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Caspase-11 promotes NLRP3 inflammasome activation via the cleavage of pannexin1 in acute kidney disease
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Caspase-11 promotes NLRP3 inflammasome activation via the cleavage of pannexin1 in acute kidney disease
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Journal Article
Caspase-11 promotes NLRP3 inflammasome activation via the cleavage of pannexin1 in acute kidney disease
2022
Overview
Ischemia/reperfusion (I/R) injury is a major cause of acute kidney injury (AKI) in clinic. The activation of NLRP3 inflammasome is associated with inflammation and renal injury in I/R-induced AKI. In the current study we explored the molecular and cellular mechanisms for NLRP3 inflammasome activation following renal I/R. Mice were subjected to I/R renal injury by clamping bilateral renal pedicles. We showed that I/R injury markedly increased caspase-11 expression and the cleavage of pannexin 1 (panx1) in the kidneys accompanied by NLRP3 inflammasome activation evidenced by the activation of caspase-1 and interlukin-1β (IL-1β) maturation. In
Casp-11
−/−
mice, I/R-induced panx1 cleavage, NLRP3 inflammasome activation as well as renal functional deterioration and tubular morphological changes were significantly attenuated. In cultured primary tubular cells (PTCs) and NRK-52E cells, hypoxia/reoxygenation (H/R) markedly increased caspase-11 expression, NLRP3 inflammasome activation, IL-1β maturation and panx1 cleavage. Knockdown of caspase-11 attenuated all those changes; similar effects were observed in PTCs isolated from
Casp-11
−/−
mice. In NRK-52E cells, overexpression of caspase-11 promoted panx1 cleavage; pretreatment with panx1 inhibitor carbenoxolone or knockdown of panx1 significantly attenuated H/R-induced intracellular ATP reduction, extracellular ATP elevation and NLRP3 inflammasome activation without apparent influence on H/R-induced caspase-11 increase; pretreatment with P2X7 receptor inhibitor AZD9056 also attenuated NLRP3 inflammasome activation. The above results demonstrate that the cleavage of panx1 by upregulated caspase-11 is involved in facilitating ATP release and then NLRP3 inflammasome activation in I/R-induced AKI. This study provides new insight into the molecular mechanism of NLRP3 inflammasome activation in AKI.
Publisher
Springer Singapore,Nature Publishing Group
Subject
Acute Kidney Injury - metabolism
/ Acute Kidney Injury - pathology
/ Animals
/ Biomedical and Life Sciences
/ Caspases, Initiator - deficiency
/ Caspases, Initiator - metabolism
/ Dose-Response Relationship, Drug
/ Hypoxia
/ IL-1β
/ Ischemia
/ Kidneys
/ Mice
/ Nerve Tissue Proteins - metabolism
/ NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Structure-Activity Relationship
/ Vaccine
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