【摘要】：目的:探討交聯(lián)CD44分子對(duì)人肥大細(xì)胞白血病HMC-1細(xì)胞株Fas表達(dá)及其介導(dǎo)的細(xì)胞凋亡的影響。方法:應(yīng)用流式細(xì)胞術(shù)檢測(cè)HMC-1細(xì)胞表面CD44及Fas的表達(dá),并觀察透明質(zhì)酸(native hyaluronan,HA)、低分子質(zhì)量透明質(zhì)酸(fragmented hyaluronan,F-HA)處理或抗體交聯(lián)CD44分子后細(xì)胞表面Fas表達(dá)的變化,進(jìn)而檢測(cè)PI3K、PKC及MAPK信號(hào)通路抑制劑、蛋白質(zhì)合成抑制劑和肌動(dòng)蛋白聚合抑制劑對(duì)CD44分子交聯(lián)后細(xì)胞表面Fas表達(dá)的影響,用Northern雜交技術(shù)檢測(cè)交聯(lián)CD44對(duì)Fas mRNA表達(dá)的影響,用Annexin V/PI雙染法檢測(cè)交聯(lián)CD44、HA或F-HA對(duì)Fas介導(dǎo)的細(xì)胞凋亡的影響。結(jié)果:HMC-1細(xì)胞高表達(dá)CD44而低表達(dá)Fas,交聯(lián)CD44分子顯著上調(diào)細(xì)胞表面Fas的表達(dá)(P0.05),而Fas mRNA轉(zhuǎn)錄水平?jīng)]有明顯變化;肌動(dòng)蛋白聚合抑制劑細(xì)胞松弛素B能抑制CD44上調(diào)的Fas表達(dá)(P0.05),所檢測(cè)細(xì)胞信號(hào)通路抑制劑和蛋白質(zhì)合成抑制劑均未能抑制Fas表達(dá)的上調(diào)(P0.05);F-HA和交聯(lián)CD44均能夠促進(jìn)Fas介導(dǎo)的細(xì)胞凋亡(P0.05)。結(jié)論:CD44分子可上調(diào)HMC-1細(xì)胞的Fas表達(dá)并放大Fas介導(dǎo)的細(xì)胞凋亡,CD44分子可能成為肥大細(xì)胞白血病治療的新靶點(diǎn)。
[Abstract]:Aim: to investigate the effect of cross-linked CD44 on Fas expression and apoptosis in HMC-1 cells of human mast cell leukemia. Methods: flow cytometry was used to detect the expression of CD44 and Fas on the surface of HMC-1 cells, and to observe the expression of native hyaluronan,HA and (fragmented hyaluronan, of low molecular weight hyaluronic acid. The changes of Fas expression on cell surface were detected after F-HA treatment or antibody crosslinking CD44 molecule, and then PI3K,PKC and MAPK signal pathway inhibitors were detected. The effects of protein synthesis inhibitor and actin polymerization inhibitor on the expression of Fas on the cell surface after CD44 molecular crosslinking were studied. The effect of cross-linked CD44 on Fas mRNA expression was detected by Northern hybridization, and cross-linked CD44, was detected by Annexin V/PI double staining. Effect of HA or F-HA on apoptosis mediated by Fas. Results: high expression of CD44 and low expression of Fas, crosslinked CD44 in HMC-1 cells significantly up-regulated the expression of Fas on the cell surface (P0.05), while the level of Fas mRNA transcription did not change significantly. Actin polymerization inhibitor cytochalasin B could inhibit the up-regulated Fas expression of CD44 (P0.05). Neither the signal pathway inhibitor nor protein synthesis inhibitor could inhibit the up-regulation of Fas expression (P0.05). Both F-HA and CD44 could promote apoptosis mediated by Fas (P0.05). Conclusion: CD44 can up-regulate the expression of Fas in HMC-1 cells and amplify the apoptosis mediated by Fas. CD44 may be a new target for the treatment of mast cell leukemia.
【作者單位】： 河北醫(yī)科大學(xué)第四醫(yī)院腫瘤研究所免疫室;河北醫(yī)科大學(xué)第四醫(yī)院科研中心;產(chǎn)業(yè)醫(yī)科大學(xué)附屬病院第一內(nèi)科;
【基金】：國(guó)家自然科學(xué)基金資助項(xiàng)目(No.81402228) 河北省自然科學(xué)基金資助項(xiàng)目(No.H2015206216) 河北省醫(yī)學(xué)基金資助項(xiàng)目(No.ZL20140334) 河北省教育基金資助項(xiàng)目(No.QN2014049)~~
【分類號(hào)】：R733.7

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本文編號(hào)：2429711