Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injury

Abstract Background Circular RNAs have emerged as important regulators in the pathogenesis of human diseases, including infantile pneumonia (IP). In this study, we aimed to explore the effects of circ_0035292 on lipopolysaccharide (LPS)‐treated Wistsar Institute (WI)‐38 cells. Methods Quantitative r...

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Main Authors: Ying Guo, Zhouzhen Li, Chen Cheng
Format: Article
Language:English
Published: Wiley 2023-06-01
Series:Immunity, Inflammation and Disease
Subjects:
Online Access:https://doi.org/10.1002/iid3.905
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author Ying Guo
Zhouzhen Li
Chen Cheng
author_facet Ying Guo
Zhouzhen Li
Chen Cheng
author_sort Ying Guo
collection DOAJ
description Abstract Background Circular RNAs have emerged as important regulators in the pathogenesis of human diseases, including infantile pneumonia (IP). In this study, we aimed to explore the effects of circ_0035292 on lipopolysaccharide (LPS)‐treated Wistsar Institute (WI)‐38 cells. Methods Quantitative real‐time polymerase chain reaction and western blot were executed to detect the levels of circ_0035292, microRNA‐370‐3p (miR‐370‐3p) and transducin β‐like 1X related protein 1 (TBL1XR1). Cell counting kit‐8, 5‐ethynyl‐2′‐deoxyuridine, and flow cytometry assessed cell proliferation and apoptosis. Concentrations of inflammatory factors were examined with enzyme linked immunosorbent assay kits. Dual‐luciferase reporter assay and RNA immunoprecipitation were adopted to analyze binding between miR‐370‐3p and circ_0035292 or TBL1XR1. Results Circ_0035292 level was increased in IP patients and LPS‐triggered WI‐38 cells. Circ_0035292 knockdown rescued LPS‐mediated WI‐38 cell proliferation suppression and WI‐38 cell apoptosis and inflammation promotion. Circ_0035292 interacted with miR‐370‐3p and miR‐370‐3p directly targeted TBL1XR1. Moreover, miR‐370‐3p overexpression alleviated LPS‐induced WI‐38 cell apoptosis and inflammatory injury, which was abrogated via TBL1XR1 upregulation. Circ_0035292 absence inhibited the NF‐κB pathway. Conclusion Knockdown of circ_0035292 rescued LPS‐triggered WI‐38 cell injury via miR‐370‐3p/TBL1XR1 axis and NF‐κB pathway.
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spelling doaj-art-ddc0b31bfcc044b3978cbb2c91a66c512025-08-20T03:08:46ZengWileyImmunity, Inflammation and Disease2050-45272023-06-01116n/an/a10.1002/iid3.905Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injuryYing Guo0Zhouzhen Li1Chen Cheng2Department of Pediatrics Wuhan Asia General Hospital Wuhan City Hubei ChinaDepartment of Pediatrics Wuhan Asia General Hospital Wuhan City Hubei ChinaDepartment of Pediatrics Wuhan Asia General Hospital Wuhan City Hubei ChinaAbstract Background Circular RNAs have emerged as important regulators in the pathogenesis of human diseases, including infantile pneumonia (IP). In this study, we aimed to explore the effects of circ_0035292 on lipopolysaccharide (LPS)‐treated Wistsar Institute (WI)‐38 cells. Methods Quantitative real‐time polymerase chain reaction and western blot were executed to detect the levels of circ_0035292, microRNA‐370‐3p (miR‐370‐3p) and transducin β‐like 1X related protein 1 (TBL1XR1). Cell counting kit‐8, 5‐ethynyl‐2′‐deoxyuridine, and flow cytometry assessed cell proliferation and apoptosis. Concentrations of inflammatory factors were examined with enzyme linked immunosorbent assay kits. Dual‐luciferase reporter assay and RNA immunoprecipitation were adopted to analyze binding between miR‐370‐3p and circ_0035292 or TBL1XR1. Results Circ_0035292 level was increased in IP patients and LPS‐triggered WI‐38 cells. Circ_0035292 knockdown rescued LPS‐mediated WI‐38 cell proliferation suppression and WI‐38 cell apoptosis and inflammation promotion. Circ_0035292 interacted with miR‐370‐3p and miR‐370‐3p directly targeted TBL1XR1. Moreover, miR‐370‐3p overexpression alleviated LPS‐induced WI‐38 cell apoptosis and inflammatory injury, which was abrogated via TBL1XR1 upregulation. Circ_0035292 absence inhibited the NF‐κB pathway. Conclusion Knockdown of circ_0035292 rescued LPS‐triggered WI‐38 cell injury via miR‐370‐3p/TBL1XR1 axis and NF‐κB pathway.https://doi.org/10.1002/iid3.905circ_0035292infantile pneumoniamiR‐370‐3pNF‐κBTBL1XR1
spellingShingle Ying Guo
Zhouzhen Li
Chen Cheng
Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injury
Immunity, Inflammation and Disease
circ_0035292
infantile pneumonia
miR‐370‐3p
NF‐κB
TBL1XR1
title Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injury
title_full Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injury
title_fullStr Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injury
title_full_unstemmed Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injury
title_short Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)‐induced WI‐38 cell apoptosis and inflammatory injury
title_sort circ 0035292 knockdown alleviates lipopolysaccharide lps induced wi 38 cell apoptosis and inflammatory injury
topic circ_0035292
infantile pneumonia
miR‐370‐3p
NF‐κB
TBL1XR1
url https://doi.org/10.1002/iid3.905
work_keys_str_mv AT yingguo circ0035292knockdownalleviateslipopolysaccharidelpsinducedwi38cellapoptosisandinflammatoryinjury
AT zhouzhenli circ0035292knockdownalleviateslipopolysaccharidelpsinducedwi38cellapoptosisandinflammatoryinjury
AT chencheng circ0035292knockdownalleviateslipopolysaccharidelpsinducedwi38cellapoptosisandinflammatoryinjury