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A Rat Lung Transplantation Model of Warm Ischemia/Reperfusion Injury: Optimizations to Improve Outcomes
Published on: October 28, 2021
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Cold ischemia-induced autophagy in rat lung tissue
Xu Chen1, Jing-Xiang Wu1, Xing-Ji You2
1Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.
Molecular Medicine Reports
|December 2, 2014
Summary
Cold ischemia preservation induces autophagy and cell death in rat lungs. This process, involving autophagy and apoptosis, may contribute to lung injury during organ preservation for transplantation.
Area of Science:
- Cell Biology
- Organ Transplantation
- Physiology
Background:
- Autophagy, a cellular recycling process, is upregulated during stress.
- Autophagy is linked to warm ischemia-reperfusion injury in rat lungs.
- The role of autophagy in cold ischemia (CI) lung preservation is largely unknown.
Purpose of the Study:
- To investigate autophagy and apoptosis in rat lungs during cold ischemia preservation.
- To determine the time course of autophagy and cell death markers following CI.
Main Methods:
- Sprague Dawley rat lungs were subjected to cold ischemia (4°C) for 0, 3, 6, 12, and 24 hours.
- Levels of autophagy, autophagic cell death, and apoptosis were measured at each time point.
Main Results:
- Cold ischemia preservation induced autophagy, starting at 3 hours and peaking at 6 hours.
- Prolonged CI preservation led to a coexistence of autophagic cell death and apoptosis.
- Autophagy levels declined after peaking at 6 hours.
Conclusions:
- Autophagy is involved in the pathophysiology of lung cold ischemia.
- Autophagic cell death, along with apoptosis and necrosis, occurs after lung CI.
- CI preservation may contribute to lung injury during organ preservation for transplantation.
