siRNA-medicated silencing of TRPM7 promotes polarization in differentiated HL-60 cells

吴娴波; 邹文英; 蔡春青; 陈新宏; 邹飞; 孟晓静

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siRNA-medicated silencing of TRPM7 promotes polarization in differentiated HL-60 cells

更新时间：2026-01-09

- siRNA-medicated silencing of TRPM7 promotes polarization in differentiated HL-60 cells
- Journal of Army Medical University Vol. 35, Issue 18, Pages: 1910-1914(2013)
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  CLC： R392.12;R394-33;R394.3
- Published：2013
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吴娴波,邹文英,蔡春青,陈新宏,邹飞,孟晓静.TRPM7对dHL-60细胞极性化的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(18):1910-1914.

　Wu Xianbo,Zou Wenying,Cai Chunqing,Chen Xinhong,Zou Fei,Meng Xiaojing.siRNA-medicated silencing of TRPM7 promotes polarization in differentiated HL-60 cells[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(18):1910-1914.
吴娴波,邹文英,蔡春青,陈新宏,邹飞,孟晓静.TRPM7对dHL-60细胞极性化的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(18):1910-1914. DOI：

　Wu Xianbo,Zou Wenying,Cai Chunqing,Chen Xinhong,Zou Fei,Meng Xiaojing.siRNA-medicated silencing of TRPM7 promotes polarization in differentiated HL-60 cells[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(18):1910-1914. DOI：

摘要

目的探讨瞬时受体电位M7(transient receptor potential melastatin 7，TRPM7)对dHL-60细胞极性化的影响及可能的分子机制。方法通过siRNA技术下调dHL-60细胞TRPM7蛋白表达，分为转染无义干扰片段的对照组和TRPM7干扰组，用Zigmond小室观察细胞极性化的变化，采用Western blot检测TRPM7和磷酸化AKT的表达，并用细胞免疫荧光方法观察磷酸化AKT的定位情况。结果与转染无义干扰片段的对照组相比，转染TRPM7靶向siRNA的dHL-60细胞中，TRPM7蛋白表达水平明显降低（

0.05）；干扰TRPM7后dHL-60细胞的极性化率与对照组相比显著增加（P0.05）；磷酸化AKT表达明显上调，并从细胞质转向了细胞膜，呈极性分布在细胞质膜上，而总AKT的表达则无明显变化。AKT的特异性抑制剂Triciribine可使dHL-60细胞在fMLP刺激下的磷酸化AKT的极性分布消失。结论 TRPM7通过AKT信号通路调控细胞极性相关分子，进而影响dHL-60细胞的极性化能力。

Abstract

Objective To determine the effect of silencing transient receptor potential melastatin 7 (TRPM7) gene on the polarization of differentiated HL-60 (dHL-60) cells. Methods Small interfering RNA (siRNA) targeting TRPM7 or targeting nonsense codons were used to transfected dHL-60 cells

and then cell polarization was observed in Zigmond chamber. Western blotting was used to examine the expression of TRPM7 and phosphorylated AKT in the transfected cells. Immunofluorescence staining was used to detect the location of phosphorylated AKT. Results Compared with th

e control cells transfected with nonsense codons

the dHL-60 cells transfected with TRPM7-specific siRNA significantly decreased the protein expression of TRPM7 (

0.05)

increased cell polarization and expression of phosphorylated AKT significantly (

0.05)

and translocated the phosphorylated AKT from the cytoplasm to cell membrane in a polarized distribution

though no change was found in total AKT. The polarized distribution of AKT disappeared when the fMLP-stimulted dHL-60 cells were pretreated with triciribine

an AKT specific inhibitor. Conclusion TRPM7 regulates the dHL-60 cell polarization probably by AKT pathway.

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