File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: IL-17a exacerbates hepatic ischemia-reperfusion injury in fatty liver by promoting neutrophil infiltration and mitochondria-driven apoptosis

TitleIL-17a exacerbates hepatic ischemia-reperfusion injury in fatty liver by promoting neutrophil infiltration and mitochondria-driven apoptosis
Authors
KeywordsLiver transplantation
Neutrophils
NF-κB signaling
MOMP
Inflammation
Apoptosis
Issue Date2020
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at https://jlb.onlinelibrary.wiley.com/journal/19383673
Citation
Journal of Leukocyte Biology, 2020 How to Cite?
AbstractHepatic ischemia–reperfusion (IR) injury is a critical issue during liver transplantation (LT). Recent studies have demonstrated that IL‐17a contributes to IR injury and steatohepatitis. However, the underlying mechanism is not understood. This study aimed to examine the role of IL‐17a on hepatic IR injury in fatty liver and to investigate the underlying mechanisms. The correlation between serum IL‐17a levels and liver function was analyzed in LT patients receiving fatty (n = 42) and normal grafts (n = 44). Rat LT model was applied to validate the clinical findings. IL‐17a knockout (KO) and wild‐type mice were fed with high‐fat diets to induce fatty liver and subjected to hepatic IR injury with major hepatectomy. Frequency of circulating neutrophils and IL‐17a expression on PBMCs were analyzed by flow cytometry. Mitochondrial outer membrane permeabilization (MOMP) was examined by a living intravital image system. Serum IL‐17a was elevated after human LT, especially with fatty grafts. The aspartate aminotransferase and alanine transaminase levels were increased in recipients with fatty grafts compared with normal grafts. In rat LT model, the intragraft IL‐17a expression was significantly higher in fatty grafts than normal ones post‐LT. KO of IL‐17a in mice notably attenuated liver damage after IR injury in fatty liver, characterized by better‐preserved liver architecture, improved liver function, and reduced neutrophil infiltration. MOMP triggered cell death after hepatic IR injury in a caspase‐independent way via IL‐17a/NF‐κB signaling pathway. KO of IL‐17a protected the fatty liver against IR injury through the suppression of neutrophil infiltration and mitochondria‐driven apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/286360
ISSN
2019 Impact Factor: 3.757
2015 SCImago Journal Rankings: 2.463
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYang, X-
dc.contributor.authorLi, C-
dc.contributor.authorNg, KTP-
dc.contributor.authorLiu, J-
dc.contributor.authorLiu, H-
dc.contributor.authorZhang, W-
dc.contributor.authorXiao, F-
dc.contributor.authorLi, X-
dc.contributor.authorLo, CM-
dc.contributor.authorLu, L-
dc.contributor.authorMan, K-
dc.date.accessioned2020-08-31T07:02:46Z-
dc.date.available2020-08-31T07:02:46Z-
dc.date.issued2020-
dc.identifier.citationJournal of Leukocyte Biology, 2020-
dc.identifier.issn0741-5400-
dc.identifier.urihttp://hdl.handle.net/10722/286360-
dc.description.abstractHepatic ischemia–reperfusion (IR) injury is a critical issue during liver transplantation (LT). Recent studies have demonstrated that IL‐17a contributes to IR injury and steatohepatitis. However, the underlying mechanism is not understood. This study aimed to examine the role of IL‐17a on hepatic IR injury in fatty liver and to investigate the underlying mechanisms. The correlation between serum IL‐17a levels and liver function was analyzed in LT patients receiving fatty (n = 42) and normal grafts (n = 44). Rat LT model was applied to validate the clinical findings. IL‐17a knockout (KO) and wild‐type mice were fed with high‐fat diets to induce fatty liver and subjected to hepatic IR injury with major hepatectomy. Frequency of circulating neutrophils and IL‐17a expression on PBMCs were analyzed by flow cytometry. Mitochondrial outer membrane permeabilization (MOMP) was examined by a living intravital image system. Serum IL‐17a was elevated after human LT, especially with fatty grafts. The aspartate aminotransferase and alanine transaminase levels were increased in recipients with fatty grafts compared with normal grafts. In rat LT model, the intragraft IL‐17a expression was significantly higher in fatty grafts than normal ones post‐LT. KO of IL‐17a in mice notably attenuated liver damage after IR injury in fatty liver, characterized by better‐preserved liver architecture, improved liver function, and reduced neutrophil infiltration. MOMP triggered cell death after hepatic IR injury in a caspase‐independent way via IL‐17a/NF‐κB signaling pathway. KO of IL‐17a protected the fatty liver against IR injury through the suppression of neutrophil infiltration and mitochondria‐driven apoptosis.-
dc.languageeng-
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at https://jlb.onlinelibrary.wiley.com/journal/19383673-
dc.relation.ispartofJournal of Leukocyte Biology-
dc.subjectLiver transplantation-
dc.subjectNeutrophils-
dc.subjectNF-κB signaling-
dc.subjectMOMP-
dc.subjectInflammation-
dc.subjectApoptosis-
dc.titleIL-17a exacerbates hepatic ischemia-reperfusion injury in fatty liver by promoting neutrophil infiltration and mitochondria-driven apoptosis-
dc.typeArticle-
dc.identifier.emailNg, KTP: ledodes@hku.hk-
dc.identifier.emailLiu, H: liuhui25@hku.hk-
dc.identifier.emailXiao, F: xiaof@hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.emailLu, L: liweilu@hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.authorityNg, KTP=rp01720-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.authorityLu, L=rp00477-
dc.identifier.authorityMan, K=rp00417-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/JLB.3MA0520-716R-
dc.identifier.pmid32531822-
dc.identifier.scopuseid_2-s2.0-85086325694-
dc.identifier.hkuros313697-
dc.identifier.hkuros313460-
dc.identifier.isiWOS:000539778900001-
dc.publisher.placeUnited Kingdom-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats