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      KCI등재 SCOPUS SCIE

      MiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses and apoptosis by targeting TLR4

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      https://www.riss.kr/link?id=A107056648

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      다국어 초록 (Multilingual Abstract)

      Background Intestinal epithelial cells are important for defending against pathogen infection. LPS is an endotoxin that is highly antigenic and cytotoxic produced by bacteria. LPS disrupts the intestine epithelium integrity and induced the intestinal epithelial cell infammation and apoptosis. Our previous study has predicted the function of exosome miRNAs through bioinformatics analysis, and we found that miR-339 had a potential function in cell infammation response. To our knowledge, no published paper has demonstrated the miR-339 function in protecting the intestine epithelium against bacterial infection. Objective The objective of this study is to evaluate the miR-339 function in regulating intestinal epithelial cells to defend against bacterial infection through biological experiments and bioinformatics analyses. Methods Through the miR-339 transfection experiment and TLR4 interfering experiment, we evaluated the function of miR339 and TLR4 in the process of infammatory responses and apoptosis. Through Bioinformatics analyses and dual-luciferase reporter experiment, we identifed the target gene of miR-339. Results miR-339 attenuates LPS-induced intestinal epithelial cells infammatory responses through the TLR4/NF-κB signaling pathway and inhibited LPS-induced apoptosis through the P53 signaling pathway. TLR4 is the target gene of miR-339. TLR4 reduced LPS-induced proinfammatory responses and apoptosis. Conclusions In conclusion, miR-339 protected the intestine epithelial cells from LPS-induced cell infammation and apoptosis through targeting TLR4. This study expanded our understanding of how miRNAs and genes work collaboratively in regulating intestinal epithelial cells to defend against bacterial infection.
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      Background Intestinal epithelial cells are important for defending against pathogen infection. LPS is an endotoxin that is highly antigenic and cytotoxic produced by bacteria. LPS disrupts the intestine epithelium integrity and induced the intestinal ...

      Background Intestinal epithelial cells are important for defending against pathogen infection. LPS is an endotoxin that is highly antigenic and cytotoxic produced by bacteria. LPS disrupts the intestine epithelium integrity and induced the intestinal epithelial cell infammation and apoptosis. Our previous study has predicted the function of exosome miRNAs through bioinformatics analysis, and we found that miR-339 had a potential function in cell infammation response. To our knowledge, no published paper has demonstrated the miR-339 function in protecting the intestine epithelium against bacterial infection. Objective The objective of this study is to evaluate the miR-339 function in regulating intestinal epithelial cells to defend against bacterial infection through biological experiments and bioinformatics analyses. Methods Through the miR-339 transfection experiment and TLR4 interfering experiment, we evaluated the function of miR339 and TLR4 in the process of infammatory responses and apoptosis. Through Bioinformatics analyses and dual-luciferase reporter experiment, we identifed the target gene of miR-339. Results miR-339 attenuates LPS-induced intestinal epithelial cells infammatory responses through the TLR4/NF-κB signaling pathway and inhibited LPS-induced apoptosis through the P53 signaling pathway. TLR4 is the target gene of miR-339. TLR4 reduced LPS-induced proinfammatory responses and apoptosis. Conclusions In conclusion, miR-339 protected the intestine epithelial cells from LPS-induced cell infammation and apoptosis through targeting TLR4. This study expanded our understanding of how miRNAs and genes work collaboratively in regulating intestinal epithelial cells to defend against bacterial infection.

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      참고문헌 (Reference)

      1 Gomez CD, "“Exosomics”: a review of biophysics, biology and biochemistry of exosomes with a focus on human breast milk" 9 : 92-, 2018

      2 Kellum JA, "Understanding the inflammatory cytokine response in pneumonia and sepsis : results of the genetic and inflammatory markers of sepsis(GenIMS)study" 167 (167): 1655-1663, 2007

      3 Allaire JM, "The intestinal epithelium : central coordinator of mucosal immunity" 39 (39): 677-696, 2018

      4 Shan T, "Roles of notch signaling in adipocyte progenitor cells and mature adipocytes" 232 (232): 1258-1261, 2017

      5 Xie MY, "Porcine milk exosome MiRNAs attenuate LPSinduced apoptosis through Iinhibiting TLR4/NF-kappa B and p53 pathways in intestinal epithelial cells" 67 (67): 9477-9491, 2019

      6 Hou L, "Pig has no uncoupling protein 1" 487 (487): 795-800, 2017

      7 Shu G, "Phloretin promotes adipocyte differentiation in vitro and improves glucose homeostasis in vivo" 25 (25): 1296-1308, 2014

      8 Shin S, "MicroRNA-513a-5p mediates TNF-alpha and LPS induced apoptosis via downregulation of X-linked inhibitor of apoptotic protein in endothelial cells" 94 (94): 1431-1436, 2012

      9 Wang T, "MicroRNA-494 inhibition protects nucleus pulposus cells from TNF-alpha-induced apoptosis by targeting JunD" 115 : 1-7, 2015

      10 Mao KR, "Innate and adaptive lymphocytes sequentially shape the gut microbiota and lipid metabolism" 554 (554): 255-255, 2018

      1 Gomez CD, "“Exosomics”: a review of biophysics, biology and biochemistry of exosomes with a focus on human breast milk" 9 : 92-, 2018

      2 Kellum JA, "Understanding the inflammatory cytokine response in pneumonia and sepsis : results of the genetic and inflammatory markers of sepsis(GenIMS)study" 167 (167): 1655-1663, 2007

      3 Allaire JM, "The intestinal epithelium : central coordinator of mucosal immunity" 39 (39): 677-696, 2018

      4 Shan T, "Roles of notch signaling in adipocyte progenitor cells and mature adipocytes" 232 (232): 1258-1261, 2017

      5 Xie MY, "Porcine milk exosome MiRNAs attenuate LPSinduced apoptosis through Iinhibiting TLR4/NF-kappa B and p53 pathways in intestinal epithelial cells" 67 (67): 9477-9491, 2019

      6 Hou L, "Pig has no uncoupling protein 1" 487 (487): 795-800, 2017

      7 Shu G, "Phloretin promotes adipocyte differentiation in vitro and improves glucose homeostasis in vivo" 25 (25): 1296-1308, 2014

      8 Shin S, "MicroRNA-513a-5p mediates TNF-alpha and LPS induced apoptosis via downregulation of X-linked inhibitor of apoptotic protein in endothelial cells" 94 (94): 1431-1436, 2012

      9 Wang T, "MicroRNA-494 inhibition protects nucleus pulposus cells from TNF-alpha-induced apoptosis by targeting JunD" 115 : 1-7, 2015

      10 Mao KR, "Innate and adaptive lymphocytes sequentially shape the gut microbiota and lipid metabolism" 554 (554): 255-255, 2018

      11 Chen T, "Exploration of microRNAs in porcine milk exosomes" 15 : 100-, 2014

      12 Valadi H, "Exosome-mediated transfer of mRNAs and microRNAs is a novel mechanism of genetic exchange between cells" 9 (9): 654-672, 2007

      13 Xu B, "Effects of harmaline on cell growth of human liver cancer through the p53/p21 and Fas/FasL signaling pathways" 15 (15): 1931-1936, 2018

      14 Eckmann L, "Cytokines in host defense against Salmonella" 3 (3): 1191-1200, 2001

      15 Yan Y, "BCFA suppresses LPS induced IL-8 mRNA expression in human intestinal epithelial cells" 116 : 27-31, 2017

      16 Li RX, "Attenuating effect of melatonin on lipopolysaccharide-induced chicken small intestine inflammation" 97 (97): 2295-2302, 2018

      17 Min X, "Anticancer effects of 10-hydroxycamptothecin induce apoptosis of human osteosarcoma through activating caspase-3, p53 and cytochrome c pathways" 15 (15): 2459-2464, 2018

      18 유형석, "Anti-Inflammatory Potential of Probiotic Strain Weissella cibaria JW15 Isolated from Kimchi through Regulation of NF-κB and MAPKs Pathways in LPS-Induced RAW 264.7 Cells" 한국미생물·생명공학회 29 (29): 1022-1032, 2019

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2015-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2012-05-07 학술지명변경 한글명 : 한국유전학회지 -> Genes & Genomics KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-04-14 학술지명변경 외국어명 : Korean Journal of Genetics -> Genes and Genomics KCI등재
      2007-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2004-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2003-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2002-01-01 평가 등재후보학술지 유지 (등재후보1차) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.51 0.12 0.38
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.32 0.27 0.258 0.02
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