التفاصيل البيبلوغرافية
| العنوان: |
Lipocalin-2 Deficiency Diminishes Canonical NLRP3 Inflammasome Formation and IL-1β Production in the Subacute Phase of Spinal Cord Injury. |
| المؤلفون: |
Müller, Nina, Scheld, Miriam, Voelz, Clara, Gasterich, Natalie, Zhao, Weiyi, Behrens, Victoria, Weiskirchen, Ralf, Baazm, Maryam, Clarner, Tim, Beyer, Cordian, Sanadgol, Nima, Zendedel, Adib |
| المصدر: |
International Journal of Molecular Sciences; May2023, Vol. 24 Issue 10, p8689, 18p |
| مصطلحات موضوعية: |
SPINAL cord injuries, NLRP3 protein, INFLAMMASOMES, LIPOCALIN-2, LIPOCALINS, TOLL-like receptors |
| مستخلص: |
Spinal cord injury (SCI) results in the production of proinflammatory cytokines due to inflammasome activation. Lipocalin 2 (LCN2) is a small secretory glycoprotein upregulated by toll-like receptor (TLR) signaling in various cells and tissues. LCN2 secretion is induced by infection, injury, and metabolic disorders. In contrast, LCN2 has been implicated as an anti-inflammatory regulator. However, the role of LCN2 in inflammasome activation during SCI remains unknown. This study examined the role of Lcn2 deficiency in the NLRP3 inflammasome-dependent neuroinflammation in SCI. Lcn2−/− and wild-type (WT) mice were subjected to SCI, and locomotor function, formation of the inflammasome complex, and neuroinflammation were assessed. Our findings demonstrated that significant activation of the HMGB1/PYCARD/caspase-1 inflammatory axis was accompanied by the overexpression of LCN2 7 days after SCI in WT mice. This signal transduction results in the cleaving of the pyroptosis-inducing protein gasdermin D (GSDMD) and the maturation of the proinflammatory cytokine IL-1β. Furthermore, Lcn2−/− mice showed considerable downregulation in the HMGB1/NLRP3/PYCARD/caspase-1 axis, IL-1β production, pore formation, and improved locomotor function compared with WT. Our data suggest that LCN2 may play a role as a putative molecule for the induction of inflammasome-related neuroinflammation in SCI. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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