LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury
Abstract The regulation of long non-coding RNAs (lncRNAs) has been implicated in the pathogenesis of sepsis-induced acute kidney injury (SI-AKI). Nevertheless, the specific roles of individual lncRNAs in this process remain unclear. This study investigated the expression of lncRNA AP001007 in lipopo...
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Nature Portfolio
2024-11-01
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| Series: | Scientific Reports |
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| Online Access: | https://doi.org/10.1038/s41598-024-79367-2 |
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| author | Sheng Lin Zuxiu Ren Lili Li Suqin Xia Rongrong Yang Hong Ye |
| author_facet | Sheng Lin Zuxiu Ren Lili Li Suqin Xia Rongrong Yang Hong Ye |
| author_sort | Sheng Lin |
| collection | DOAJ |
| description | Abstract The regulation of long non-coding RNAs (lncRNAs) has been implicated in the pathogenesis of sepsis-induced acute kidney injury (SI-AKI). Nevertheless, the specific roles of individual lncRNAs in this process remain unclear. This study investigated the expression of lncRNA AP001007 in lipopolysaccharide (LPS)-induced HK-2 cells and in the peripheral blood of sepsis patients. The result shows that LPS treatment downregulated the expression of AP001007 in HK-2 cells and that circulating levels of AP001007 were lower in sepsis patients. Furthermore, overexpressing AP001007 in HK-2 cells improved cell viability, mitochondrial activity, and survival when exposed to LPS. Additionally, LPS-treated HK-2 cells secreted fewer pro-inflammatory cytokines when AP001007 was overexpressed. Similar protective effects were observed in human kidney organoids (HKOs) subjected to LPS. These findings suggest that AP001007 confers protection against LPS-induced damage in HK-2 cells and HKOs, highlighting its potential as a regulator of SI-AKI. |
| format | Article |
| id | doaj-art-c8e99e9603ba4497a99bc7dc9af33931 |
| institution | OA Journals |
| issn | 2045-2322 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj-art-c8e99e9603ba4497a99bc7dc9af339312025-08-20T02:33:31ZengNature PortfolioScientific Reports2045-23222024-11-0114111010.1038/s41598-024-79367-2LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injurySheng Lin0Zuxiu Ren1Lili Li2Suqin Xia3Rongrong Yang4Hong Ye5Fujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical UniversityFujian Children’s Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical UniversityFujian Children’s Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical UniversityFujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical UniversityFujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical UniversityFujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical UniversityAbstract The regulation of long non-coding RNAs (lncRNAs) has been implicated in the pathogenesis of sepsis-induced acute kidney injury (SI-AKI). Nevertheless, the specific roles of individual lncRNAs in this process remain unclear. This study investigated the expression of lncRNA AP001007 in lipopolysaccharide (LPS)-induced HK-2 cells and in the peripheral blood of sepsis patients. The result shows that LPS treatment downregulated the expression of AP001007 in HK-2 cells and that circulating levels of AP001007 were lower in sepsis patients. Furthermore, overexpressing AP001007 in HK-2 cells improved cell viability, mitochondrial activity, and survival when exposed to LPS. Additionally, LPS-treated HK-2 cells secreted fewer pro-inflammatory cytokines when AP001007 was overexpressed. Similar protective effects were observed in human kidney organoids (HKOs) subjected to LPS. These findings suggest that AP001007 confers protection against LPS-induced damage in HK-2 cells and HKOs, highlighting its potential as a regulator of SI-AKI.https://doi.org/10.1038/s41598-024-79367-2Long non-coding RNAAP001007SepsisKidneyLipopolysaccharide |
| spellingShingle | Sheng Lin Zuxiu Ren Lili Li Suqin Xia Rongrong Yang Hong Ye LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury Scientific Reports Long non-coding RNA AP001007 Sepsis Kidney Lipopolysaccharide |
| title | LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury |
| title_full | LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury |
| title_fullStr | LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury |
| title_full_unstemmed | LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury |
| title_short | LncRNA AP001007 protects human renal tubular epithelial HK-2 cells and kidney organoids from LPS-induced injury |
| title_sort | lncrna ap001007 protects human renal tubular epithelial hk 2 cells and kidney organoids from lps induced injury |
| topic | Long non-coding RNA AP001007 Sepsis Kidney Lipopolysaccharide |
| url | https://doi.org/10.1038/s41598-024-79367-2 |
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