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Current Pharmaceutical Biotechnology

Editor-in-Chief

ISSN (Print): 1389-2010
ISSN (Online): 1873-4316

Research Article

Effect of TRAF1 on Phenotypic Changes Of Kupffer Cells In Liver Transplantation Ischemic-Reperfusion

Author(s): Zhen Zhang, KeTing Que, Yu You, XiaoPing Zhao, DiGuang Wen, ZhiHao Feng and ZuoJin Liu*

Volume 22, Issue 12, 2021

Published on: 11 January, 2021

Page: [1602 - 1611] Pages: 10

DOI: 10.2174/1389201022666210111113900

Price: $65

Abstract

Objective: The purpose of this study was to explore the effect of TRAF1 on phenotypic changes of KCs in I/R in liver transplantation.

Methods: SD rats were randomly divided into sham group and liver transplantation I/R group. KCs were extracted from rat livers in each group. KCs were transfected by lentivirus of si-TRAF1 or si-HOIP, and induced by Lipopolysaccharide (LPS). Flow cytometry was used to detect cell apoptosis. Western blot and RT-PCR were used to detect the protein and mRNA expression levels.

Results: Compared with the sham group, the expression levels of TRAF1, TNF-α and IL-1β were significantly increased in the I/R group (P<0.05). In addition, compared with the control group, the expression levels of NF-κB (P65 and p-P65) and M1 phenotype (TNF-α and IL-1β) were notably increased in si-TRAF1 and si-HOIP group (all P<0.05). Furthermore, the levels of Linear Ubiquitin Complex (LUBAC) were markedly increased in LPS-induced KCs in comparison with the control group (P<0.05). Moreover, compared with the control group, the expression levels of P65, p-P65, TNF-α and IL-1β were notably decreased in the si-TRAF1 and si-HOIP group (P<0.05). The expression levels of P65, p-P65, TNF-α and IL-1β were significantly increased in si-TRAF1 and si-HOIP group when compared to the control group (P<0.05).

Conclusion: TRAF1 was an important negative regulator of liver transplantation I/R by inhibiting the activation of NF-κB in KCs and preventing its M1 phenotype transformation.

Keywords: Kupffer cells, TRAF1, NF-κB, liver transplantation, ischemia reperfusion, M1 phenotype, lipopolysaccharide.

Graphical Abstract

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