GPR4 aggravates ferroptosis in nucleus pulposus cells by inhibiting mitophagy via MAPK pathway activation

GPR4 aggravates ferroptosis in nucleus pulposus cells by inhibiting mitophagy via MAPK pathway activation | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article GPR4 aggravates ferroptosis in nucleus pulposus cells by inhibiting mitophagy via MAPK pathway activation Jie Zhao, Zhaoqiang Xu, Jiawen Niu, Hang Du, Yang Zhang, Yachao Zhao, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7509828/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Graphical Abstract Abstract Inflammatory diseases are known to lower the pH of the extracellular microenvironment. However, the role of proton-activated G protein-coupled receptors (GPRs) in the progression of intervertebral disc degeneration (IVDD) remains largely unexplored. In this study, we identified GPR4 as a key regulator of IVDD progression. Our analysis revealed a significant upregulation of GPR4 in degenerative human intervertebral discs. The expression of GPR4 was assessed in 58 human disc samples (male: female = 31:27) and rat models (n = 3 per group) using western blotting (WB) and immunohistochemistry (IHC). Functional assays, including flow cytometry, immunofluorescence, and WB, were performed to evaluate the impact of GPR4 on ferroptosis. We observed that GPR4 expression was significantly elevated in tert-butyl hydroperoxide (TBHP)-treated degenerative nucleus pulposus cells (NPCs). Proteomic sequencing of primary NPCs further demonstrated that GPR4 overexpression altered gene expression related to mitochondrial energy metabolism and ferritin homeostasis. Notably, knockdown of GPR4 via shRNA (shGPR4) enhanced MAPK-mediated mitophagy while suppressing ferroptosis in TBHP-exposed NPCs. These findings suggest that GPR4 plays a critical role in IVDD pathogenesis and may serve as a potential therapeutic target for mitigating disc degeneration. GPR4 Ferroptosis Mitophagy MAPK IVDD Full Text Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7509828","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":524823108,"identity":"68f56938-23b8-41b8-8254-df88c6950501","order_by":0,"name":"Jie Zhao","email":"","orcid":"","institution":"The Second Hospital of Shandong University","correspondingAuthor":false,"prefix":"","firstName":"Jie","middleName":"","lastName":"Zhao","suffix":""},{"id":524823110,"identity":"83278823-7f7d-496a-b8e5-38b24ff069c0","order_by":1,"name":"Zhaoqiang Xu","email":"","orcid":"","institution":"The Second Hospital of Shandong 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However, the role of proton-activated G protein-coupled receptors (GPRs) in the progression of intervertebral disc degeneration (IVDD) remains largely unexplored. In this study, we identified GPR4 as a key regulator of IVDD progression. Our analysis revealed a significant upregulation of GPR4 in degenerative human intervertebral discs. The expression of GPR4 was assessed in 58 human disc samples (male: female\u0026thinsp;=\u0026thinsp;31:27) and rat models (n\u0026thinsp;=\u0026thinsp;3 per group) using western blotting (WB) and immunohistochemistry (IHC). Functional assays, including flow cytometry, immunofluorescence, and WB, were performed to evaluate the impact of GPR4 on ferroptosis. We observed that GPR4 expression was significantly elevated in tert-butyl hydroperoxide (TBHP)-treated degenerative nucleus pulposus cells (NPCs). Proteomic sequencing of primary NPCs further demonstrated that GPR4 overexpression altered gene expression related to mitochondrial energy metabolism and ferritin homeostasis. Notably, knockdown of GPR4 via shRNA (shGPR4) enhanced MAPK-mediated mitophagy while suppressing ferroptosis in TBHP-exposed NPCs. These findings suggest that GPR4 plays a critical role in IVDD pathogenesis and may serve as a potential therapeutic target for mitigating disc degeneration.","description":"","filename":"Onlinefloatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-7509828/v1/f5f8bc8279a40affcda8e696.png"},{"id":97250797,"identity":"99ae2b86-b352-47e2-8104-5d1deb448498","added_by":"auto","created_at":"2025-12-02 13:15:16","extension":"pdf","order_by":1,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1866904,"visible":true,"origin":"","legend":"","description":"","filename":"ManuscriptZJ.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7509828/v1_covered_7e5f25bd-d1b4-43bd-817b-5af53e81b356.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"GPR4 aggravates ferroptosis in nucleus pulposus cells by inhibiting mitophagy via MAPK pathway activation","fulltext":[],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":false,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":true,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":true,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"GPR4, Ferroptosis, Mitophagy; MAPK, IVDD","lastPublishedDoi":"10.21203/rs.3.rs-7509828/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7509828/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"Inflammatory diseases are known to lower the pH of the extracellular microenvironment. However, the role of proton-activated G protein-coupled receptors (GPRs) in the progression of intervertebral disc degeneration (IVDD) remains largely unexplored. In this study, we identified GPR4 as a key regulator of IVDD progression. Our analysis revealed a significant upregulation of GPR4 in degenerative human intervertebral discs. The expression of GPR4 was assessed in 58 human disc samples (male: female\u0026thinsp;=\u0026thinsp;31:27) and rat models (n\u0026thinsp;=\u0026thinsp;3 per group) using western blotting (WB) and immunohistochemistry (IHC). Functional assays, including flow cytometry, immunofluorescence, and WB, were performed to evaluate the impact of GPR4 on ferroptosis. We observed that GPR4 expression was significantly elevated in tert-butyl hydroperoxide (TBHP)-treated degenerative nucleus pulposus cells (NPCs). Proteomic sequencing of primary NPCs further demonstrated that GPR4 overexpression altered gene expression related to mitochondrial energy metabolism and ferritin homeostasis. Notably, knockdown of GPR4 via shRNA (shGPR4) enhanced MAPK-mediated mitophagy while suppressing ferroptosis in TBHP-exposed NPCs. These findings suggest that GPR4 plays a critical role in IVDD pathogenesis and may serve as a potential therapeutic target for mitigating disc degeneration.","manuscriptTitle":"GPR4 aggravates ferroptosis in nucleus pulposus cells by inhibiting mitophagy via MAPK pathway activation","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-10-07 18:51:18","doi":"10.21203/rs.3.rs-7509828/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"870a162a-7e11-4577-af44-7f94393014f8","owner":[],"postedDate":"October 7th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-12-01T19:53:27+00:00","versionOfRecord":[],"versionCreatedAt":"2025-10-07 18:51:18","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7509828","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7509828","identity":"rs-7509828","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}