TAX1BP1 regulates the apoptosis of renal tubular epithelial cells in ischemia/reperfusion injury via the NF-kB/PMAIP1 signaling pathway
Background The pathogenesis of acute kidney injury (AKI) is not fully understood. Tax1-binding protein 1 (TAX1BP1) modulates inflammation and apoptosis through the NF-kB signaling pathway, however, its specific role in ischemic AKI remains unclear. Methods We injected a TAX1BP1 overexpression plasmi...
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| Veröffentlicht in: | Inflammation research 2025-12, Vol.74 (1), p.9, Article 9 |
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| creator | Wu, Zhifen Tan, Wei Wang, Chunxuan Lin, Lirong Tian, En Huo, Bengang Zheng, Luquan Yang, Xujia Li, Ke Yang, Jurong |
| description | Background
The pathogenesis of acute kidney injury (AKI) is not fully understood. Tax1-binding protein 1 (TAX1BP1) modulates inflammation and apoptosis through the NF-kB signaling pathway, however, its specific role in ischemic AKI remains unclear.
Methods
We injected a TAX1BP1 overexpression plasmid into the tail vein of male C57BL/6 mice, followed by clamping the bilateral renal arteries to induce AKI. Additionally, TAX1BP1 overexpression and silencing vectors were transfected into NRK52E cells to establish an in vitro hypoxia-reoxygenation model. Renal tubular necrosis was assessed using PAS and H&E staining. Expression levels of TAX1BP1, caspase-3, Bcl2, phosphorylated p65, and total p65 were measured through Western blot in both models. RT-PCR was used to evaluate KIM-1, NGAL, IL-6, and TNFα expression, while TUNEL staining detected apoptosis in renal tubular epithelial cells. RNA sequencing identified potential TAX1BP1 targets, which were validated via Western blot and RT-PCR.
Results
Our results indicate that TAX1BP1 significantly influences ischemic AKI by modulating apoptosis and inflammation in kidney tissues. In vitro studies confirmed its critical role in renal tubular epithelial cell apoptosis and inflammation through NF-kB activation, potentially via PMAIP1.
Conclusion
TAX1BP1 may protect renal tubular epithelial cells by targeting PMAIP1 through the NF-kB signaling pathway in ischemic AKI. |
| doi_str_mv | 10.1007/s00011-024-01976-4 |
| format | Article |
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The pathogenesis of acute kidney injury (AKI) is not fully understood. Tax1-binding protein 1 (TAX1BP1) modulates inflammation and apoptosis through the NF-kB signaling pathway, however, its specific role in ischemic AKI remains unclear.
Methods
We injected a TAX1BP1 overexpression plasmid into the tail vein of male C57BL/6 mice, followed by clamping the bilateral renal arteries to induce AKI. Additionally, TAX1BP1 overexpression and silencing vectors were transfected into NRK52E cells to establish an in vitro hypoxia-reoxygenation model. Renal tubular necrosis was assessed using PAS and H&E staining. Expression levels of TAX1BP1, caspase-3, Bcl2, phosphorylated p65, and total p65 were measured through Western blot in both models. RT-PCR was used to evaluate KIM-1, NGAL, IL-6, and TNFα expression, while TUNEL staining detected apoptosis in renal tubular epithelial cells. RNA sequencing identified potential TAX1BP1 targets, which were validated via Western blot and RT-PCR.
Results
Our results indicate that TAX1BP1 significantly influences ischemic AKI by modulating apoptosis and inflammation in kidney tissues. In vitro studies confirmed its critical role in renal tubular epithelial cell apoptosis and inflammation through NF-kB activation, potentially via PMAIP1.
Conclusion
TAX1BP1 may protect renal tubular epithelial cells by targeting PMAIP1 through the NF-kB signaling pathway in ischemic AKI.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-024-01976-4</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allergology ; Apoptosis ; Bcl-2 protein ; Biomedical and Life Sciences ; Biomedicine ; Caspase-3 ; Cell activation ; Dermatology ; Epithelial cells ; Epithelium ; Expression vectors ; Gene expression ; Gene sequencing ; Hypoxia ; Immunology ; Inflammation ; Ischemia ; Kidneys ; Necrosis ; Neurology ; NF-κB protein ; Original Research Paper ; Pathogenesis ; Pharmacology/Toxicology ; Polymerase chain reaction ; Renal artery ; Reperfusion ; Rheumatology ; Signal transduction ; Staining ; Target detection</subject><ispartof>Inflammation research, 2025-12, Vol.74 (1), p.9, Article 9</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Switzerland AG 2024 Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>Copyright Springer Nature B.V. Dec 2025</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c1154-b2213980cc047cf8b45f4489cc538605e2b70749e618a13abbe9ebd54e20bdef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00011-024-01976-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00011-024-01976-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids></links><search><creatorcontrib>Wu, Zhifen</creatorcontrib><creatorcontrib>Tan, Wei</creatorcontrib><creatorcontrib>Wang, Chunxuan</creatorcontrib><creatorcontrib>Lin, Lirong</creatorcontrib><creatorcontrib>Tian, En</creatorcontrib><creatorcontrib>Huo, Bengang</creatorcontrib><creatorcontrib>Zheng, Luquan</creatorcontrib><creatorcontrib>Yang, Xujia</creatorcontrib><creatorcontrib>Li, Ke</creatorcontrib><creatorcontrib>Yang, Jurong</creatorcontrib><title>TAX1BP1 regulates the apoptosis of renal tubular epithelial cells in ischemia/reperfusion injury via the NF-kB/PMAIP1 signaling pathway</title><title>Inflammation research</title><addtitle>Inflamm. Res</addtitle><description>Background
The pathogenesis of acute kidney injury (AKI) is not fully understood. Tax1-binding protein 1 (TAX1BP1) modulates inflammation and apoptosis through the NF-kB signaling pathway, however, its specific role in ischemic AKI remains unclear.
Methods
We injected a TAX1BP1 overexpression plasmid into the tail vein of male C57BL/6 mice, followed by clamping the bilateral renal arteries to induce AKI. Additionally, TAX1BP1 overexpression and silencing vectors were transfected into NRK52E cells to establish an in vitro hypoxia-reoxygenation model. Renal tubular necrosis was assessed using PAS and H&E staining. Expression levels of TAX1BP1, caspase-3, Bcl2, phosphorylated p65, and total p65 were measured through Western blot in both models. RT-PCR was used to evaluate KIM-1, NGAL, IL-6, and TNFα expression, while TUNEL staining detected apoptosis in renal tubular epithelial cells. RNA sequencing identified potential TAX1BP1 targets, which were validated via Western blot and RT-PCR.
Results
Our results indicate that TAX1BP1 significantly influences ischemic AKI by modulating apoptosis and inflammation in kidney tissues. In vitro studies confirmed its critical role in renal tubular epithelial cell apoptosis and inflammation through NF-kB activation, potentially via PMAIP1.
Conclusion
TAX1BP1 may protect renal tubular epithelial cells by targeting PMAIP1 through the NF-kB signaling pathway in ischemic AKI.</description><subject>Allergology</subject><subject>Apoptosis</subject><subject>Bcl-2 protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caspase-3</subject><subject>Cell activation</subject><subject>Dermatology</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Expression vectors</subject><subject>Gene expression</subject><subject>Gene sequencing</subject><subject>Hypoxia</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Kidneys</subject><subject>Necrosis</subject><subject>Neurology</subject><subject>NF-κB protein</subject><subject>Original Research Paper</subject><subject>Pathogenesis</subject><subject>Pharmacology/Toxicology</subject><subject>Polymerase chain reaction</subject><subject>Renal artery</subject><subject>Reperfusion</subject><subject>Rheumatology</subject><subject>Signal transduction</subject><subject>Staining</subject><subject>Target detection</subject><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><recordid>eNp9kMtOwzAQRSMEEs8fYGWJten4kcRZthWPSuWxAImd5ZhJ6hKSYCegfgG_jaFI7FjNaObcO6ObJKcMzhlAPgkAwBgFLimwIs-o3EkOmORAC1BPu7EHLqhQAvaTwxDWEVdc8YPk82H6xGb3jHisx8YMGMiwQmL6rh-64ALpqrhqTUOGsYyAJ9i7SDQujiw2TSCuJS7YFb46M_HYo6_G4Lo4bNej35B3Z34sby_py2xyfzNdxGvB1dHTtTXpzbD6MJvjZK8yTcCT33qUPF5ePMyv6fLuajGfLqllLJW05JyJQoG1IHNbqVKmlZSqsDYVKoMUeZlDLgvMmDJMmLLEAsvnVCKH8hkrcZScbX17372NGAa97kYffwlasJQVRaryLFJ8S1nfheCx0r13r8ZvNAP9HbjeBq5j4PoncC2jSGxFIcJtjf7P-h_VF63_hBk</recordid><startdate>20251201</startdate><enddate>20251201</enddate><creator>Wu, Zhifen</creator><creator>Tan, Wei</creator><creator>Wang, Chunxuan</creator><creator>Lin, Lirong</creator><creator>Tian, En</creator><creator>Huo, Bengang</creator><creator>Zheng, Luquan</creator><creator>Yang, Xujia</creator><creator>Li, Ke</creator><creator>Yang, Jurong</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope></search><sort><creationdate>20251201</creationdate><title>TAX1BP1 regulates the apoptosis of renal tubular epithelial cells in ischemia/reperfusion injury via the NF-kB/PMAIP1 signaling pathway</title><author>Wu, Zhifen ; Tan, Wei ; Wang, Chunxuan ; Lin, Lirong ; Tian, En ; Huo, Bengang ; Zheng, Luquan ; Yang, Xujia ; Li, Ke ; Yang, Jurong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1154-b2213980cc047cf8b45f4489cc538605e2b70749e618a13abbe9ebd54e20bdef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2025</creationdate><topic>Allergology</topic><topic>Apoptosis</topic><topic>Bcl-2 protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caspase-3</topic><topic>Cell activation</topic><topic>Dermatology</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Expression vectors</topic><topic>Gene expression</topic><topic>Gene sequencing</topic><topic>Hypoxia</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Kidneys</topic><topic>Necrosis</topic><topic>Neurology</topic><topic>NF-κB protein</topic><topic>Original Research Paper</topic><topic>Pathogenesis</topic><topic>Pharmacology/Toxicology</topic><topic>Polymerase chain reaction</topic><topic>Renal artery</topic><topic>Reperfusion</topic><topic>Rheumatology</topic><topic>Signal transduction</topic><topic>Staining</topic><topic>Target detection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Zhifen</creatorcontrib><creatorcontrib>Tan, Wei</creatorcontrib><creatorcontrib>Wang, Chunxuan</creatorcontrib><creatorcontrib>Lin, Lirong</creatorcontrib><creatorcontrib>Tian, En</creatorcontrib><creatorcontrib>Huo, Bengang</creatorcontrib><creatorcontrib>Zheng, Luquan</creatorcontrib><creatorcontrib>Yang, Xujia</creatorcontrib><creatorcontrib>Li, Ke</creatorcontrib><creatorcontrib>Yang, Jurong</creatorcontrib><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Zhifen</au><au>Tan, Wei</au><au>Wang, Chunxuan</au><au>Lin, Lirong</au><au>Tian, En</au><au>Huo, Bengang</au><au>Zheng, Luquan</au><au>Yang, Xujia</au><au>Li, Ke</au><au>Yang, Jurong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TAX1BP1 regulates the apoptosis of renal tubular epithelial cells in ischemia/reperfusion injury via the NF-kB/PMAIP1 signaling pathway</atitle><jtitle>Inflammation research</jtitle><stitle>Inflamm. Res</stitle><date>2025-12-01</date><risdate>2025</risdate><volume>74</volume><issue>1</issue><spage>9</spage><pages>9-</pages><artnum>9</artnum><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Background
The pathogenesis of acute kidney injury (AKI) is not fully understood. Tax1-binding protein 1 (TAX1BP1) modulates inflammation and apoptosis through the NF-kB signaling pathway, however, its specific role in ischemic AKI remains unclear.
Methods
We injected a TAX1BP1 overexpression plasmid into the tail vein of male C57BL/6 mice, followed by clamping the bilateral renal arteries to induce AKI. Additionally, TAX1BP1 overexpression and silencing vectors were transfected into NRK52E cells to establish an in vitro hypoxia-reoxygenation model. Renal tubular necrosis was assessed using PAS and H&E staining. Expression levels of TAX1BP1, caspase-3, Bcl2, phosphorylated p65, and total p65 were measured through Western blot in both models. RT-PCR was used to evaluate KIM-1, NGAL, IL-6, and TNFα expression, while TUNEL staining detected apoptosis in renal tubular epithelial cells. RNA sequencing identified potential TAX1BP1 targets, which were validated via Western blot and RT-PCR.
Results
Our results indicate that TAX1BP1 significantly influences ischemic AKI by modulating apoptosis and inflammation in kidney tissues. In vitro studies confirmed its critical role in renal tubular epithelial cell apoptosis and inflammation through NF-kB activation, potentially via PMAIP1.
Conclusion
TAX1BP1 may protect renal tubular epithelial cells by targeting PMAIP1 through the NF-kB signaling pathway in ischemic AKI.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><doi>10.1007/s00011-024-01976-4</doi></addata></record> |
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| subjects | Allergology Apoptosis Bcl-2 protein Biomedical and Life Sciences Biomedicine Caspase-3 Cell activation Dermatology Epithelial cells Epithelium Expression vectors Gene expression Gene sequencing Hypoxia Immunology Inflammation Ischemia Kidneys Necrosis Neurology NF-κB protein Original Research Paper Pathogenesis Pharmacology/Toxicology Polymerase chain reaction Renal artery Reperfusion Rheumatology Signal transduction Staining Target detection |
| title | TAX1BP1 regulates the apoptosis of renal tubular epithelial cells in ischemia/reperfusion injury via the NF-kB/PMAIP1 signaling pathway |
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