中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (15): 2833-2837.doi: 10.3969/j.issn.1673-8225.2011.15.042

• 组织构建临床实践 clinical practice in tissue construction • 上一篇    下一篇

绝经后骨质疏松肾阴虚证相关基因的信息学分析

谢丽华,赵毅鹏,陈  可,赖玉链,葛继荣   

  1. 福建省中医药研究院中基室,福建省福州市 350003
  • 收稿日期:2010-12-17 修回日期:2011-03-10 出版日期:2011-04-09 发布日期:2013-11-06
  • 通讯作者: 葛继荣,博士,副研究员,福建省中医药研究院,福建省福州市 350003 gjrrjgcy@sohu. com
  • 作者简介:谢丽华★,女,1982年生,福建省沙县人,汉族,2007年福建师范大学毕业,硕士,助理研究员,主要从事医学分子生物学研究。 xlhat@163.com
  • 基金资助:

    课题受福建省自然科学基金项目(2009J01160)和福建省科技厅公益类科研院所自主选题项目(2009R10007-3)资助。

Bioinformatics analysis of genes expression profiles of postmenopausal osteoporosis with Kidney Yin deficiency

Xie Li-hua, Zhao Yi-peng, Chen Ke, Lai Yu-lian, Ge Ji-rong   

  1. Department of Basic Theory of Traditional Chinese Medicine, Fujian Institute of Chinese Medicine, Fuzhou  350003, Fujian Province, China
  • Received:2010-12-17 Revised:2011-03-10 Online:2011-04-09 Published:2013-11-06
  • Contact: Ge Ji-rong, Doctor, Associate researcher, Department of Basic Theory of Traditional Chinese Medicine, Fujian Institute of Chinese Medicine, Fuzhou 350003, Fujian Province, China gjrrjgcy@sohu.com
  • About author:Xie Li-hua★, Master, Assistant researcher, Department of Basic Theory of Traditional Chinese Medicine, Fujian Institute of Chinese Medicine, Fuzhou 350003, Fujian Province, China xlhat@163.com
  • Supported by:

    the Natural Science Foundation of Fujian Province, No. 2009J01160*; the Independent Topic Selection of Commonweal Scientific Institutes of Fujian Provincial Science and Technology Commission, No. 2009R10007-3*

摘要:

背景:在绝经后骨质疏松症患者中,不同中医证型在骨质疏松易感基因不同表型中分布存在差异,但其基因组学机制尚未见报道。
目的:通过基因表达谱的差比性分析,探讨绝经后骨质疏松症肾阴虚证相关基因的信息学特征。
方法:随机选择绝经后骨质疏松症受试者,分为肾阴虚证组4例,肾阳虚证组3例、非肾虚证组3例,并选择健康绝经后妇女3例设为正常对照组。用人全基因组表达谱芯片检测4组基因表达谱,肾阴虚证组分别与其他3组比较,筛选共同的差异表达基因,进行GO和Pathway分析。
结果与结论:肾阴虚证组与正常对照组、肾阳虚证组、非肾虚证组的差异表达基因分别为197,354和54条;肾阴虚证组与其他3组比较共同的差异表达基因有9条:PROK2,ASB1,MUC12,GSTM5,CLCF1,GPR27,C3orf35和未知基因chr3:113822408-113822347,chr18:34851804-34851745。与正常对照组相比,表达上调基因为GSTM5,MUC12,表达下调基因为GPR27,C3orf35,ASB1,CLCF1和PROK2。Pathway分析GSTM5参与谷胱甘肽代谢通路,CLCF1参与细胞因子与受体之间干扰通路和JAK-STAT信号转导通路。结果证实,绝经后骨质疏松症肾阴虚证与GPR27,ASB1,PROK2,CLCF1和GSTM5基因的表达有关,并与谷胱甘肽代谢通路、细胞因子与其受体相互作用通路和JAK-STAT信号转导通路存在关联。

关键词: 肾阴虚证, 绝经后骨质疏松症, 基因表达, 功能分类, 信号通路, 基因组学, 组织构建

Abstract:

BACKGROUND: Gene differential expression exists in various types of postmenopausal osteoporosis, but its genomics mechanism has not been studied and reported.
OBFECTIVE: Through analyzing the gene expression spectrum’s difference, to investigate characteristics of genes expression profiles of postmenopausal osteoporosis with Kidney Yin deficiency.
METHODS: By TCM syndrome, 13 patients with postmenopausal osteoporosis were randomly divided into three groups: kidney Yin deficiency (n=4), kidney Yang deficiency (n=3), non-kidney deficiency (n=3), another 3 healthy postmenopausal women also were selected as control group. Human gene expression microarrays were applied to explore gene expression spectrum's difference of the groups. Kidney Yin deficiency group was compared with other three groups respectively. The genes with common significant difference were studied by Go and Pathway analysis.
RESULTS AND CONCLUSION: Compared with control group, kidney Yang deficiency and non-kidney deficiency groups, there were 197, 354 and 54 genes expressed differentially in the kidney Yin deficiency group. Nine genes were expressed differentially among kidney Yin deficiency group with other three groups: PROK2, ASB1, MUC12, GSTM5, CLCF1, GPR27, C3orf35 and unknown genes chr3:113822408-11382234, chr18:34851804-34851745. Compared with control group, GSTM5 and MUC12 showed up-regulated expression, GPR27, C3orf35, ASB1, CLCF1 and PROK2 showed down-regulated expression. The pathway analysis showed GSTM5 was involved in glutathione metabolism, and CLCF1 was involved in cytokine-cytokine receptor interaction and Jak-STAT signaling. The pathogenesis of postmenopausal osteoporosis with kidney Yin deficiency is associated with the genes expression of GPR27, ASB1, PROK2, CLCF1 and GSTM5, and it has association with glutathione metabolism pathway, cytokine-cytokine receptor interaction pathway and Jak-STAT signaling pathway.

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