Min Liu1, Weixin Li2, Fuxing Song1, Ling Zhang1, Xianjun Sun1. 1. Department of Pediatrics, Jinan People's Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China. 2. Department of Infectious Diseases, Jinan Hospital of Integrated Traditional Chinese and Western Medicine, Jinan, Shandong Province, China.
Abstract
PURPOSE: Pneumonia is a respiratory disease with an increasing incidence in recent years. More and more studies have revealed that lncRNAs can regulate the transcriptional expression of target genes at different stage. Herein, we aimed to explore the effect of lncRNA MIAT in LPS-induced pneumonia, and further illuminate the possible underlying mechanisms. METHOD AND RESULTS: Mice were intraperitoneally injected with LPS, and the lung inflammation was evaluated. Microarray showed lncRNA MIAT was up-regulated in LPS-induced pulmonary inflammation. And qRT-PCR and FISH assay indicated that MIAT was increased in mice with LPS injection. Functional analysis showed sh-MIAT inhibited LPS-induced inflammation response, inhibited apoptosis level and protected lung function. As well, si-MIAT removed the injury of LPS on mouse lung epithelial TC-1 cells, and inhibited the activation of NF-κB signaling. Furthermore, MIAT acted as a sponge of miR-147a, and miR-147a directly targeted NKAP. Functionally, AMO-147a or NKAP remitted the beneficial effects of si-MIAT on LPS-induced inflammation response of TC-1 cells. CONCLUSION: Deletion of MIAT protected against LPS-induced lung inflammation via regulating miR-147a/NKAP, which might provide new insight for pneumonia treatment.
PURPOSE:Pneumonia is a respiratory disease with an increasing incidence in recent years. More and more studies have revealed that lncRNAs can regulate the transcriptional expression of target genes at different stage. Herein, we aimed to explore the effect of lncRNA MIAT in LPS-induced pneumonia, and further illuminate the possible underlying mechanisms. METHOD AND RESULTS:Mice were intraperitoneally injected with LPS, and the lung inflammation was evaluated. Microarray showed lncRNA MIAT was up-regulated in LPS-induced pulmonary inflammation. And qRT-PCR and FISH assay indicated that MIAT was increased in mice with LPS injection. Functional analysis showed sh-MIAT inhibited LPS-induced inflammation response, inhibited apoptosis level and protected lung function. As well, si-MIAT removed the injury of LPS on mouse lung epithelial TC-1 cells, and inhibited the activation of NF-κB signaling. Furthermore, MIAT acted as a sponge of miR-147a, and miR-147a directly targeted NKAP. Functionally, AMO-147a or NKAP remitted the beneficial effects of si-MIAT on LPS-induced inflammation response of TC-1 cells. CONCLUSION: Deletion of MIAT protected against LPS-induced lung inflammation via regulating miR-147a/NKAP, which might provide new insight for pneumonia treatment.
Authors: Dinesh Devadoss; Christopher Long; Raymond J Langley; Marko Manevski; Madhavan Nair; Michael A Campos; Glen Borchert; Irfan Rahman; Hitendra S Chand Journal: Am J Respir Cell Mol Biol Date: 2019-12 Impact factor: 6.914
Authors: Nathan J Klingensmith; Katherine T Fay; John D Lyons; Ching-Wen Chen; Shunsuke Otani; Zhe Liang; Deena B Chihade; Eileen M Burd; Mandy L Ford; Craig M Coopersmith Journal: Shock Date: 2019-04 Impact factor: 3.454
Authors: J B Kral-Pointner; W C Schrottmaier; V Horvath; H Datler; L Hell; C Ay; B Niederreiter; B Jilma; J A Schmid; A Assinger; N Mackman; S Knapp; G Schabbauer Journal: J Thromb Haemost Date: 2017-06-20 Impact factor: 5.824
Authors: Caroline M Weight; Cristina Venturini; Sherin Pojar; Simon P Jochems; Jesús Reiné; Elissavet Nikolaou; Carla Solórzano; Mahdad Noursadeghi; Jeremy S Brown; Daniela M Ferreira; Robert S Heyderman Journal: Nat Commun Date: 2019-07-16 Impact factor: 14.919