节点文献

Small RNA sequencing reveals differentially expressed miRNAs in necrotizing enteracolitis in rats

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 余仁强王敏姜善雨张颖慧周勤

【机构】 江苏省无锡市妇幼保健院新生儿科

【摘要】 Necrotizing enterocolitis(NEC) is the leading cause of death due to gastrointestinal disease in preterm infants.The role of miRNAs in NEC is still unknown.The objective of this study was to identify differentially expressed(DE) miRNAs in rats with NEC and analyze their possible roles.In this study,an NEC rat model was established using Sprague-Dawley rat pups.Next-generation RNA sequencing was used to analyze the miRNA expression profiles in the NEC and control rats.Gene ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analyses were carried out to identify target mRNAs for the DE miRNAs and to explore their potential roles.The DE miRNAs were verified by real-time quantitative PCR(RTqPCR).The status of intestinal injury as well as the elevated levels of inflammatory cytokines in the NEC group confirmed that the NEC model was successfully established.16 miRNAs were found to be differentially expressed between the NEC group and the control group of rats.Bioinformatics analysis indicated that the parental genes of the DE miRNAs were predominantly implicated in the phosphorylation,cell migration and protein phosphorylation processes.Moreover,the DE miRNAs were mainly found to be involved in the pathways of axon guidance,endocytosis and focal adhesion,as well as,in the Wnt signaling pathway,which is related to colitis.The expression patterns of the candidate miRNAs(rno-miR-27 a-5 p and mo-miR-187-3 p),as assessed by RT-qPCR,were in accordance with the expression patterns obtained by miRNA-sequencing.The miRNA-mRNA-pathway network revealed that mo-miR-27 a-5 p and mo-miR-187-3 p might be involved in NEC via the Wnt signaling pathway.We found an altered miRNA expression pattern in rats with NEC.We hypothesize that rno-miR-27 a-5 p and rno-miR-187-3 p might mediate the NEC pathophysiological processes via the Wnt signaling pathway.

【Abstract】 Necrotizing enterocolitis(NEC) is the leading cause of death due to gastrointestinal disease in preterm infants.The role of miRNAs in NEC is still unknown.The objective of this study was to identify differentially expressed(DE) miRNAs in rats with NEC and analyze their possible roles.In this study,an NEC rat model was established using Sprague-Dawley rat pups.Next-generation RNA sequencing was used to analyze the miRNA expression profiles in the NEC and control rats.Gene ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analyses were carried out to identify target mRNAs for the DE miRNAs and to explore their potential roles.The DE miRNAs were verified by real-time quantitative PCR(RTqPCR).The status of intestinal injury as well as the elevated levels of inflammatory cytokines in the NEC group confirmed that the NEC model was successfully established.16 miRNAs were found to be differentially expressed between the NEC group and the control group of rats.Bioinformatics analysis indicated that the parental genes of the DE miRNAs were predominantly implicated in the phosphorylation,cell migration and protein phosphorylation processes.Moreover,the DE miRNAs were mainly found to be involved in the pathways of axon guidance,endocytosis and focal adhesion,as well as,in the Wnt signaling pathway,which is related to colitis.The expression patterns of the candidate miRNAs(rno-miR-27 a-5 p and mo-miR-187-3 p),as assessed by RT-qPCR,were in accordance with the expression patterns obtained by miRNA-sequencing.The miRNA-mRNA-pathway network revealed that mo-miR-27 a-5 p and mo-miR-187-3 p might be involved in NEC via the Wnt signaling pathway.We found an altered miRNA expression pattern in rats with NEC.We hypothesize that rno-miR-27 a-5 p and rno-miR-187-3 p might mediate the NEC pathophysiological processes via the Wnt signaling pathway.

  • 【会议录名称】 中国生物化学与分子生物学会2020全国学术在线会议摘要集
  • 【会议名称】中国生物化学与分子生物学会2020全国学术在线会议
  • 【会议时间】2020-10-22
  • 【会议地点】中国上海
  • 【分类号】R574.62
  • 【主办单位】中国生物化学与分子生物学会
节点文献中: 

本文链接的文献网络图示:

本文的引文网络