足细胞

本文应用组织学和电镜技术对性早熟与未成熟雄性大黄鱼精巢中间质细胞和足细胞进行显微与亚显微结构的研究。

Microstructure and submicrostructure of Leydig cell and Sertoli cell in the testis of gonadal precocity and immature in cultured large yellow croakers were studied using histology and electron microscopic technique .

大黄鱼性早熟的机制：精巢中间质细胞和足细胞的显微与亚显微结构

Mechanism of gonadal precocity in cultured Pseudosciaena crocea : a study of microstructure and submicrostructure of Leydig cell and Sertoli cell in testis

多胚水稻品系APⅣ反足细胞多样性的观察

Observation on diversity of antipodal cells in polyembryonic rice strain ap ⅳ

吡格列酮还能显著减轻PAN诱导的足细胞凋亡和坏死，而恢复足细胞的分化功能。

Further , pioglitazone significantly decreased PAN-induced podocyte apoptosis and necrosis while restoring podocyte differentiation .

高糖通过ERK（1/2）途径调节足细胞产生明胶酶B

High glucose regulates the production of MMP-9 in podocyte through ERK_ ( 1 / 2 ) signal pathway

在PAN肾病模型第3和第10天，透射电镜显示足细胞足突融合；

The foot process fusion was seen on the third and tenth days following the injection of PAN ;

目的了解足细胞上晚期糖基化产物受体（RAGE）激活后的细胞内信号的传导途径。

Objective To investigate the signalling events follow the activation of RAGE in podocytes .

目的：（1）观察肾小球足细胞上结缔组织生长因子（ConnectiveTissueGrowthFactor，CTGF）的表达，以及转化生长因子？

Objective : ( 1 ) To observe the expression and regulation of connective tissue growth factor ( CTGF ) by transforming growth factor ?

结果：ANGⅡ诱导足细胞凋亡呈时间和剂量依赖性；

Results : ANG ⅱ promoted podocyte apoptosis in a time and dose dependent manner ;

我们利用氨基核苷嘌呤霉素（PAN）肾脏损伤模型在小鼠永生足细胞中检验了这些可能性。

We tested these possibilities utilizing the puromycin aminonucleoside ( PAN ) model of renal injury in immortalized mouse podocytes .

结论足细胞上RAGE激活后，通过ROS-p21Ras-ERK信号途径诱导足细胞表达MCP-1。

Conclusion Activation of RAGE induces MCP-1 expression in podocytes via ROS-ERK signalling pathway .

醛固酮抑制Akt活性诱导大鼠足细胞凋亡

Aldosterone inhibits Akt activation and induces apoptosis in rat podocytes

方法：以体外培养的小鼠肾小球足细胞为研究对象，应用Western印迹分析技术，检测高糖刺激不同时间对足细胞表达CTGF蛋白的影响。

Methods : The effects of high glucose on the expression of CTGF and its receptor LRP were analyzed by western blotting .

抑制FAK的活化可改善ox-LDL诱导的足细胞损伤。

Inhibition of FAK activation ameliorated podocyte injury induced by ox-LDL .

FAK在ox-LDL诱导的足细胞损伤过程中激活。

FAK was activated in podocytes treated with ox-LDL .

长期高糖环境对足细胞上CTGF的受体LRP蛋白的表达无影响。

Long-term high glucose had no effect on the expression of LRP in podocytes .

结果ALD以时间和剂量依赖方式诱导足细胞凋亡。

Results ALD induced podocyte apoptosis in a dose - and time-dependent manner .

多聚酶链反应（RT-PCR）检测足细胞盐皮质激素受体（MR）和11β-羟类固醇脱氢酶2（11β-HSD2）mRNA表达。

RT-PCR was used to examine the expression of mineralocorticoid receptor ( MR ) and 11 Beta-hydroxysteroid dehydrogenase type 2 ( 11 β - HSD2 ) mRNA in podocyte .

50ng/mlIL-13作用24小时即可造成足细胞明显损伤。

50ng / ml IL-13 treated for 24 hours can damage podocyte distinctly .

在各个时间点，长期高糖环境对足细胞CTGF的受体LRP蛋白没有明显作用。

High glucose had no effect on the expression of LRP protein at each time point .

使用MTS法及流式细胞学方法检测足细胞的细胞增殖活性及凋亡率。

MTS assay and flow cytometry method were performed for detection of podocyte cell proliferation activity and apoptotic rate .

正常情况下VEGF在足细胞合成，以旁分泌的形式作用于临近EC表面的VEGF受体，是维持毛细血管袢完整和EC增殖的必要条件。

VEGF is synthesized in podocytes and will paracrine to VEGF receptors on jacent ECs which is the essential condition of EC proliferation and the glomerular capillary loop maintenance .

1,25-二羟基维生素D3减少Heymann肾炎鼠足细胞凋亡脱落

1,25-Dihydroxyvitamin D_3 Decreases Podocyte Apoptosis and Detachment in Rats with Passive Heymann Nephritis

血管紧张素Ⅱ灌注诱导nephrin表达改变与足细胞凋亡

Angiotensin ⅱ infusion induces nephrin expression change and podocyte apoptosis

SngⅡ灌注14d时，足细胞裂隙膜变窄；

At day 14 , Ang ⅱ infusion induced the narrowing of slit diaphragm .

蛋白尿是难溶性补体C5b-9攻击足细胞的结果。

Proteinuria is a consequence of sublytic complement C5b-9 attack on podocytes .

人肾小球足细胞表达Nephrin的体外研究

Expression of nephrin by human glomerular podocyte in vitro

方法以RT-PCR和ELISA的方法检测AGE、羰甲基化白蛋白（CML）、S100蛋白和RAGE中和抗体对小鼠足细胞的MCP-1的基因和蛋白质表达的影响。

MethodsThe effects of AGE , CML , S100 protein and neutralizing antibody against RAGE on MCP-1 gene and protein expressions were examined by RT-PCR and ELISA in mouse podocytes .

但是糖尿病可使这一平衡遭到破坏，ROS产生增多或清除减少，导致ROS在体内蓄积而引起多种肾脏细胞尤其是足细胞损伤。

ROS generation increasing or ROS clearing reduction result in accumulate of ROS in the body which will lead to kidney cells damage , especially podocyte cell injury .

细胞培养及分组：体外培养永生化小鼠足细胞系（由哈佛医学院PeterMundel教授惠赠）。

Cell culture . Conditionally immortalized mouse podocytes were kindly provided by Professor Peter Mundel ( Harvard Medical School ) .