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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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在KLF4相关的实验性细胞病变中,特定于细胞的STAT3删除

Yogesh Gowthaman1, Chelsea C Estrada1,2, Joseph Kim1

  • 1Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, NY.

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向细胞中的STAT3信号,可以防止由克鲁佩尔样因子4 (Klf4) 损失引起的损伤. 这种方法可以阻止细胞损失,细胞激活和焦点分片样硬化 (FSGS) 的发展,从而保持功能.

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科学领域:

  • 肝脏病学
  • 分子生物学
  • 遗传学

背景情况:

  • 多种类型的血小板炎和焦点细分血小板硬化 (FSGS) 的关键特征是细胞损失和表皮细胞激活.
  • 特别是在受体细胞中的克鲁佩尔样因子4 (Klf4) 损失会触发异常的球STAT3激活,导致受体细胞枯竭,细胞增殖和FSGS.
  • 虽然系统性STAT3抑制显示出有前途,但 podocyte STAT3在调解Klf4损失效应中的内在作用仍然不清楚.

研究的目的:

  • 调查是否可以通过抑制细胞内部的STAT3信号来预防由Klf4缺乏引起的FSGS表型.
  • 阐明细胞内在STAT3激活对Klf4缺陷驱动的FSGS病变的直接贡献.

主要方法:

  • 在 podocytes (Klf4ΔPodStat3ΔPod) 中同时有条件淘汰的小鼠的生成和表征.
  • 从人类细胞活检 (Nephroseq) 和大量RNA-seq数据 (NEPTUNE) 分析基因表达阵列,以评估质细胞疾病中的STAT3信号.
  • 使用基于scRNA-seq的解卷方法来确定FSGS和对照样本中的细胞特异性STAT3基因表达.

主要成果:

  • 与Klf4PodStat3Pod小鼠相比,Klf4Pod小鼠没有显著的细胞损失,细胞激活,FSGS病变,白蛋白尿或功能障碍.
  • 这些小鼠也表现出减少的状肌纤维细胞和恢复的整体存活率.
  • 患有血管炎的人类脏活检显示了富含的STAT3信号基因,与eGFR负相关,细胞表现出这些基因的更高表达.

结论:

  • 足以抵消Klf4损失的有害影响.
  • 这种向性抑制可以防止FSGS的发展,包括细胞损失,细胞激活,膜尿和功能衰竭.
  • 这些发现突出显示细胞STAT3是Klf4缺陷引起的病的关键调解者.