Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophages

Objective To investigate the regulatory mechanism of long-chain noncoding RNA metastasis-associated lung adenocarcinoma 1 (lnc-MALAT1) in the inflammatory response of lipopolysaccharide (LPS)-induced alveolar macrophages (AMOs). Methods AMOs cells were treated with LPS for 12 hours to create an in...

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Main Author: LUO Chuan-ling, SUN Li-ping, QI Cheng-dong
Format: Article
Language:zho
Published: Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. 2021-03-01
Series:Jichu yixue yu linchuang
Subjects:
Online Access:http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/a200432.pdf
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author LUO Chuan-ling, SUN Li-ping, QI Cheng-dong
author_facet LUO Chuan-ling, SUN Li-ping, QI Cheng-dong
author_sort LUO Chuan-ling, SUN Li-ping, QI Cheng-dong
collection DOAJ
description Objective To investigate the regulatory mechanism of long-chain noncoding RNA metastasis-associated lung adenocarcinoma 1 (lnc-MALAT1) in the inflammatory response of lipopolysaccharide (LPS)-induced alveolar macrophages (AMOs). Methods AMOs cells were treated with LPS for 12 hours to create an inflammation model, and liposome method was used to transfect pcDNA, pcDNA-MALAT1, miR-NC, miR-217 mimics, pcDNA-MALAT1 and miR-NC, pcDNA-MALAT1 and miR-217 mimics to AMOs. The level of IL-1β and TNF-α was detected by ELISA. RT-qPCR was used to detect the expression of MALAT1 and miR-217 in cells. The dual luciferase report experiment and RIP experiment were used to detect potential target-attacking relationship between MALAT1 and miR-217. Results Compared with the AMOs group, the expression of IL-1β and TNFα, MALAT1 in the cells of the LPS+AMOs group were significantly increased (P<0.05) and the expression level of miR-217 was significantly reduced(P<0.05). The dual luciferase report experiment and RIP experiment confirmed that MALAT1 targeted at miR-217. Over-expression of MALAT1 could obviously promote the secretion of IL-1β and TNF-α induced by LPS in AMOs, while over-expression of miR-217 inhibited the secretion of IL-1β and TNF-α induced by LPS in AMOs. Furthermore, over-expression of miR-217 reduced the secretion of IL-1β and TNF-α induced by MALAT1 in LPS-induced AMOs. Conclusions Lnc-MALAT1, a long non-coding RNA, can promote the inflammatory response of AMOs induced by LPS, and its mechanism is related to its targeting at miR-217.
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spelling doaj.art-cc4062dc82464182b1522d61840c0db62024-01-05T03:04:40ZzhoInstitute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.Jichu yixue yu linchuang1001-63252021-03-01413404408Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophagesLUO Chuan-ling, SUN Li-ping, QI Cheng-dong01. Department of Critical Medicine; 2. Department of Pediatric Medicine, Zaozhuang Mining Group Central Hospital, Zaozhuang 277100,ChinaObjective To investigate the regulatory mechanism of long-chain noncoding RNA metastasis-associated lung adenocarcinoma 1 (lnc-MALAT1) in the inflammatory response of lipopolysaccharide (LPS)-induced alveolar macrophages (AMOs). Methods AMOs cells were treated with LPS for 12 hours to create an inflammation model, and liposome method was used to transfect pcDNA, pcDNA-MALAT1, miR-NC, miR-217 mimics, pcDNA-MALAT1 and miR-NC, pcDNA-MALAT1 and miR-217 mimics to AMOs. The level of IL-1β and TNF-α was detected by ELISA. RT-qPCR was used to detect the expression of MALAT1 and miR-217 in cells. The dual luciferase report experiment and RIP experiment were used to detect potential target-attacking relationship between MALAT1 and miR-217. Results Compared with the AMOs group, the expression of IL-1β and TNFα, MALAT1 in the cells of the LPS+AMOs group were significantly increased (P<0.05) and the expression level of miR-217 was significantly reduced(P<0.05). The dual luciferase report experiment and RIP experiment confirmed that MALAT1 targeted at miR-217. Over-expression of MALAT1 could obviously promote the secretion of IL-1β and TNF-α induced by LPS in AMOs, while over-expression of miR-217 inhibited the secretion of IL-1β and TNF-α induced by LPS in AMOs. Furthermore, over-expression of miR-217 reduced the secretion of IL-1β and TNF-α induced by MALAT1 in LPS-induced AMOs. Conclusions Lnc-MALAT1, a long non-coding RNA, can promote the inflammatory response of AMOs induced by LPS, and its mechanism is related to its targeting at miR-217.http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/a200432.pdflnc-malat1|alveolar macrophages|mir-217|lipopolysaccharide(lps)
spellingShingle LUO Chuan-ling, SUN Li-ping, QI Cheng-dong
Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophages
Jichu yixue yu linchuang
lnc-malat1|alveolar macrophages|mir-217|lipopolysaccharide(lps)
title Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophages
title_full Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophages
title_fullStr Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophages
title_full_unstemmed Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophages
title_short Lnc-MALAT1 attenuates miR-217 inhibiting LPS-induced inflammatory response in rat alveolar macrophages
title_sort lnc malat1 attenuates mir 217 inhibiting lps induced inflammatory response in rat alveolar macrophages
topic lnc-malat1|alveolar macrophages|mir-217|lipopolysaccharide(lps)
url http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/a200432.pdf
work_keys_str_mv AT luochuanlingsunlipingqichengdong lncmalat1attenuatesmir217inhibitinglpsinducedinflammatoryresponseinratalveolarmacrophages