代突起和细胞体形状的动态变化,导致细胞间的相互交错消失,该现象通过延时摄影可清晰地显示出来。FGF2 降低了足突裂孔隔膜组成成分、nephrin 阳性细胞间连接的弯曲度和细胞间隙的宽度的基因表达。在没有 FGF2 的情况下,增殖标志物 Ki-67 的免疫染色很少见且染色较弱,而在存在 FGF2 的情况下,染色强烈的细胞频繁出现。双核和细胞分裂也观察到了,尽管细胞数量没有显著增加。体外划痕实验显示 FGF2 可增强足细胞的迁移。这些发现表明,FGF2 可使足细胞从静止状态进入细胞周期,并因增强的运动能力而改变其形态,本研究中的培养系统可用于分析体内足细胞的病理变化。