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| Format: | Artículo científico |
| Langue: | en |
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Life sciences
2025
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| Accès en ligne: | https://pubmed.ncbi.nlm.nih.gov/40164332/ |
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| author | Long, Luosha Li, Meng Wang, Minghui Liang, Baien Huang, Meiying Yuan, Xi Wu, Xinyan Guo, Xiangdong Li, Suchun Liu, Zhende Liu, Weizhi Chen, Wei Wang, Weidong Lyu, Qianqian Li, Chunling |
| author_facet | Long, Luosha Li, Meng Wang, Minghui Liang, Baien Huang, Meiying Yuan, Xi Wu, Xinyan Guo, Xiangdong Li, Suchun Liu, Zhende Liu, Weizhi Chen, Wei Wang, Weidong Lyu, Qianqian Li, Chunling Long, Luosha Li, Meng Wang, Minghui Liang, Baien Huang, Meiying Yuan, Xi Wu, Xinyan Guo, Xiangdong Li, Suchun Liu, Zhende Liu, Weizhi Chen, Wei Wang, Weidong Lyu, Qianqian Li, Chunling |
| collection | PubMed - marine biology |
| contents | Activation of mannose receptor C type 1 in macrophages improves renal fibrosis through mediating fibronectin endocytosis. Long, Luosha Li, Meng Wang, Minghui Liang, Baien Huang, Meiying Yuan, Xi Wu, Xinyan Guo, Xiangdong Li, Suchun Liu, Zhende Liu, Weizhi Chen, Wei Wang, Weidong Lyu, Qianqian Li, Chunling Animals Mice Fibronectins Macrophages Fibrosis Endocytosis Mice, Knockout Mice, Inbred C57BL RAW 264.7 Cells Receptors, Cell Surface Male Kidney Diseases Ureteral Obstruction Lectins, C-Type Mannose Receptor Kidney Mannose-Binding Lectins Reperfusion Injury Transforming Growth Factor beta1 Signal Transduction Excess extracellular matrix (ECM) deposition is the characteristic of renal fibrosis, owing to the imbalance between synthesis and degradation. Fibronectin could regulate the deposition of other ECM, thus plays a crucial role in the progression of renal fibrosis. Mannose receptor C type 1 (MRC1), largely expressed on macrophages, owns an extracellular fibronectin type II domain that binds to and internalizes collagen and thus involves in fibrosis modulation. The purpose of the present study was to investigate whether MRC1 participates in the internalization of fibronectin and whether alginate oligosaccharides (AOSC), a degradation product of alginate, has beneficial effects in the resolution of renal fibrosis via MRC1. Renal fibrosis models were constructed by unilateral ureteral obstruction (UUO) and unilateral ischemia-reperfusion injury (UIRI) in MRC1-WT and MRC1-KO mice. RAW264.7 cells were treated with TGF-β1 to induce pro-fibrotic responses. Expression of fibrotic markers and fibronectin endocytosis were examined. MRC1 gene knockout aggravated renal fibrosis in UUO and UIRI models. Inhibition of MRC1 exacerbated TGF-β1-induced pro-fibrotic responses in RAW264.7 cells. MRC1 regulated integrin β1-mediated fibronectin endocytosis through Arp2/3-Kindlin-2 signaling pathway. AOSC improved renal fibrosis by increasing MRC1 expression and endocytosis of fibronectin. Our findings highlight the importance of MRC1 and fibronectin endocytosis in the development of renal fibrosis, suggesting that activation of MRC1 by AOSC is probably a therapeutic option to delay the progress of kidney fibrosis. |
| format | Artículo científico |
| id | pubmed_40164332 |
| institution | PubMed |
| language | en |
| publishDate | 2025 |
| publisher | Life sciences |
| record_format | pubmed |
| spellingShingle | Activation of mannose receptor C type 1 in macrophages improves renal fibrosis through mediating fibronectin endocytosis. Long, Luosha Li, Meng Wang, Minghui Liang, Baien Huang, Meiying Yuan, Xi Wu, Xinyan Guo, Xiangdong Li, Suchun Liu, Zhende Liu, Weizhi Chen, Wei Wang, Weidong Lyu, Qianqian Li, Chunling Animals Mice Fibronectins Macrophages Fibrosis Endocytosis Mice, Knockout Mice, Inbred C57BL RAW 264.7 Cells Receptors, Cell Surface Male Kidney Diseases Ureteral Obstruction Lectins, C-Type Mannose Receptor Kidney Mannose-Binding Lectins Reperfusion Injury Transforming Growth Factor beta1 Signal Transduction Activation of mannose receptor C type 1 in macrophages improves renal fibrosis through mediating fibronectin endocytosis. Long, Luosha Li, Meng Wang, Minghui Liang, Baien Huang, Meiying Yuan, Xi Wu, Xinyan Guo, Xiangdong Li, Suchun Liu, Zhende Liu, Weizhi Chen, Wei Wang, Weidong Lyu, Qianqian Li, Chunling Animals Mice Fibronectins Macrophages Fibrosis Endocytosis Mice, Knockout Mice, Inbred C57BL RAW 264.7 Cells Receptors, Cell Surface Male Kidney Diseases Ureteral Obstruction Lectins, C-Type Mannose Receptor Kidney Mannose-Binding Lectins Reperfusion Injury Transforming Growth Factor beta1 Signal Transduction Excess extracellular matrix (ECM) deposition is the characteristic of renal fibrosis, owing to the imbalance between synthesis and degradation. Fibronectin could regulate the deposition of other ECM, thus plays a crucial role in the progression of renal fibrosis. Mannose receptor C type 1 (MRC1), largely expressed on macrophages, owns an extracellular fibronectin type II domain that binds to and internalizes collagen and thus involves in fibrosis modulation. The purpose of the present study was to investigate whether MRC1 participates in the internalization of fibronectin and whether alginate oligosaccharides (AOSC), a degradation product of alginate, has beneficial effects in the resolution of renal fibrosis via MRC1. Renal fibrosis models were constructed by unilateral ureteral obstruction (UUO) and unilateral ischemia-reperfusion injury (UIRI) in MRC1-WT and MRC1-KO mice. RAW264.7 cells were treated with TGF-β1 to induce pro-fibrotic responses. Expression of fibrotic markers and fibronectin endocytosis were examined. MRC1 gene knockout aggravated renal fibrosis in UUO and UIRI models. Inhibition of MRC1 exacerbated TGF-β1-induced pro-fibrotic responses in RAW264.7 cells. MRC1 regulated integrin β1-mediated fibronectin endocytosis through Arp2/3-Kindlin-2 signaling pathway. AOSC improved renal fibrosis by increasing MRC1 expression and endocytosis of fibronectin. Our findings highlight the importance of MRC1 and fibronectin endocytosis in the development of renal fibrosis, suggesting that activation of MRC1 by AOSC is probably a therapeutic option to delay the progress of kidney fibrosis. |
| title | Activation of mannose receptor C type 1 in macrophages improves renal fibrosis through mediating fibronectin endocytosis. |
| topic | Animals Mice Fibronectins Macrophages Fibrosis Endocytosis Mice, Knockout Mice, Inbred C57BL RAW 264.7 Cells Receptors, Cell Surface Male Kidney Diseases Ureteral Obstruction Lectins, C-Type Mannose Receptor Kidney Mannose-Binding Lectins Reperfusion Injury Transforming Growth Factor beta1 Signal Transduction |
| url | https://pubmed.ncbi.nlm.nih.gov/40164332/ |