title: Cold ischemia-induced autophagy in rat lung tissue.
abstract: Autophagy is a highly conserved pathway that permits recycling of nutrients within the cell and is rapidly upregulated during starvation or cell stress. Autophagy has been implicated in the pathophysiological process of warm ischemia‑reperfusion injury in the rat lung. Cold ischemia (CI) preservation for lung transplantation also exhibits cell stress and nutrient deprivation, however, little is known with regard to the involvement of autophagy in this process. In the present study, CI preservation‑induced autophagy and apoptosis was investigated in the lungs of Sprague Dawley rats. Sprague Dawley rat lungs were flushed and preserved at 4˚C (i.e. CI) for various durations (0, 3, 6, 12 and 24 h). The levels of autophagy, autophagic cell death and apoptosis were measured at each time point following CI. The results revealed that autophagy was induced by CI preservation, which was initiated at 3 h, peaked at 6 h after CI and declined thereafter. Additionally, a coexistence of autophagic cell death and apoptosis was observed in rat lung tissues following prolonged CI. These findings demonstrate that autophagy is involved in the pathophysiological process of lung CI. Furthermore, autophagic cell death in addition to necrosis and apoptosis occurs following CI in the lung. CI preservation may therefore be a potential mechanism of lung injury during organ preservation prior to lung transplantation.
authors.affiliation: Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.
authors.forename: Xu
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.
authors.forename: Jing-Xiang
authors.initials: JX
authors.lastname: Wu
authors.affiliation: Department of Physiology, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Xing-Ji
authors.initials: XJ
authors.lastname: You
authors.affiliation: Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.
authors.forename: Hong-Wei
authors.initials: HW
authors.lastname: Zhu
authors.affiliation: Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.
authors.forename: Jiong-Lin
authors.initials: JL
authors.lastname: Wei
authors.affiliation: Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.
authors.forename: Mei-Ying
authors.initials: MY
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism; D001343:Autophagy / Q000235:genetics; D000071186:Beclin-1; D050377:Cold Ischemia; D008168:Lung / Q000378:metabolism*; D016040:Lung Transplantation; D008297:Male; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D023421:Models, Animal; D009926:Organ Preservation; D051381:Rats
chemical_list: D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; C512829:Becn1 protein, rat; D008869:Microtubule-Associated Proteins