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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Wiley
2023-06-01
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| Series: | Immunity, Inflammation and Disease |
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| 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. |
| format | Article |
| id | doaj-art-ddc0b31bfcc044b3978cbb2c91a66c51 |
| institution | DOAJ |
| issn | 2050-4527 |
| language | English |
| publishDate | 2023-06-01 |
| publisher | Wiley |
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| series | Immunity, Inflammation and Disease |
| 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 |