• 中文核心期刊要目总览
  • 中国科技核心期刊
  • 中国科学引文数据库(CSCD)
  • 中国科技论文与引文数据库(CSTPCD)
  • 中国学术期刊文摘数据库(CSAD)
  • 中国学术期刊(网络版)(CNKI)
  • 中文科技期刊数据库
  • 万方数据知识服务平台
  • 中国超星期刊域出版平台
  • 国家科技学术期刊开放平台
  • 荷兰文摘与引文数据库(SCOPUS)
  • 日本科学技术振兴机构数据库(JST)
王光, 王永峰, 李江岚, 彭如及, 梁馨尹, 陈学东, 姜桂华, 史进方, 司马杨虎, 徐世清. 2022: 高蛋白血症诱导的动物模型中血细胞稳态失衡的机制. 动物学研究, 43(3): 301-318. DOI: 10.24272/j.issn.2095-8137.2021.397
引用本文: 王光, 王永峰, 李江岚, 彭如及, 梁馨尹, 陈学东, 姜桂华, 史进方, 司马杨虎, 徐世清. 2022: 高蛋白血症诱导的动物模型中血细胞稳态失衡的机制. 动物学研究, 43(3): 301-318. DOI: 10.24272/j.issn.2095-8137.2021.397
Guang Wang, Yong-Feng Wang, Jiang-Lan Li, Ru-Ji Peng, Xin-Yin Liang, Xue-Dong Chen, Gui-Hua Jiang, Jin-Fang Shi, Yang-Hu Si-Ma, Shi-Qing Xu. 2022: Mechanism of hyperproteinemia-induced blood cell homeostasis imbalance in an animal model. Zoological Research, 43(3): 301-318. DOI: 10.24272/j.issn.2095-8137.2021.397
Citation: Guang Wang, Yong-Feng Wang, Jiang-Lan Li, Ru-Ji Peng, Xin-Yin Liang, Xue-Dong Chen, Gui-Hua Jiang, Jin-Fang Shi, Yang-Hu Si-Ma, Shi-Qing Xu. 2022: Mechanism of hyperproteinemia-induced blood cell homeostasis imbalance in an animal model. Zoological Research, 43(3): 301-318. DOI: 10.24272/j.issn.2095-8137.2021.397

高蛋白血症诱导的动物模型中血细胞稳态失衡的机制

Mechanism of hyperproteinemia-induced blood cell homeostasis imbalance in an animal model

  • 摘要: 高蛋白血症是一种以血浆蛋白浓度(PPC)显著升高为指标的严重代谢紊乱疾病,临床常并发于多种恶性疾病或重度感染。然而,由于临床无法剥离原发性疾病的影响,目前对高PPC的分子机理研究甚少。该文在无脊椎模式动物家蚕中构建了一个原发性高蛋白血症动物模型,调查了高PPC对循环血细胞的影响。结果发现,高PPC严重影响血细胞稳态,导致活性氧水平升高,诱导了依赖内质网-钙离子信号途径的血细胞程序性死亡发生。另一方面,高PPC通过激活血细胞的JAK/STAT信号通路,诱导以颗粒细胞为主的血细胞增殖。补充内分泌激素活性物质20E治疗后,能够显著减轻高PPC对循环血细胞稳态的影响。因此,该文发现了一条高PPC影响血细胞稳态不同于高血糖、高血脂和高胆固醇的信号通路。此外发现,造血因子Gcm的基因表达下调可作为潜在的高蛋白血症早期检测指标。

     

    Abstract: Hyperproteinemia is a metabolic disorder associated with increased plasma protein concentration (PPC) and is often clinically complicated by malignant diseases or severe infections. At present, however, research on the molecular mechanism underlying high PPC (HPPC) is scant. Here, an animal model of primary hyperproteinemia was constructed in an invertebrate (Bombyx mori) to investigate the effects of HPPC on circulating blood cells. Results showed that HPPC affected blood cell homeostasis, leading to increased reactive oxygen species levels, and induced programmed cell death dependent on the endoplasmic reticulum-calcium ion signaling pathway. HPPC induced the proliferation of blood cells, mainly granulocytes, by activating the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. Supplementation with the endocrine hormone active substance 20E significantly reduced the impact of HPPC on blood cell homeostasis. Thus, we identified a novel signaling pathway by which HPPC affects blood cell homeostasis, which differs from hyperglycemia, hyperlipidemia, and hypercholesterolemia. In addition, we showed that down-regulation of gene expression of the hematopoietic factor Gcm could be used as a potential early detection indicator for hyperproteinemia.

     

/

返回文章
返回