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The Ninj1/Dusp1 Axis Contributes to Liver Ischemia Reperfusion Injury by Regulating Macrophage Activation and Neutrophil Infiltration. | LitMetric

The Ninj1/Dusp1 Axis Contributes to Liver Ischemia Reperfusion Injury by Regulating Macrophage Activation and Neutrophil Infiltration.

Cell Mol Gastroenterol Hepatol

Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China. Electronic address:

Published: April 2023

AI Article Synopsis

  • Liver ischemia-reperfusion (IR) injury poses significant risks in liver surgeries, and the role of Ninj1, a protein involved in inflammation, in this context is explored.
  • In experiments, mice lacking Ninj1 showed reduced liver injury and inflammation due to decreased neutrophil activity and proinflammatory cytokine production after IR events.
  • The study suggests that the Ninj1/Dusp1 pathway is crucial in managing liver inflammation and neutrophil infiltration, offering potential targets for improving recovery following liver surgeries.

Article Abstract

Background & Aims: Liver ischemia-reperfusion (IR) injury represents a major risk factor in both partial hepatectomy and liver transplantation. Nerve injury-induced protein 1 (Ninj1) is widely recognized as an adhesion molecule in leukocyte trafficking under inflammatory conditions, but its role in regulating sterile inflammation during liver IR injury remains unclear.

Methods: Myeloid Ninj1-deficient mice were generated by bone marrow chimeric models using Ninj1 knockout mice and wild-type mice. In vivo, a liver partial warm ischemia model was applied. Liver injury and hepatic inflammation were investigated. In vitro, primary Kupffer cells (KCs) isolated from Ninj1 knockout and wild-type mice were used to explore the function and mechanism of Ninj1 in modulating KC inflammation upon lipopolysaccharide stimulation.

Results: Ninj1 deficiency in KCs protected mice against liver IR injury during the later phase of reperfusion, especially in neutrophil infiltration, intrahepatic inflammation, and hepatocyte apoptosis. This prompted ischemia-primed KCs to decrease proinflammatory cytokine production. In vitro and in vivo, using small-interfering RNA against dual-specificity phosphatase 1 (DUSP1), we found that Ninj1 deficiency diminished the inflammatory response in KCs and neutrophil infiltration through DUSP1-dependent deactivation of the c-Jun-N-terminal kinase and p38 pathways. Sivelestat, a neutrophil elastase inhibitor, functioned similarly to Ninj1 deficiency, resulting in both mitigated hepatic IR injury in mice and a more rapid recovery of liver function in patients undergoing liver resection.

Conclusions: The Ninj1/Dusp1 axis contributes to liver IR injury by regulating the proinflammatory response of KCs, and influences neutrophil infiltration, partly by subsequent regulation of C-X-C motif chemokine ligand 1 (CXCL1) production after IR.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10036740PMC
http://dx.doi.org/10.1016/j.jcmgh.2023.01.008DOI Listing

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