Suppression of long noncoding RNA SNHG6 alleviates cigarette smoke-induced lung inflammation by modulating NF-κB signaling
© 2024 Wiley Periodicals LLC..
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a widespread inflammatory disease with a high mortality rate. Long noncoding RNAs play important roles in pulmonary diseases and are potential targets for inflammation intervention.
METHODS: The expression of small nucleolar RNA host gene 6 (SNHG6) in mouse lung epithelial cell line MLE12 with or without cigarette smoke extract (CSE) treatment was first detected using quantitative reverse-transcription PCR. ELISA was used to evaluate the release of inflammatory cytokines (TNF-α, IL-1β, and IL-6). The binding site of miR-182-5p with SNHG6 was predicted by using miRanda, which was verified by double luciferase reporter assay.
RESULTS: Here, we revealed that SNHG6 was upregulated in CS-exposed MLE12 alveolar epithelial cells and lungs from COPD-model mice. SNHG6 silencing weakened CS-induced inflammation in MLE12 cells and mouse lungs. Mechanistic investigations revealed that SNHG6 could upregulate IκBα kinase through sponging the microRNA miR-182-5p, followed by activated NF-κB signaling. The suppressive effects of SNHG6 silencing on CS-induced inflammation were blocked by an miR-182-5p inhibitor.
CONCLUSION: Overall, our findings suggested that SNHG6 regulates CS-induced inflammation in COPD by activating NF-κB signaling, thereby offering a novel potential target for COPD treatment.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:39 |
|---|---|
| Enthalten in: |
Environmental toxicology - 39(2024), 5 vom: 15. Apr., Seite 2634-2641 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Yang, Junxia [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Chronic obstructive pulmonary disease |
|---|
| Anmerkungen: |
Date Completed 17.04.2024 Date Revised 17.04.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1002/tox.24132 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM366964909 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM366964909 | ||
| 003 | DE-627 | ||
| 005 | 20240417232356.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240114s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1002/tox.24132 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1378.xml |
| 035 | |a (DE-627)NLM366964909 | ||
| 035 | |a (NLM)38205902 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Yang, Junxia |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Suppression of long noncoding RNA SNHG6 alleviates cigarette smoke-induced lung inflammation by modulating NF-κB signaling |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 17.04.2024 | ||
| 500 | |a Date Revised 17.04.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2024 Wiley Periodicals LLC. | ||
| 520 | |a BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a widespread inflammatory disease with a high mortality rate. Long noncoding RNAs play important roles in pulmonary diseases and are potential targets for inflammation intervention | ||
| 520 | |a METHODS: The expression of small nucleolar RNA host gene 6 (SNHG6) in mouse lung epithelial cell line MLE12 with or without cigarette smoke extract (CSE) treatment was first detected using quantitative reverse-transcription PCR. ELISA was used to evaluate the release of inflammatory cytokines (TNF-α, IL-1β, and IL-6). The binding site of miR-182-5p with SNHG6 was predicted by using miRanda, which was verified by double luciferase reporter assay | ||
| 520 | |a RESULTS: Here, we revealed that SNHG6 was upregulated in CS-exposed MLE12 alveolar epithelial cells and lungs from COPD-model mice. SNHG6 silencing weakened CS-induced inflammation in MLE12 cells and mouse lungs. Mechanistic investigations revealed that SNHG6 could upregulate IκBα kinase through sponging the microRNA miR-182-5p, followed by activated NF-κB signaling. The suppressive effects of SNHG6 silencing on CS-induced inflammation were blocked by an miR-182-5p inhibitor | ||
| 520 | |a CONCLUSION: Overall, our findings suggested that SNHG6 regulates CS-induced inflammation in COPD by activating NF-κB signaling, thereby offering a novel potential target for COPD treatment | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a NF‐κB signaling | |
| 650 | 4 | |a chronic obstructive pulmonary disease | |
| 650 | 4 | |a cigarette smoke | |
| 650 | 4 | |a long noncoding RNA SNHG6 | |
| 650 | 4 | |a miR‐182‐5p | |
| 650 | 7 | |a NF-kappa B |2 NLM | |
| 650 | 7 | |a RNA, Long Noncoding |2 NLM | |
| 650 | 7 | |a MicroRNAs |2 NLM | |
| 700 | 1 | |a Yuan, Yaping |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Linxuan |e verfasserin |4 aut | |
| 700 | 1 | |a Deng, Guoping |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Jiaru |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Yuan |e verfasserin |4 aut | |
| 700 | 1 | |a Gu, Wenchao |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Environmental toxicology |d 2001 |g 39(2024), 5 vom: 15. Apr., Seite 2634-2641 |w (DE-627)NLM112466567 |x 1522-7278 |7 nnns |
| 773 | 1 | 8 | |g volume:39 |g year:2024 |g number:5 |g day:15 |g month:04 |g pages:2634-2641 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1002/tox.24132 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 39 |j 2024 |e 5 |b 15 |c 04 |h 2634-2641 | ||