4.3 Article

LncRNA-AK149641 associated with airway inflammation in an OVA-induced asthma mouse model

期刊

JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
卷 52, 期 5, 页码 355-365

出版社

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10863-020-09844-6

关键词

lncRNA-AK149641; OVA-induced asthma mouse model; TNF-alpha; IL-6 and NF-kappa B signaling pathway

资金

  1. National Natural Science Foundation of China [81700035]
  2. Jiangsu Province Young Medical Talents [QNRC2016087]
  3. Nanjing Medical Science and Technique Development Foundation [JQX15008]
  4. Nanjing Science and Technology Commission (Social Development) [201723003]
  5. Southeast University-Nanjing Medical University Cooperative Research Project [2242018K3DN20]
  6. Key Projects of Nanjing Health and Planning Commission [ZKX18041]
  7. General Projects of Nanjing Health and Planning Commission [YKK18194]
  8. Project of Nanjing Medical University [2017njmuzd054]

向作者/读者索取更多资源

Asthma is defined as a heterogeneous disease, usually characterized by chronic airway inflammation. Long noncoding RNAs (lncRNAs) play important roles in various biological processes. To know more about the relationships between lncRNAs and asthma, gene microarray analysis was performed to screen differentially expressed lncRNAs between the lung tissue of ovalbumin (OVA) mice and control mice. Further studies showed that downregulating differentially expressed lncRNA-AK149641 by adeno-associated virus 6 (AAV6) in OVA mice inhibited airway inflammation, with improved airway compliance and resistance, diminished infiltration of inflammatory cells, as well as less secretions of mucus, tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6). Moreover, the activity of nuclear factor-kappa B (NF-kappa B) in the lung tissue was reduced after downregulating lncRNA-AK149641. In conclusion, we proposed that downregulation of lncRNA-AK149641 attenuated the airway inflammatory response in an OVA-induced asthma mouse model, probably in association with modulation of the NF-kappa B signaling pathway.

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