MicroRNA-155 Deficiency in Kupffer Cells Ameliorates Liver Ischemia-Reperfusion Injury in Mice

Li, Yakun; Ma, Dongxia; Wang, Zhimin; Yang, Jun

doi:10.1097/tp.0000000000001765

Cited by 48 publications

(34 citation statements)

References 40 publications

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“…Further, KC in these mice produced IL‐10 which improved the viability of hepatocytes. Elimination of miRNA‐155 negative KC led to increased injury after hepatic ischaemia …”

Section: Molecular Mechanisms Of Irimentioning

confidence: 99%

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Dar

Sullivan

Bynon

et al. 2019

Liver International

273

245

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Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia‐reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll‐like receptor signalling, alterations in micro‐RNA expression, production of ROS, regulation of autophagy and activation of hypoxia‐inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation – a process that will lead to improved outcomes for patients suffering from end‐stage liver disease.

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“…Further, KC in these mice produced IL‐10 which improved the viability of hepatocytes. Elimination of miRNA‐155 negative KC led to increased injury after hepatic ischaemia …”

Section: Molecular Mechanisms Of Irimentioning

confidence: 99%

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Dar

Sullivan

Bynon

et al. 2019

Liver International

273

245

View full text Add to dashboard Cite

show abstract

“…The literature contains a large number of markers and molecules which purport to assess the liver IRI [23]. Many have been studied in small animal models involving warm IRI only [24][25][26][27][28] and this might in large part be due to the highly technical nature of small animal models of liver transplantation. Nonetheless these models might provide utility in the use of clinical transplantation, particularly when assessing or predicting the extent of liver damage.…”

Section: Biomarkers Of Liver Ischaemia-reperfusion Injurymentioning

confidence: 99%

Biomarkers of Liver Injury during Transplantation in an Era of Machine Perfusion

Bhogal

Mirza

Afford

et al. 2020

IJMS

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Liver ischaemia–reperfusion injury (IRI) is an intrinsic part of the transplantation process and damages the parenchymal cells of the liver including hepatocytes, endothelial cells and cholangiocytes. Many biomarkers of IRI have been described over the past two decades that have attempted to quantify the extent of IRI involving different hepatic cellular compartments, with the aim to allow clinicians to predict the suitability of donor livers for transplantation. The advent of machine perfusion has added an additional layer of complexity to this field and has forced researchers to re-evaluate the utility of IRI biomarkers in different machine preservation techniques. In this review, we summarise the current understanding of liver IRI biomarkers and discuss them in the context of machine perfusion.

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“…It is well known that the abnormal expression and location of miRNA are involved in several pathophysiology and disease, including inflammatory response, ischemia reperfusion injury, and cancer, through regulated target gene posttranscription [42]. Several documents showed that miR-155 promoted inflammatory response involved in atherosclerosis [43], obesity-induced renal inflammation [44,45], and ischemia-reperfusion injury [46][47][48]. In this study, we found that the serum miR-155 level was higher at baseline than at 50 th day and 100 th day.…”

Section: Journal Of Immunology Researchmentioning

confidence: 99%

Efficacy of Shenqi Pollen Capsules for High-Altitude Deacclimatization Syndrome via Suppression of the Reoxygenation Injury and Inflammatory Response

Liang

et al. 2019

Journal of Immunology Research

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High-altitude deacclimatization syndrome (HADAS) is involved in hypoxia-reoxygenation injury and inflammatory response, induced a series of symptoms, and has emerged as a severe public health issue. Here, we investigated the mechanism as well as potential means to prevent HADAS using Shenqi pollen capsules (SPCs) in subjects with HADAS in a multicenter, double-blinded, randomized, placebo-controlled study. All subjects were at the same high altitude (3650 m) for 4-8 months before returning to lower altitudes. Subjects (n=288) in 20 clusters were diagnosed with mild or moderate HADAS on the third day of the study. We randomly allocated 20 clusters of subjects (1 : 1) to receive SPCs or a placebo for 7 weeks, and they were then followed up to the 14th week. The primary endpoints were subjects’ HADAS scores recorded during the 14 weeks of follow-up. Compared with the placebo, SPC treatment significantly decreased the subjects’ HADAS scores and reduced the incidence of symptom persistence. SPC therapy also reduced the serum levels of CK, CK-MB, LDH, IL-17A, TNF-α, and miR-155 and elevated IL-10 and miR-21 levels. We thus demonstrate that SPCs effectively ameliorated HADAS symptoms in these subjects via suppression of the hypoxia-reoxygenation injury and inflammatory response.

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MicroRNA-155 Deficiency in Kupffer Cells Ameliorates Liver Ischemia-Reperfusion Injury in Mice

Abstract: miR-155 deficiency plays an effective role in attenuating liver IR injury likely by regulating the activation and inflammatory response, as well as modifying the polarization of KCs.

Cited by 48 publications

References 40 publications

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Biomarkers of Liver Injury during Transplantation in an Era of Machine Perfusion

Efficacy of Shenqi Pollen Capsules for High-Altitude Deacclimatization Syndrome via Suppression of the Reoxygenation Injury and Inflammatory Response

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