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氨肽酶N干扰腺病毒感染的子宫内膜间质细胞子宫内膜容受性因子表达情况观察 被引量:2

Expression of endometrial receptivity factors in endometrial stromal cells infected with ANPEP interference adenovirus
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摘要 目的观察氨肽酶N(ANPEP)干扰腺病毒感染人类子宫内膜间质细胞(hmESCs)后,细胞中子宫内膜容受性(ER)相关因子的表达变化。方法用刮匙轻刮取得正常妇女子宫腔内膜组织,分离培养hmESCs。将细胞分为干扰组和空载病毒组,分别加入ANPEP干扰腺病毒和空载腺病毒。感染48 h后,采用实时荧光定量PCR法检测两组ANPEPmRNA以及ER相关因子同源框基因A10(HOXA10)、整合素β3、白血病抑制因子(LIF)、白细胞介素1(IL-1)mRNA表达。结果与空载病毒组比较,干扰组ANPEPmRNA表达下调,HOXA10、整合素β3、LIFmRNA表达下降(P均<0.05),IL-1 mRNA表达无明显变化(P>0.05)。结论干扰hmESCs中ANPEP表达可影响ER因子表达,这可能是ANPEP参与调节ER的机制之一。 Objective To observe the expression changes of endometrial receptivity factors in human endometrial stromal cells(hmESCs)infected with aminopeptidase N(ANPEP)interference adenovirus Methods The hmESCs were isolated and cultured from the endometrial tissues of normal women by curettage.The cells were divided into the interfer⁃ence group and the no-load virus group,and ANPEP interference adenovirus and no-load adenovirus were added,respec⁃tively.At 48 h after infection,the mRNA expression levels of ANPEP and ER transcription factors HOXA10,integrinβ3,leukemia inhibitory factor(LIF)and interleukin-1(IL-1)were detected by real-time quantitative PCR.Results Com⁃pared with the no-load virus group,the mRNA expression of ANPEP was down-regulated,the mRNA expression levels of HOXA10,integrinβ3,and LIF were down-regulated in the interference group(all P<0.05),and there was no significant change in the mRNA expression of IL-1(P>0.05).Conclusion Interfering with the expression of ANPEP in hmESCs can affect the expression of ER,which may be one of the mechanisms by which ANPEP participates in the regulation of ER.
作者 水丽君 孟艳 郑圣霞 黄存 钱易 SHUI Lijun;MENG Yan;ZHENG Shengxia;HUANG Cun;QIAN Yi(Clinical Center of Reproductive Medicine,The First Affiliated Hospital of University of Science and Technology of China(Anhui Provincial Hospital),Hefei 230001,China;不详)
出处 《山东医药》 CAS 2021年第26期39-42,共4页 Shandong Medical Journal
基金 国家自然科学基金项目(81701517)。
关键词 人子宫内膜间质细胞 氨肽酶N 子宫内膜容受性 human endometrial stromal cells aminopeptidase N endometrial receptivity
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