慢性高原病患者骨髓有核紅細胞Ras-GTP分泌水平及BRaf、MEK、ERK1、ERK2 mRNA表達變化
發(fā)布時間:2018-02-02 12:45
本文關(guān)鍵詞: 高原病 骨髓有核紅細胞 Ras/Raf/MEK/ERK信號通路 出處:《山東醫(yī)藥》2016年03期 論文類型:期刊論文
【摘要】:目的觀察慢性高原病(CMS)患者骨髓有核紅細胞Ras相關(guān)GTP酶(Ras-GTP)分泌水平及B型絲/蘇氨酸蛋白激酶(BRaf)、絲裂原活化蛋白激酶(MEK)、細胞信號調(diào)節(jié)激酶1(ERK1)、細胞信號調(diào)節(jié)激酶2(ERK2)表達變化。方法 CMS患者15例(觀察組),單純陳舊性骨折患者15例(對照組),采用ELISA法檢測骨髓有核紅細胞Ras-GTP,實時熒光定量PCR法檢測骨髓有核紅細胞BRaf、MEK、ERK1、ERK2 mRNA。結(jié)果與對照組比較,觀察組Ras-GTP分泌水平升高,BRaf、MEK、ERK1、ERK2 mRNA的相對表達量增加(P均0.05)。觀察組Ras-GTP、Braf mRNA、MEK mRNA、ERK1 mRNA、ERK2 mRNA與HGB呈正相關(guān)(r分別為0.860、0.849、0.653、0.773、0.746,P均0.01)。結(jié)論 CMS患者骨髓有核紅細胞Ras-GTP分泌水平及BRaf、MEK、ERK1、ERK2表達升高,Ras/Raf/MEK/ERK通路可能與CMS紅細胞的過度累積有關(guān),推測其可能是CMS發(fā)病機制中的重要通路之一。
[Abstract]:Objective to observe the level of Ras-GTPsecretion of nucleated red blood cells (Ras) and B-type serine / threonine protein kinase (BRafA) in patients with chronic high altitude disease (CMS). The expression of mitogen activated protein kinase (MEKK), cell signal regulated kinase 1 (ERK1) and cell signal regulated kinase (2 ERK2) were observed in 15 patients with CMS (observation group). Ras-GTPof nucleated erythrocytes in bone marrow was detected by ELISA method and BRaf of nucleated erythrocytes in bone marrow was detected by real-time fluorescence quantitative PCR in 15 patients with simple old fracture (control group). Results compared with the control group, the level of Ras-GTP secretion in the observation group was higher than that in the control group. The relative expression of ERK2 mRNA was increased (P < 0.05). The Ras-GTPTP-Braf mRNA-MEK mRNA-ERK1 mRNA was observed in the observation group. The positive correlation between ERK2 mRNA and HGB was 0.860 ~ 0. 849 ~ 0. 653 ~ 0. 773 ~ 0. 746, respectively. Conclusion the level of Ras-GTP secretion and the expression of ERK1 ERK2 in bone marrow nucleated erythrocytes in patients with CMS were increased. The Ras/Raf/MEK/ERK pathway may be related to the excessive accumulation of CMS erythrocytes, which may be one of the important pathways in the pathogenesis of CMS.
【作者單位】: 青海大學(xué)醫(yī)學(xué)院;青海大學(xué)附屬醫(yī)院;青海大學(xué);青海省人民醫(yī)院;
【基金】:青海省科技廳國際合作項目(2014-HZ-808) 國家自然科學(xué)基金資助項目(81441116) 青海省科技廳(應(yīng)用)基礎(chǔ)研究計劃項目(2012-Z-729)
【分類號】:R594.3
【正文快照】: 慢性高原病(CMS)既往又稱為高原紅細胞增多癥,以過度紅細胞增多和嚴重低氧血癥為特征[1],并伴有血紅蛋白(HGB)及紅細胞壓積升高,但目前其發(fā)病機制尚未完全闡明。研究[2]認為,CMS發(fā)生病理生理改變的主要機制是機體對高原環(huán)境失適應(yīng),導(dǎo)致細胞內(nèi)低氧,引起低氧誘導(dǎo)因子表達增加,促
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