1. Donor Hepatic Steatosis Induce Exacerbated Ischemia-Reperfusion Injury through Activation of Innate Immune Response Molecular Pathways
- Author
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Helen P. Cathro, Valeria R. Mas, Ricardo C. Gehrau, Ashish Sharma, Daniel G. Maluf, Catherine I. Dumur, and Jihee L. Suh
- Subjects
Male ,medicine.medical_treatment ,Biopsy ,Ischemia ,Biology ,Liver transplantation ,Real-Time Polymerase Chain Reaction ,Article ,Nitric oxide ,Proinflammatory cytokine ,chemistry.chemical_compound ,medicine ,Humans ,Transplantation ,Innate immune system ,Fatty liver ,Middle Aged ,medicine.disease ,Immunity, Innate ,Tissue Donors ,Liver Transplantation ,Fatty Liver ,chemistry ,Gene Expression Regulation ,Liver ,Reperfusion Injury ,Immunology ,Cytokines ,RNA ,Female ,Steatosis ,Reperfusion injury ,Biomarkers - Abstract
BACKGROUND Severe liver steatosis is a known risk factor for increased ischemia-reperfusion injury (IRI) and poor outcomes after liver transplantation (LT). This study aimed to identify steatosis-related molecular mechanisms associated with IRI exacerbation after LT. METHODS Paired graft biopsies (n = 60) were collected before implantation (L1) and 90 minutes after reperfusion (L2). The LT recipients (n = 30) were classified by graft macrosteatosis: without steatosis (WS) of 5% or less (n = 13) and with steatosis (S) of 25% or greater (n = 17). Plasma samples were collected at L1, L2, and 1 day after LT (postoperative [POD]1) for cytokines evaluation. Tissue RNA was isolated for gene expression microarrays. Probeset summaries were obtained using robust multiarray average algorithm. Pairwise comparisons were fit using 2-sample t test. P values 0.01 or less were significant (false discovery rate
- Published
- 2015