LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis
Abstract Objective The present study was implemented to unravel the effect of lncRNA GAS5 on renal fibrosis induced by diabetic nephropathy (DN) by regulating the miR-542-3p/ERBB4 axis. Methods db/db mice were injected with lncRNA GAS5 high expression or miR-542-3p low expression related vectors. Bi...
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BMC
2025-01-01
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| Series: | Diabetology & Metabolic Syndrome |
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| Online Access: | https://doi.org/10.1186/s13098-025-01593-z |
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| author | Qinghua Yin Na Guo Ruoxi Liao |
| author_facet | Qinghua Yin Na Guo Ruoxi Liao |
| author_sort | Qinghua Yin |
| collection | DOAJ |
| description | Abstract Objective The present study was implemented to unravel the effect of lncRNA GAS5 on renal fibrosis induced by diabetic nephropathy (DN) by regulating the miR-542-3p/ERBB4 axis. Methods db/db mice were injected with lncRNA GAS5 high expression or miR-542-3p low expression related vectors. Biochemical experiments were performed to assess blood glucose level and urine protein concentration. HE, TUNEL and Masson stainings were employed to observe the cellular morphology, apoptosis, and fibrosis of renal tissues, respectively. ELISA was executed to examine the levels of IL-1β, IL-6, and TNF-α; and the superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) activities were evaluated. Bioinformatics analysis, dual-luciferase and RIP assays were performed to verify the relationship between lncRNA GAS5 and miR-542-3p, and miR-542-3p and ERBB4. Results LncRNA GAS5 and ERBB4 were lowly expressed and miR-542-3p was highly expressed in the renal tissues of DN mice. Overexpression of lncRNA GAS5 or low-expression of miR-542-3p diminished DN-induced renal fibrosis. LncRNA GAS5 could bind to miR-542-3p and miR-542-3p further modulating ERBB4 expression. Up-regulation of miR-542-3p neutralized the suppressive effect of lncRNA GAS5 overexpression and down-regulation of ERBB4 also counteracted the inhibitory impact of down-regulation of miR-542-3p on renal fibrosis in DN mice. Conclusion Up-regulation of lncRNA GAS5 alleviates renal fibrosis in DN mice via down-regulation of miR-542-3p and up-regulation of ERBB4. |
| format | Article |
| id | doaj-art-d9296fa267584fbd9ca6065971b725c2 |
| institution | Kabale University |
| issn | 1758-5996 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | BMC |
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| series | Diabetology & Metabolic Syndrome |
| spelling | doaj-art-d9296fa267584fbd9ca6065971b725c22025-01-26T12:45:31ZengBMCDiabetology & Metabolic Syndrome1758-59962025-01-0117111110.1186/s13098-025-01593-zLncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axisQinghua Yin0Na Guo1Ruoxi Liao2Division of Nephrology, Kidney Research Institute, West China Hospital of Sichuan UniversityOccupational Disease and Toxicosis/Nephrology, West China School of Public Health and West China Fourth Hospital, Sichuan UniversityDivision of Nephrology, West China Hospital of Sichuan UniversityAbstract Objective The present study was implemented to unravel the effect of lncRNA GAS5 on renal fibrosis induced by diabetic nephropathy (DN) by regulating the miR-542-3p/ERBB4 axis. Methods db/db mice were injected with lncRNA GAS5 high expression or miR-542-3p low expression related vectors. Biochemical experiments were performed to assess blood glucose level and urine protein concentration. HE, TUNEL and Masson stainings were employed to observe the cellular morphology, apoptosis, and fibrosis of renal tissues, respectively. ELISA was executed to examine the levels of IL-1β, IL-6, and TNF-α; and the superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) activities were evaluated. Bioinformatics analysis, dual-luciferase and RIP assays were performed to verify the relationship between lncRNA GAS5 and miR-542-3p, and miR-542-3p and ERBB4. Results LncRNA GAS5 and ERBB4 were lowly expressed and miR-542-3p was highly expressed in the renal tissues of DN mice. Overexpression of lncRNA GAS5 or low-expression of miR-542-3p diminished DN-induced renal fibrosis. LncRNA GAS5 could bind to miR-542-3p and miR-542-3p further modulating ERBB4 expression. Up-regulation of miR-542-3p neutralized the suppressive effect of lncRNA GAS5 overexpression and down-regulation of ERBB4 also counteracted the inhibitory impact of down-regulation of miR-542-3p on renal fibrosis in DN mice. Conclusion Up-regulation of lncRNA GAS5 alleviates renal fibrosis in DN mice via down-regulation of miR-542-3p and up-regulation of ERBB4.https://doi.org/10.1186/s13098-025-01593-zDiabetic nephropathyRenal fibrosisLncRNA GAS5miR-542-3pERBB4Blood glucose level |
| spellingShingle | Qinghua Yin Na Guo Ruoxi Liao LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis Diabetology & Metabolic Syndrome Diabetic nephropathy Renal fibrosis LncRNA GAS5 miR-542-3p ERBB4 Blood glucose level |
| title | LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis |
| title_full | LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis |
| title_fullStr | LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis |
| title_full_unstemmed | LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis |
| title_short | LncRNA GAS5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the miR-542-3p/ERBB4 axis |
| title_sort | lncrna gas5 reduces blood glucose levels and alleviates renal fibrosis in diabetic nephropathy by regulating the mir 542 3p erbb4 axis |
| topic | Diabetic nephropathy Renal fibrosis LncRNA GAS5 miR-542-3p ERBB4 Blood glucose level |
| url | https://doi.org/10.1186/s13098-025-01593-z |
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