大鼠创伤性深静脉血栓形成中Ca2+通道相关基因表达研究

分析Ca2 通道相关关键基因在大鼠创伤性肢体深静脉血栓形成中的表达变化,初步探讨该信号通路在此病理过程中的生物学意义。采用定量击打双侧大腿 双后肢石膏固定的方式,对150只SD大鼠造模,建立创伤性深静脉血栓形成动物模型。应用Genechip Rat Genome 430 2.0芯片,检测创伤性深静脉血栓形成过程中8种不同生物学状态下(正常对照、创伤即刻、血栓形成初始期、高峰期血栓形成、高峰期血栓不形成、血栓消退、血栓不消退、血栓不形成)股静脉RNA表达情况,筛查出差异表达基因,并进行pathway分析。重点关注高峰期血栓形成与不形成两种生物学状态下C,a2 通道相关关键基因表达变化。结果显示:高峰期血栓形成组与不形成组比较,Ca2 通道中CaMK、IP3 3K、CaN等多个关键基因表达均呈现下调,可能使包括内皮细胞在内的多种血管细胞,增殖、分化、代谢等功能受到抑制,并影响下游信号通路,引起组织细胞功能失调,最终导致血栓发生。因此,推测Ca2 通道功能受抑制可能与TDVT发生有关。

The Study of Genes Expressions Related to Ca2+ Signaling Pathway in a Rat Model of Traumatic Deep Vein Thrombosis

Based on the analysis of the juncture gene expressional changes related to Ca2 signaling pathway in a rat model of traumatic deep vein thrombosis(TDVT),to initially explore the biological significance of this pathway in TDVT.Beating on bilateral posterior limbs combined with hip spica cast fixation was applied in 150 SD rats to establish the TDVT rat model.Under 8 different biological states,(the control,the post-traumatic instant,the initial period of thrombosis,with and without thrombosis at the crest-time,thrombi solution,thrombi insolution and no thrombosis),the RNA expression in femoral vein was detected through Genechip Rat Genome 430 2.0 gene chips.Then the differential expression genes were selected for pathway analysis.The genes related to Ca2 signaling pathway in the two biological states at the crest-time of thrombosis(with and without thrombosis)was studied mainly.The results showed that at the crest-time of thrombosis,a series of juncture genes including CaMK,IP3 3K,CaN,etc.were down-regulated in thrombosis group compared with no thrombosis group at the crest-time.These changes could inhibit the functions(proliferation,differentiation,metabolism,etc.) of several vascular cells including endothelial cell and affect following pathways.Finally,thrombosis would be resulted from cell dysfunction.Thus,it is concluded that the inhibition of Ca2 signaling pathway may be related to TDVT.