CXCR4基因轉染對骨髓間充質(zhì)干細胞體外生物學行為的影響
發(fā)布時間:2018-03-28 01:27
本文選題:骨髓間充質(zhì)干細胞 切入點:趨化因子受體CXCR 出處:《中國藥理學通報》2017年06期
【摘要】:目的觀察對轉染CXCR4基因的骨髓間充質(zhì)干細胞體外生物學行為的影響。方法將培養(yǎng)的骨髓間充質(zhì)干細胞分為3組,GFP組、CXCR4~+組、CXCR4~-組,轉染趨化因子受體CXCR4,并用免疫熒光細胞化學法、流式細胞儀法及Transwell小室細胞趨化實驗,體外研究了CXCR4高表達及低表達對MSCs增殖、分化與遷移能力的影響。結果 CXCR4高表達及低表達均不影響MSCs的增殖能力,對其向肺組織分化的能力也沒有影響。與GFP-MSCs組相比,CXCR4~+-MSCs組遷移的細胞數(shù)量明顯升高,而CXCR4~--MSCs組遷移細胞數(shù)量差異無顯著性。結論 CXCR4高表達及低表達不改變MSCs的增殖、分化能力,然而CXCR4高表達明顯增強MSCs向炎癥病灶的遷移能力。說明CXCR4高表達的MSCs移植入體后將會更快速、更大量地到達病變區(qū)域參與組織修復,明顯增強療效。
[Abstract]:Objective to observe the effect of transfection of CXCR4 gene on the biological behavior of bone marrow mesenchymal stem cells (BMSCs) in vitro. Methods the cultured BMSCs were divided into three groups: CXCR4- group and CXCR4- group. The chemokine receptor CXCR4 was transfected into CXCR4- group, and the chemokine receptor CXCR4 was transfected into CXCR4- group by immunofluorescence cytochemistry. The effects of high and low expression of CXCR4 on the proliferation, differentiation and migration of MSCs were studied by flow cytometry and chemotaxis assay of Transwell chamber. Results the high expression and low expression of CXCR4 did not affect the proliferation of MSCs. Compared with GFP-MSCs group, the number of migration cells in CXCR4 ~ -MSCs group was significantly increased, but there was no significant difference in the number of migration cells in CXCR4~--MSCs group. Conclusion the high and low expression of CXCR4 does not change the proliferation and differentiation ability of MSCs. However, the high expression of CXCR4 significantly enhanced the ability of MSCs to migrate to inflammatory focus, which indicated that MSCs with high expression of CXCR4 would reach the lesion area more quickly and participate in tissue repair, and enhance the curative effect obviously.
【作者單位】: 遼寧中醫(yī)藥大學藥學院藥理學教研室;大連醫(yī)科大學;
【基金】:國家自然科學基金資助項目(No 81273923)
【分類號】:R329.2
【相似文獻】
相關期刊論文 前1條
1 倪吉祥;劉先哲;查運紅;梅元武;;Snail基因修飾對骨髓間充質(zhì)干細胞CXCR4表達水平及向SDF-1趨化能力的影響[J];生物工程學報;2009年02期
,本文編號:1674154
本文鏈接:http://sikaile.net/xiyixuelunwen/1674154.html
最近更新
教材專著