Prolonged Cold Ischemia Does Not Trigger Lethal Rejection or Accelerate the Acute Rejection in Two Allogeneic Rat Liver Transplantation Models

Jin, Hao; Dahmen, Uta; Liu, Anding; Huang, Hai; Gu, Yanli; Dirsch, Olaf

doi:10.1016/j.jss.2011.03.078

Cited by 4 publications

(2 citation statements)

References 41 publications

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“…We demonstrated previously that HMGB1 was released into the effluent during prolonged cold saline preservation of liver grafts [28]. We also demonstrated that transplantation of a cold-preserved liver graft did not interfere with spontaneous graft acceptance [29]. These data indicate that HMGB1-release did not result in continuing inflammatory injury in this setting.…”

Section: Introductionsupporting

confidence: 57%

Oxidation of HMGB1 Causes Attenuation of Its Pro-Inflammatory Activity and Occurs during Liver Ischemia and Reperfusion

et al. 2012

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High mobility group box 1 (HMGB1) is a nuclear transcription factor. Once HMGB1 is released by damaged cells or activated immune cells, it acts as danger molecule and triggers the inflammatory signaling cascade. Currently, evidence is accumulating that posttranslational modifications such as oxidation may modulate the pro-inflammatory potential of danger signals. We hypothesized that oxidation of HMGB1 may reduce its pro-inflammatory potential and could take place during prolonged ischemia and upon reperfusion.Liver grafts were cold preserved for 24 h and flushed with saline in hourly intervals to collect the effluent. Liver grafts, cold-preserved for 6 h, were transplanted into syngeneic recipients to obtain serum and liver samples 24 h after initiation of reperfusion. Addition of the effluent to a macrophage culture induced the synthesis of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. The stimulatory activity of graft effluent was reduced after depletion of HMGB1 via immunoprecipitation. Oxidation of the effluent HMGB1 using H2O2 attenuated its stimulatory activity as well. Liver transplantation of cold preserved grafts caused HMGB1 translocation and release as determined by immunohistochemistry and ELISA-assay, respectively. Using Western blot with non-reducing conditions revealed the presence of oxidized HMGB1 in liver samples obtained after 12 h and in effluent samples after 16 h of cold preservation as well as in liver and serum samples obtained 24 h after reperfusion.These observations confirm that post-translational oxidation of HMGB1 attenuates its pro-inflammatory activity. Oxidation of HMGB1 as induced during prolonged ischemia and by reoxygenation during reperfusion in vivo might also attenuate its pro-inflammatory activity. Our findings also call for future studies to investigate the mechanism of the inhibitory effect of oxidized HMGB1 on the pro-inflammatory potential.

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Section: Introductionsupporting

confidence: 57%

Oxidation of HMGB1 Causes Attenuation of Its Pro-Inflammatory Activity and Occurs during Liver Ischemia and Reperfusion

et al. 2012

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“…However, the role of the allogeneic immune response in this process has yet to be empirically demonstrated. In a paper recently published in the Journal of Surgical Research, Jin and colleagues advance our understanding of the mechanisms of the allogeneic immune response and its role in the induction and propagation of the injury responsible for cold ischemia [6].…”

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confidence: 99%

Prolonged Cold Ischemia Enhances Alloimmune Response to Liver Grafts

Kotecha¹,

Toledo‐Pereyra²

2012

Journal of Surgical Research

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CD47 blockade alleviates acute rejection of allogeneic mouse liver transplantation by reducing ischemia/reperfusion injury

Xie

Wang

et al. 2020

Biomedicine & Pharmacotherapy

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Prolonged Cold Ischemia Does Not Trigger Lethal Rejection or Accelerate the Acute Rejection in Two Allogeneic Rat Liver Transplantation Models

Cited by 4 publications

References 41 publications

Oxidation of HMGB1 Causes Attenuation of Its Pro-Inflammatory Activity and Occurs during Liver Ischemia and Reperfusion

Oxidation of HMGB1 Causes Attenuation of Its Pro-Inflammatory Activity and Occurs during Liver Ischemia and Reperfusion

Prolonged Cold Ischemia Enhances Alloimmune Response to Liver Grafts

CD47 blockade alleviates acute rejection of allogeneic mouse liver transplantation by reducing ischemia/reperfusion injury

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