LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axis
Renal interstitial fibrosis (RIF) is a common pathway in chronic kidney disease (CKD) that ultimately leads to end-stage renal failure, worsening both glomerulosclerosis and interstitial fibrosis. Ten percent of the adult population in the world suffers from CKD, and as the ageing population continu...
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Elsevier
2025-01-01
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844024169228 |
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| author | Luoxiang Qian Wanru Hu Yanping Wang Yousuf Abdulkarim Waheed Shuqun Hu Dong Sun Shulin Li |
| author_facet | Luoxiang Qian Wanru Hu Yanping Wang Yousuf Abdulkarim Waheed Shuqun Hu Dong Sun Shulin Li |
| author_sort | Luoxiang Qian |
| collection | DOAJ |
| description | Renal interstitial fibrosis (RIF) is a common pathway in chronic kidney disease (CKD) that ultimately leads to end-stage renal failure, worsening both glomerulosclerosis and interstitial fibrosis. Ten percent of the adult population in the world suffers from CKD, and as the ageing population continues to rise, it is increasingly regarded as a global threat—a silent epidemic. CKD has been discovered to be closely associated with both long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), while the precise molecular processes behind this relationship are still unclear. This study evaluated the impact of miR-542-3p and lncRNA TUG1 on renal fibrosis, along with the underlying regulatory mechanisms. Through in vitro tube formation assays, research demonstrated that knocking down lncRNA TUG1 may enhance angiogenesis and repair damaged endothelial cell-cell connections. We used Western blot and qRT-PCR methods in the unilateral ureteral obstruction (UUO) model to identify tissue hypoxia and fibrotic lesions. Additionally, a cutting-edge method known as fluorescence microangiography (FMA) was employed to detect damage to the peritubular capillaries (PTCs), with MATLAB software utilised for data evaluation. Furthermore, the coexpression of CD31 and α-SMA helped identify cells in the obstructed kidney that were transitioning from endothelium to myofibroblasts. On the contrary, lncRNA TUG1 downregulation showed a protective effect against the transition from endothelial cells to myofibroblasts. Additionally, knocking down lncRNA TUG1 has been shown to reduce the expression of fibrotic markers by alleviating tissue hypoxia. This effect was significantly counteracted by the inhibition of miR-542-3p. Collectively, our findings offer fresh perspectives on how lncRNA TUG1 and the miR-542-3p/HIF-1α/VEGF axis are regulated as renal fibrosis advances. |
| format | Article |
| id | doaj-art-447bd385668a414c8d67f7549209d918 |
| institution | Kabale University |
| issn | 2405-8440 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj-art-447bd385668a414c8d67f7549209d9182025-01-17T04:49:51ZengElsevierHeliyon2405-84402025-01-01111e40891LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axisLuoxiang Qian0Wanru Hu1Yanping Wang2Yousuf Abdulkarim Waheed3Shuqun Hu4Dong Sun5Shulin Li6Department of Nephrology, Affiliated Hospital of Xuzhou Medical University, 221002, China; Department of Internal Medicine, Weinan Maternal and Child Health Hospital, Weinan, 714000, ChinaDepartment of Nephrology, Affiliated Hospital of Xuzhou Medical University, 221002, ChinaDepartment of Nephrology, Affiliated Hospital of Xuzhou Medical University, 221002, ChinaDepartment of Nephrology, Affiliated Hospital of Xuzhou Medical University, 221002, ChinaLaboratory of Emergency Medicine, Second Clinical Medical College of Xuzhou Medical University, Xuzhou, 221002, China; Corresponding author. Laboratory of Emergency Medicine, Second Clinical Medical College of Xuzhou Medical University, Xuzhou 221002, China.Department of Nephrology, Affiliated Hospital of Xuzhou Medical University, 221002, China; Department of Internal Medicine and Diagnostics, Xuzhou Medical University, Xuzhou, 221002, China; Corresponding author. Department of Internal Medicine and Diagnostics, Xuzhou Medical University, Xuzhou, 221002, China.Department of Nephrology, Affiliated Hospital of Xuzhou Medical University, 221002, China; Corresponding author. Department of Nephrology, Affiliated Hospital of Xuzhou Medical University 221002, China.Renal interstitial fibrosis (RIF) is a common pathway in chronic kidney disease (CKD) that ultimately leads to end-stage renal failure, worsening both glomerulosclerosis and interstitial fibrosis. Ten percent of the adult population in the world suffers from CKD, and as the ageing population continues to rise, it is increasingly regarded as a global threat—a silent epidemic. CKD has been discovered to be closely associated with both long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), while the precise molecular processes behind this relationship are still unclear. This study evaluated the impact of miR-542-3p and lncRNA TUG1 on renal fibrosis, along with the underlying regulatory mechanisms. Through in vitro tube formation assays, research demonstrated that knocking down lncRNA TUG1 may enhance angiogenesis and repair damaged endothelial cell-cell connections. We used Western blot and qRT-PCR methods in the unilateral ureteral obstruction (UUO) model to identify tissue hypoxia and fibrotic lesions. Additionally, a cutting-edge method known as fluorescence microangiography (FMA) was employed to detect damage to the peritubular capillaries (PTCs), with MATLAB software utilised for data evaluation. Furthermore, the coexpression of CD31 and α-SMA helped identify cells in the obstructed kidney that were transitioning from endothelium to myofibroblasts. On the contrary, lncRNA TUG1 downregulation showed a protective effect against the transition from endothelial cells to myofibroblasts. Additionally, knocking down lncRNA TUG1 has been shown to reduce the expression of fibrotic markers by alleviating tissue hypoxia. This effect was significantly counteracted by the inhibition of miR-542-3p. Collectively, our findings offer fresh perspectives on how lncRNA TUG1 and the miR-542-3p/HIF-1α/VEGF axis are regulated as renal fibrosis advances.http://www.sciencedirect.com/science/article/pii/S2405844024169228lncRNA Taurine-upregulated gene 1miR-542-3pHypoxia-inducible factor-1-alphaChronic kidney disease |
| spellingShingle | Luoxiang Qian Wanru Hu Yanping Wang Yousuf Abdulkarim Waheed Shuqun Hu Dong Sun Shulin Li LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axis Heliyon lncRNA Taurine-upregulated gene 1 miR-542-3p Hypoxia-inducible factor-1-alpha Chronic kidney disease |
| title | LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axis |
| title_full | LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axis |
| title_fullStr | LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axis |
| title_full_unstemmed | LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axis |
| title_short | LncRNA TUG1 mitigates chronic kidney disease through miR-542-3p/HIF-1α/VEGF axis |
| title_sort | lncrna tug1 mitigates chronic kidney disease through mir 542 3p hif 1α vegf axis |
| topic | lncRNA Taurine-upregulated gene 1 miR-542-3p Hypoxia-inducible factor-1-alpha Chronic kidney disease |
| url | http://www.sciencedirect.com/science/article/pii/S2405844024169228 |
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