Alterations in the proteome of pulmonary alveolar type II cells in the rat after hepatic ischemia-reperfusion

Abstract

The proteins identified by quantitative proteomics indicated significant changes in moderators of cell metabolism and host defense in ATII. These findings provide new insights into possible mechanisms responsible for hepatic ischemia-reperfusion-related acute lung injury and suggest that ATII cells in the lung sense and respond to hepatic injury.

TLR4 as receptor for HMGB1-mediated acute lung injury after liver ischemia/reperfusion injury

“…31 The lung is frequently damaged by proinflammatory mediators released from the injured liver after liver IR, as the lungs are the first capillary bed that is reached by the blood after leaving the hepatic circulation. [3][4][5][6][7] was recently found to act as a potent proinflammatory cytokine and participated in the development of systemic inflammatory response, when it was released into the extracellular environment. 32,33 HMGB1 was also found to be involved in many other types of ALI, such as endotoxin, ventilator, and hemorrhage-induced ALI.…”

“…In addition, HMGB1 was reported to be released from macrophages and monocytes after exposure to proinflammatory cytokines. [36][37][38][39] Given that proinflammatory cytokines might be transported to lung tissue after liver I/R injury, [3][4][5][6][7] lung cells might be activated by proinflammatory cytokines and then release HMGB1. 40,41 For this reason, we examined HMGB1 mRNA in the lung tissue, and found that HMGB1 mRNA was significantly increased in the lung tissue after liver I/R injury.…”

“…1,2 This form of lung injury has been attributed to hepatic I/R injury, but the underlying mechanisms have not been fully elucidated. [3][4][5] The aim of this study was to investigate whether HMGB1 was involved as a stimulating factor, and whether TLR4, p38MAPK, and AP-1 signaling pathways act as mediators in the development of liver I/R injury induced ALI. We found that levels of serum and lung HMGB1 increased significantly after liver I/R injury; that TLR4, p38MAPK, and AP-1 signaling pathways were activated in the pathologic process of liver I/R injuryinduced ALI; and that ALI and lung inflammatory response can be attenuated by knockdown of TLR4 in the lung tissue.…”

“…Since the lungs are the first capillary bed that is reached by the blood after leaving the hepatic circulation, one proposed mechanism is that ALI may be induced by proinflammatory mediators released from the injured liver into system circulation. [3][4][5][6][7] High-mobility group box protein 1 (HMGB1), originally identified as a DNA-binding protein, is a proximal trigger that is sufficient to induce the release of other cytokines classically associated with mediating inflammatory responses, including tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), and interleukin-6 (IL-6). 8 Interestingly, HMGB1 was rapidly mobilized and released into system circulation by hepatocytes in the setting of liver I/R injury.…”

Propofol alleviates acute lung injury following orthotopic autologous liver transplantation in rats via inhibition of the NADPH oxidase pathway

“…Reactive oxygen species (ROS), endotoxins and cytokines enter into the circulation and damage remote organs and systems, of which the lungs are considered to be the most vulnerable (2). Therefore, therapeutic strategies alleviating ALI induced by liver transplantation are required to improve patient prognosis.…”