Inhibition of RIP1-RIP3-mediated necroptosis attenuates renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in unilateral ureteral obstruction
Renal fibrosis represents the final common outcome of chronic kidney disease of virtually any etiology. However, the mechanism underlying the evolution of renal fibrosis remains to be addressed. This study sought to clarify whether RIP1-RIP3-mediated necroptosis is involved in renal fibrosis via Wnt...
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| Veröffentlicht in: | PloS one 2022-10, Vol.17 (10), p.e0274116 |
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| creator | Piao, Shang Guo Ding, Jun Lin, Xue Jing Nan, Qi Yan Xuan, Mei Ying Jiang, Yu Ji Zheng, Hai Lan Jin, Ji Zhe Li, Can |
| description | Renal fibrosis represents the final common outcome of chronic kidney disease of virtually any etiology. However, the mechanism underlying the evolution of renal fibrosis remains to be addressed. This study sought to clarify whether RIP1-RIP3-mediated necroptosis is involved in renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in vitro and in a rat model of unilateral ureteral obstruction (UUO). Rats with UUO were administered RIP inhibitors (necrostatin-1 or GSK872) or β-catenin/TCF inhibitor ICG-001 daily for 7 consecutive days. UUO caused significant renal tubular necrosis and overexpression of RIP1-RIP3-MLKL axis proteins, and was accompanied by activation of the NLRP3 inflammasome and renal fibrosis. Oxidative stress caused by UUO was closely associated with endoplasmic reticulum stress and mitochondrial dysfunction, which resulted in apoptotic cell death via Wnt3α/β-catenin/GSK-3β signaling. All of these effects were abolished by an RIP inhibitor (necrostatin-1 or GSK872) or ICG-001. In H2O2-treated HK-2 cells, both RIP inhibitor and ICG-001 decreased intracellular reactive oxygen species production and apoptotic cells, but increased cell viability. Activated Wnt3α/β-catenin/GSK-3β signaling was decreased by either RIP inhibitor or ICG-001. Our findings suggest that RIP1-RIP3-mediated necroptosis contributes to the development of renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in UUO and may be a therapeutic target for protection against renal scarring of other origins. |
| doi_str_mv | 10.1371/journal.pone.0274116 |
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However, the mechanism underlying the evolution of renal fibrosis remains to be addressed. This study sought to clarify whether RIP1-RIP3-mediated necroptosis is involved in renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in vitro and in a rat model of unilateral ureteral obstruction (UUO). Rats with UUO were administered RIP inhibitors (necrostatin-1 or GSK872) or β-catenin/TCF inhibitor ICG-001 daily for 7 consecutive days. UUO caused significant renal tubular necrosis and overexpression of RIP1-RIP3-MLKL axis proteins, and was accompanied by activation of the NLRP3 inflammasome and renal fibrosis. Oxidative stress caused by UUO was closely associated with endoplasmic reticulum stress and mitochondrial dysfunction, which resulted in apoptotic cell death via Wnt3α/β-catenin/GSK-3β signaling. All of these effects were abolished by an RIP inhibitor (necrostatin-1 or GSK872) or ICG-001. In H2O2-treated HK-2 cells, both RIP inhibitor and ICG-001 decreased intracellular reactive oxygen species production and apoptotic cells, but increased cell viability. Activated Wnt3α/β-catenin/GSK-3β signaling was decreased by either RIP inhibitor or ICG-001. Our findings suggest that RIP1-RIP3-mediated necroptosis contributes to the development of renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in UUO and may be a therapeutic target for protection against renal scarring of other origins.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0274116</identifier><identifier>PMID: 36223414</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Apoptosis ; beta Catenin - metabolism ; Biology and Life Sciences ; Cell death ; Cell viability ; Cytokines ; Disease ; Endoplasmic reticulum ; Etiology ; Fibrosis ; Gene expression ; Glycogen Synthase Kinase 3 beta ; Hydrogen Peroxide ; Inflammasomes ; Inflammation ; Inhibitors ; Kidney diseases ; Kidney Diseases - complications ; Kidneys ; Kinases ; Medicine and Health Sciences ; Mitochondria ; Morphology ; Necroptosis ; Necrosis ; NLR Family, Pyrin Domain-Containing 3 Protein ; Oxidative stress ; Oxygen ; Pathogenesis ; Proteins ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism ; Research and Analysis Methods ; Signaling ; Therapeutic targets ; Transmission electron microscopy ; Ureteral Obstruction - complications ; β-Catenin</subject><ispartof>PloS one, 2022-10, Vol.17 (10), p.e0274116</ispartof><rights>2022 Piao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 Piao et al 2022 Piao et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-aa012dca455769a98b9913737af83228cb9dad88e138395d6e00472079e4b6c73</citedby><cites>FETCH-LOGICAL-c526t-aa012dca455769a98b9913737af83228cb9dad88e138395d6e00472079e4b6c73</cites><orcidid>0000-0002-9412-4412</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555645/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555645/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36223414$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Mukhopadhyay, Partha</contributor><creatorcontrib>Piao, Shang Guo</creatorcontrib><creatorcontrib>Ding, Jun</creatorcontrib><creatorcontrib>Lin, Xue Jing</creatorcontrib><creatorcontrib>Nan, Qi Yan</creatorcontrib><creatorcontrib>Xuan, Mei Ying</creatorcontrib><creatorcontrib>Jiang, Yu Ji</creatorcontrib><creatorcontrib>Zheng, Hai Lan</creatorcontrib><creatorcontrib>Jin, Ji Zhe</creatorcontrib><creatorcontrib>Li, Can</creatorcontrib><title>Inhibition of RIP1-RIP3-mediated necroptosis attenuates renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in unilateral ureteral obstruction</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Renal fibrosis represents the final common outcome of chronic kidney disease of virtually any etiology. 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In H2O2-treated HK-2 cells, both RIP inhibitor and ICG-001 decreased intracellular reactive oxygen species production and apoptotic cells, but increased cell viability. Activated Wnt3α/β-catenin/GSK-3β signaling was decreased by either RIP inhibitor or ICG-001. 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metabolism</topic><topic>Biology and Life Sciences</topic><topic>Cell death</topic><topic>Cell viability</topic><topic>Cytokines</topic><topic>Disease</topic><topic>Endoplasmic reticulum</topic><topic>Etiology</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Hydrogen Peroxide</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Inhibitors</topic><topic>Kidney diseases</topic><topic>Kidney Diseases - complications</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Medicine and Health Sciences</topic><topic>Mitochondria</topic><topic>Morphology</topic><topic>Necroptosis</topic><topic>Necrosis</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein</topic><topic>Oxidative stress</topic><topic>Oxygen</topic><topic>Pathogenesis</topic><topic>Proteins</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptor-Interacting Protein Serine-Threonine Kinases - 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However, the mechanism underlying the evolution of renal fibrosis remains to be addressed. This study sought to clarify whether RIP1-RIP3-mediated necroptosis is involved in renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in vitro and in a rat model of unilateral ureteral obstruction (UUO). Rats with UUO were administered RIP inhibitors (necrostatin-1 or GSK872) or β-catenin/TCF inhibitor ICG-001 daily for 7 consecutive days. UUO caused significant renal tubular necrosis and overexpression of RIP1-RIP3-MLKL axis proteins, and was accompanied by activation of the NLRP3 inflammasome and renal fibrosis. Oxidative stress caused by UUO was closely associated with endoplasmic reticulum stress and mitochondrial dysfunction, which resulted in apoptotic cell death via Wnt3α/β-catenin/GSK-3β signaling. All of these effects were abolished by an RIP inhibitor (necrostatin-1 or GSK872) or ICG-001. In H2O2-treated HK-2 cells, both RIP inhibitor and ICG-001 decreased intracellular reactive oxygen species production and apoptotic cells, but increased cell viability. Activated Wnt3α/β-catenin/GSK-3β signaling was decreased by either RIP inhibitor or ICG-001. Our findings suggest that RIP1-RIP3-mediated necroptosis contributes to the development of renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in UUO and may be a therapeutic target for protection against renal scarring of other origins.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>36223414</pmid><doi>10.1371/journal.pone.0274116</doi><orcidid>https://orcid.org/0000-0002-9412-4412</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Apoptosis beta Catenin - metabolism Biology and Life Sciences Cell death Cell viability Cytokines Disease Endoplasmic reticulum Etiology Fibrosis Gene expression Glycogen Synthase Kinase 3 beta Hydrogen Peroxide Inflammasomes Inflammation Inhibitors Kidney diseases Kidney Diseases - complications Kidneys Kinases Medicine and Health Sciences Mitochondria Morphology Necroptosis Necrosis NLR Family, Pyrin Domain-Containing 3 Protein Oxidative stress Oxygen Pathogenesis Proteins Rats Reactive oxygen species Reactive Oxygen Species - metabolism Receptor-Interacting Protein Serine-Threonine Kinases - metabolism Research and Analysis Methods Signaling Therapeutic targets Transmission electron microscopy Ureteral Obstruction - complications β-Catenin |
| title | Inhibition of RIP1-RIP3-mediated necroptosis attenuates renal fibrosis via Wnt3α/β-catenin/GSK-3β signaling in unilateral ureteral obstruction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T14%3A09%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inhibition%20of%20RIP1-RIP3-mediated%20necroptosis%20attenuates%20renal%20fibrosis%20via%20Wnt3%CE%B1/%CE%B2-catenin/GSK-3%CE%B2%20signaling%20in%20unilateral%20ureteral%20obstruction&rft.jtitle=PloS%20one&rft.au=Piao,%20Shang%20Guo&rft.date=2022-10-12&rft.volume=17&rft.issue=10&rft.spage=e0274116&rft.pages=e0274116-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0274116&rft_dat=%3Cproquest_plos_%3E2724213731%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2724213731&rft_id=info:pmid/36223414&rft_doaj_id=oai_doaj_org_article_b0da6ae3ff3840fa939873295063584b&rfr_iscdi=true |