دورية أكاديمية
أعرض في EDS

DAMPs Released From Injured Renal Tubular Epithelial Cells Activate Innate Immune Signals in Healthy Renal Tubular Epithelial Cells.

التفاصيل البيبلوغرافية
العنوان: DAMPs Released From Injured Renal Tubular Epithelial Cells Activate Innate Immune Signals in Healthy Renal Tubular Epithelial Cells.
المؤلفون: DeWolf SE; Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA.; Department of Pulmonary and Critical Care Medicine, University of California San Diego, San Diego, CA., Kasimsetty SG; Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA., Hawkes AA; Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA., Stocks LM; LifeSharing Organ Procurement Organization, San Diego, CA., Kurian SM; Division of Cell and Organ Transplantion, Scripps Clinic and Green Hospital, La Jolla, CA., McKay DB; Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA.; Division of Cell and Organ Transplantion, Scripps Clinic and Green Hospital, La Jolla, CA.
المصدر: Transplantation [Transplantation] 2022 Aug 01; Vol. 106 (8), pp. 1589-1599. Date of Electronic Publication: 2021 Dec 23.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 0132144 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1534-6080 (Electronic) Linking ISSN: 00411337 NLM ISO Abbreviation: Transplantation Subsets: MEDLINE
أسماء مطبوعة: Publication: Hagerstown, MD : Lippincott Williams & Wilkins
Original Publication: Baltimore, Williams & Wilkins.
مواضيع طبية MeSH: Acute Kidney Injury* , Reperfusion Injury*/metabolism, Alarmins ; Epithelial Cells/metabolism ; Humans ; Immunity, Innate ; Kidney/metabolism
مستخلص: Background: Renal ischemia-reperfusion injury (IRI) predictably causes acute kidney injury after shock and major cardiovascular procedures in all kidneys procured for transplantation. The earliest events of IRI are triggered by molecules released from injured cells, damage-associated molecular patterns (DAMPs), that bind pattern recognition receptors (PRRs) constitutively expressed on many cells within the kidney. Activation of PRR signaling leads to production of proinflammatory molecules, which incite a cascade of inflammatory events leading to acute kidney injury. Renal tubular epithelial cells (RTECs) are particularly susceptible to ischemic injury, and proximal RTEC injury is pathognomonic of renal IRI. To better understand how injured RTECs contribute to the cycle of deleterious inflammation in the setting of renal IRI, this study asked whether DAMPs released from injured RTECs induced PRR signals in healthy RTECs.
Methods: Human RTECs were necrosed ex vivo to release intracellular DAMPs and resulting necrotic supernatant used to stimulate healthy RTECs, T lymphocytes, and monocytes.
Results: DAMPs released from necrosed RTECs upregulated PRRs known to be associated with renal IRI and activated mitogen-activated protein kinase signaling pathways. Proinflammatory cytokines were upregulated in response to necrotic supernatant, and this upregulation was abrogated by MEK-1 inhibition. The RTEC-derived DAMPs were also potent inducers of T-cell activation/proliferation and monocyte migration.
Conclusions: This is the first study to our knowledge to show that endogenous DAMPs released from injured RTECs directly activate PRR signaling in healthy RTECs. These findings provide new insights directed to therapeutics for renal IRI.
Competing Interests: The authors declare no conflicts of interest.
(Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)
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معلومات مُعتمدة: R01 DK113162 United States DK NIDDK NIH HHS; R01 DK128547 United States DK NIDDK NIH HHS; R21 AI154471 United States AI NIAID NIH HHS
المشرفين على المادة: 0 (Alarmins)
تواريخ الأحداث: Date Created: 20211226 Date Completed: 20220728 Latest Revision: 20231002
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC9218002
DOI: 10.1097/TP.0000000000004038
PMID: 34954736
قاعدة البيانات: MEDLINE
الوصف
تدمد:1534-6080
DOI:10.1097/TP.0000000000004038