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Involvement of Aldehyde Dehydrogenase 2 (ALDH2) in Fatty Liver Graft Protection Mechanisms against Cold Ischemic Injury

A. Panisello-Rosello,1 A. Lopez,2 C. Castro,2 S. Bellogi,1 E. Folch-Puy,1 A. Rolo,3 C. Palmeira,3 R. Adam, J. Roselló-Catafau.

1Experimental Pathology, Instituto de Investigaciones Biomédicas de Barcelona, Barcelona, Catalonia, Spain
2INSERM U935, Hôpital Paul Brousse, Paris, France
3Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.

Meeting: 2018 American Transplant Congress

Abstract number: A33

Keywords: Apoptosis, Ischemia, Liver grafts, Preservation solutions

Session Information

Session Name: Poster Session A: Biomarkers, Immune Monitoring and Outcomes

Session Type: Poster Session

Date: Saturday, June 2, 2018

Session Time: 5:30pm-7:30pm

 Presentation Time: 5:30pm-7:30pm

Location: Hall 4EF

Aldehyde dehydogenase (ALDH2) is a mitochondrial enzyme that recently has been involved in the cardioprotection against ischemia injury. No data are reported on the potential involvement of ALDH2 in fatty liver graft preservation against cold ischemia injury. In this communication we demonstrate the relevance of ALDH2 activity in the underlying patophysiological mechanisms responsible for the fatty liver graft protection against cold ischemia injury when two solutions, as HTK and IGL-1, are used. Fatty liver from Male obese Zücker rats (11 weeks aged) were washed and stored in IGL-1 and HTK solutions at 4[ordm]C. After rinsing with Ringer solution, livers were stored at -80[ordm]C for subsequent analyses. We measured liver damage with alanine aminotransferase and aspartate aminotransferase (ALT/AST), mitochondrial damage with glutamate dehydrogenase (GLDH), aldehyde dehydrogenase 2 (ALDH2), adenosine monophosphate protein kinase (AMPK), mamalian target of rapamycin (m-TOR), several autophagy markers (beclin-1, beclin 2 and LCB3) and apoptosis (caspases 9 and 3). Nitric oxide generation (eNOS and nitrites/nitrates) and High mobility box 1 (HMGB1) were also measured. Data revealed that ALDH2 was more enhanced in liver preserved in IGL-1 than in HTK, correlating with increases in phosphorylated AMPK and a p-mTOR expression decrease. Data also showed increases in autophagy markers, which were accompanied by significant decreases in apoptosis. All these changes well correlated with decreases in AST/ALT and GLDH levels. These data confirm that ALDH2 plays an essential role in liver graft protection against cold ischemia injury, being part of the underlying protection mechanism of AMPK/mTOR autophagy induction and apoptosis prevention. These data suggest that ALDH2 could be a promising marker of graft protection against cold ischemic injury during static preservation. Supported by FIS project (PI 12/0056); S.R is a fellowship-holder Marie Curie programme (Agreement 722619).

CITATION INFORMATION: Panisello-Rosello A., Lopez A., Castro C., Bellogi S., Folch-Puy E., Rolo A., Palmeira C., Adam R., Roselló-Catafau J. Involvement of Aldehyde Dehydrogenase 2 (ALDH2) in Fatty Liver Graft Protection Mechanisms against Cold Ischemic Injury Am J Transplant. 2017;17 (suppl 3).

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To cite this abstract in AMA style:

Panisello-Rosello A, Lopez A, Castro C, Bellogi S, Folch-Puy E, Rolo A, Palmeira C, Adam R, Roselló-Catafau J. Involvement of Aldehyde Dehydrogenase 2 (ALDH2) in Fatty Liver Graft Protection Mechanisms against Cold Ischemic Injury [abstract]. https://atcmeetingabstracts.com/abstract/involvement-of-aldehyde-dehydrogenase-2-aldh2-in-fatty-liver-graft-protection-mechanisms-against-cold-ischemic-injury/. Accessed May 16, 2025.

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