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m iR-21在周围神经损伤时调控雪旺细胞凋亡

陆新华 王辉 宁昕杰 罗骏成 梁家骥

中国病理生理杂志Issue(11):2047-2052,6.
中国病理生理杂志Issue(11):2047-2052,6.DOI:10.3969/j.issn.1000-4718.2015.11.020

m iR-21在周围神经损伤时调控雪旺细胞凋亡

miR-21 inhibits apoptosis of Schwann cells following peripheral nerve in-jury

陆新华 1王辉 1宁昕杰 1罗骏成 1梁家骥1

作者信息

  • 1. 中山大学附属第三医院神经外科,广东广州510630
  • 折叠

摘要

Abstract

AIM:To explore the relationship and molecular mechanism between microRNA-21(miR-21) and Schwann cells ( SC) following peripheral nerve injury.METHODS: The mRNA expression of miR-21 and phosphatase and tensin homologue deleted on chromosome ten ( PTEN) in animal model were detected by real-time PCR.The over-ex-pression of miR-21 and inhibition of miR-21 expression in the Schwann cells according to transfection of lentiviral vectors were performed, the nonspecific miRNA was used as a negative control ( NC) .The cell apoptosis was measured by flow cy-tometry.The mRNA expression of miR-21 and PTEN in the cells was detected by real-time PCR.The protein expression of PTEN and cleaved caspase-3 was determined by Western blot.RESULTS: The level of miR-21 was significantly higher and the mRNA level of PTEN was significantly lower in the model of nerve injury than those in control group.miR-21 over-expression decreased the number of apoptotic Schwann cells compared with NC-SC.The mRNA expression of PTEN was down-regulated by over-expression of miR-21.The protein expression of PTEN and cleaved caspase-3 was down-regulated by over-expression of miR-21 (P<0.05).CONCLUSION: miR-21 may play an important role in the peripheral nerve injury through inhibiting apoptosis of Schwann cells by down-regulating the expression of PTEN.

关键词

周围神经损伤/微小RNA-21/雪旺细胞/细胞凋亡

Key words

Peripheral nerve injury/MicroRNA-21/Schwann cells/Apoptosis

分类

医药卫生

引用本文复制引用

陆新华,王辉,宁昕杰,罗骏成,梁家骥..m iR-21在周围神经损伤时调控雪旺细胞凋亡[J].中国病理生理杂志,2015,(11):2047-2052,6.

基金项目

国家自然科学基金资助项目(No.30901542);广东省自然科学基金自由申请项目(No.2014A030313055);产学研合作项目(No.2014B090901043);广东省科技计划(No.2012B031800056);中山大学高校基本业务费青年教师培育资助项目 ()

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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