miR-155 Aggravates Liver Ischemia/reperfusion Injury by Suppressing SOCS1 in Mice
| Autor: | L. Tan, Liang-Liang Kong, Weiwei Jiang, A. Lu, H. Cai |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male medicine.medical_treatment Liver transplantation Proinflammatory cytokine miR-155 03 medical and health sciences Mice 0302 clinical medicine Immune system Suppressor of Cytokine Signaling 1 Protein Downregulation and upregulation Medicine Animals Receptor Transplantation business.industry medicine.disease Liver Transplantation Mice Inbred C57BL MicroRNAs 030104 developmental biology medicine.anatomical_structure Gene Expression Regulation Liver Hepatocyte Reperfusion Injury Cancer research 030211 gastroenterology & hepatology Surgery business Reperfusion injury Signal Transduction |
| Zdroj: | Transplantation proceedings. 50(10) |
| ISSN: | 1873-2623 |
| Popis: | Liver ischemia/reperfusion injury (IRI) occurs during partial liver resection and liver transplantation. Activation of Toll-like receptors (TLRs) is a key event triggered by a range of proinflammatory cytokines during liver I/R. Although it has been reported that miR-155 takes part in both innate and adaptive immune responses, the potential role of miR-155 in liver IRI remains unknown. In this study, we found that expression of miR-155 was upregulated during liver I/R by many inflammatory cytokines, and forced expression of miR-155 aggravated hepatocyte injury following liver I/R both in vivo and in vitro. Mice transfected with Ago-miR-155—a chemically modified miR-155—showed enhanced liver severity compared to those transfected with negative control miRNA by inhibiting the expression of SOCS1, the target of miR-155. Thus by the inhibition of SOCS1, the overexpression of miR-155 promoted activation of NF-κB, and elevating the production of proinflammatory cytokines, such TNF-α and IL-6. In conclusion, miR-155 aggravates liver I/R injury in vivo and hepatocyte hypoxia/reoxygenation injury by suppressing the expression of SOCS1. |
| Databáze: | OpenAIRE |
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