首页|LncRNA MALAT1靶向调控miR-155抑制炎症性肠病肠道上皮细胞损伤

LncRNA MALAT1靶向调控miR-155抑制炎症性肠病肠道上皮细胞损伤

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[目的]探究LncRNA MALAT1与miR-155在炎症性肠病肠道损伤中的作用。[方法]用实时荧光定量PCR分析YAMC细胞的MALAT1与miR-155水平。将YAMC细胞分为4组:si NC组、si MALAT1组、miR NC组和miR-155 mimic组。采用荧光素酶报告基因实验分析MALAT1与miR-155的作用关系。采用流式细胞术分析细胞凋亡率。采用细胞克隆形成实验分析细胞生长能力。采用酶联免疫吸附剂测定炎症因子水平。[结果]TNF-α处理YAMC 细胞后，MALAT1 表达水平降低(0。98±0。02 vs 0。23±0。01，P＜0。05)，miR-155 表达水平增加(0。98±0。02 vs 0。23±0。01，P＜0。05)。si MALAT1 组的 YAMC 细胞形成集落数量显著降低(68。28±8。02 vs 38。53±7。01，P＜0。05);miR-155 mimic 组的 YAMC 细胞形成集落数量显著降低(73。56±10。32 vs 30。13±6。21，P＜0。05)。si MAL-AT1 组的 YAMC 细胞凋亡率显著增加(20。18±1。02 vs 33。61±6。21，P＜0。05);miR-155 mimic 组的 YAMC 细胞凋亡率显著增加(22。37±3。61 vs 60。31±10。61，P＜0。05)。si MALAT1组的YAMC细胞炎症因子水平显著增加(P＜0。05);miR-155 mimic组的YAMC细胞炎症因子水平显著增加(P＜0。05)。在MALAT1 WT组中转染miR-155 mimic后荧光素酶活性显著降低(1。01±0。11vs0。43±0。02，P＜0。05)。[结论]LncRNA MALAT1能够促进炎症性肠病肠道上皮细胞生长，并抑制肠道上皮细胞凋亡，减少炎症因子释放，这一作用可能与MALAT1靶向抑制miR-155表达有关。
LncRNA MALAT1 targets miR-155 to inhibit intestinal epithelial cell injury in inflammatory bowel disease
[Objective]To investigate the role of LncRNA MALAT1 and miR-155 in intestinal injury in inflammatory bowel disease.[Method]MALAT1 and miR-155 levels were analyzed by real-time fluorescence quantitative PCR.The YAMC cells were divided into 4 groups:si NC group,si MALAT1 group,miR NC group and miR-155 mimic group.The luciferase reporter gene assay was used to analyze the relationship between the action of MALAT1 and miR-155.Flow cytometry was used to ana-lyze the apoptosis rate.Cell growth ability was analyzed using cell clone formation assay.The levels of inflammatory factors were measured using enzyme-linked immunosorbent.[Result]The expression levels of MALAT1 decreased(0.98±0.02 vs 0.23±0.01,P＜0.05)and miR-155 increased(0.98±0.02 vs 0.23±0.01,P＜0.05)after TNF-α treatment of YAMC cells.si MALAT1 group had a significantly lower number of YAMC cells forming colonies(68.28±8.02 vs 38.53±7.01,P＜0.05);miR-155 mimic group had a significantly lower number of YAMC cells forming colonies(73.56±10.32 vs 30.13±6.21,P＜0.05).The rate of YAMC cell apoptosis was significantly increased in the si MALAT1 group(20.18±1.02 vs 33.61±6.21,P＜0.05);the rate of YAMC cell apoptosis was significantly increased in the miR-155 mimic group(22.37±3.61 vs 60.31±10.61,P＜0.05).si MALAT1 group had significantly increased levels of inflammatory factors in YAMC cells(P＜0.05);the levels of inflammatory factors in YAMC cells were significantly increased in the miR-155 mimic group(P＜0.05).The luciferase activity was significantly decreased after transfection of miR-155 mimic in MALAT1 WT group(1.01±0.11 vs 0.43±0.02,P＜0.05).[Conclusion]LncRNA MALAT1 can promote the growth of intestinal epithelial cells in inflammatory bowel disease and inhibit apoptosis of intestinal epithelial cells and reduce the release of inflammatory factors,and this effect may be related to the targeting of MALAT1 to inhibit miR-155 expression.

LncRNA MALAT1miR-155inflammatory bowel diseaseintestinal injuryepithelial cellsapoptosis

郭峰健、诸葛萦、王俊珊

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同济大学附属上海市第十人民医院崇明分院消化内科,上海 202157

上海交通大学附属第一人民医院心内科,上海 200085

同济大学附属上海市第十人民医院消化内科,上海 200072

LncRNA MALAT1 miR-155 炎症性肠病 肠道损伤 上皮细胞 凋亡

上海市崇明区可持续发展科技创新行动计划(2020)上海市第十人民医院院内课题上海市松江区科委科技攻关计划重点课题上海交通大学转化医学国家重大科技基础设施(上海)开放课题

CKY-2020-0504.03.18.0622020SJ288TMSK-2021-149

2024

10.16519/j.cnki.1004-311x.2024.02.0028

生物技术
黑龙江省微生物学会 黑龙江省生物工程学会 黑龙江省科学院微生物研究所

生物技术

CSTPCD
影响因子：0.611
ISSN：1004-311X
年,卷(期)：2024.34(2)
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