• Login
    View Item 
    •   Home
    • UMass Chan Faculty and Staff Research and Publications
    • UMass Chan Faculty and Researcher Publications
    • View Item
    •   Home
    • UMass Chan Faculty and Staff Research and Publications
    • UMass Chan Faculty and Researcher Publications
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of eScholarship@UMassChanCommunitiesPublication DateAuthorsUMass Chan AffiliationsTitlesDocument TypesKeywordsThis CollectionPublication DateAuthorsUMass Chan AffiliationsTitlesDocument TypesKeywords

    My Account

    LoginRegister

    Help

    AboutSubmission GuidelinesData Deposit PolicySearchingAccessibilityTerms of UseWebsite Migration FAQ

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    JUN Amino-Terminal Kinase 1 Signaling in the Proximal Tubule Causes Cell Death and Acute Renal Failure in Rat and Mouse Models of Renal Ischemia/Reperfusion Injury

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    Publisher version
    View Source
    Access full-text PDFOpen Access
    View Source
    Check access options
    Check access options
    Authors
    Grynberg, Keren
    Ozols, Elyce
    Mulley, William R.
    Davis, Roger J.
    Flavell, Richard A.
    Nikolic-Paterson, David J.
    Ma, Frank Y.
    UMass Chan Affiliations
    Davis Lab
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2021-02-16
    Keywords
    Amino Acids, Peptides, and Proteins
    Cell Biology
    Cellular and Molecular Physiology
    Enzymes and Coenzymes
    Female Urogenital Diseases and Pregnancy Complications
    Male Urogenital Diseases
    Nephrology
    Pathological Conditions, Signs and Symptoms
    Pathology
    
    Metadata
    Show full item record
    Link to Full Text
    https://doi.org/10.1016/j.ajpath.2021.02.004
    Abstract
    Activation of the JUN amino-terminal kinase (JNK) pathway is prominent in most forms of acute and progressive tubulointerstitial damage, including acute renal ischemia/reperfusion injury (IRI). There are two forms of JNK expressed in the kidney, JNK1 and JNK2. Systemic administration of pan-JNK inhibitors suppresses renal IRI; however, the contribution of JNK1 versus JNK2, and the specific role of JNK activation in the proximal tubule in IRI, remains unknown. These questions were addressed in rat and mouse models of acute bilateral renal IRI. Administration of the JNK inhibitor, CC-930, substantially reduced the severity of renal failure, tubular damage, and inflammation at 24 hours in a rat IRI model. Next, Jnk1(-/-) mice, but not Jnk2(-/-) mice, were shown to be significantly protected against acute renal failure, tubular damage, and inflammation in the IRI model. Furthermore, mice with conditional Jnk1 deletion in the proximal tubule also showed considerable protection from IRI-induced renal failure, tubular damage, and inflammation. Finally, primary cultures of Jnk1(-/-), but not Jnk2(-/-), tubular epithelial cells were protected from oxidant-induced cell death, in association with preventing phosphorylation of proteins (receptor interacting serine/threonine kinase 3 and mixed lineage kinase domain-like pseudokinase) in the necroptosis pathway. In conclusion, JNK1, but not JNK2, plays a specific role in IRI-induced cell death in the proximal tubule, leading to acute renal failure.
    Source

    Grynberg K, Ozols E, Mulley WR, Davis RJ, Flavell RA, Nikolic-Paterson DJ, Ma FY. JUN Amino-Terminal Kinase 1 Signaling in the Proximal Tubule Causes Cell Death and Acute Renal Failure in Rat and Mouse Models of Renal Ischemia/Reperfusion Injury. Am J Pathol. 2021 Feb 16:S0002-9440(21)00049-3. doi: 10.1016/j.ajpath.2021.02.004. Epub ahead of print. PMID: 33607044. Link to article on publisher's site

    DOI
    10.1016/j.ajpath.2021.02.004
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/29702
    PubMed ID
    33607044
    Related Resources

    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1016/j.ajpath.2021.02.004
    Scopus Count
    Collections
    UMass Chan Faculty and Researcher Publications

    entitlement

    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Lamar Soutter Library, UMass Chan Medical School | 55 Lake Avenue North | Worcester, MA 01655 USA
    Quick Guide | escholarship@umassmed.edu
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.