Resolving the graft ischemia-reperfusion injury during liver transplantation at the single cell resolution

Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transc...

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Published inCell death & disease Vol. 12; no. 6; pp. 589 - 17
Main Authors Wang, Linhe, Li, Jie, He, Shuai, Liu, Yang, Chen, Haitian, He, Shujiao, Yin, Meixian, Zou, Dawei, Chen, Shirui, Luo, Tao, Yu, Xinyu, Wan, Xuesi, Huang, Shunwei, Guo, Zhiyong, He, Xiaoshun
Format Journal Article
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Published London Nature Publishing Group UK 08.06.2021
Springer Nature B.V
Nature Publishing Group
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Abstract Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transcriptional profile of intrahepatic cells during liver transplantation is still unclear. We performed a single-cell transcriptome analysis of 14,313 cells from liver tissues collected from pre-procurement, at the end of preservation and 2 h post-reperfusion. We made detailed annotations of mononuclear phagocyte, endothelial cell, NK/T, B and plasma cell clusters, and we described the dynamic changes of the transcriptome of these clusters during IRI and the interaction between mononuclear phagocyte clusters and other cell clusters. In addition, we found that TNFAIP3 interacting protein 3 ( TNIP3) , specifically and highly expressed in Kupffer cell clusters post-reperfusion, may have a protective effect on IRI. In summary, our study provides the first dynamic transcriptome map of intrahepatic cell clusters during liver transplantation at single-cell resolution.
AbstractList Abstract Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transcriptional profile of intrahepatic cells during liver transplantation is still unclear. We performed a single-cell transcriptome analysis of 14,313 cells from liver tissues collected from pre-procurement, at the end of preservation and 2 h post-reperfusion. We made detailed annotations of mononuclear phagocyte, endothelial cell, NK/T, B and plasma cell clusters, and we described the dynamic changes of the transcriptome of these clusters during IRI and the interaction between mononuclear phagocyte clusters and other cell clusters. In addition, we found that TNFAIP3 interacting protein 3 (TNIP3), specifically and highly expressed in Kupffer cell clusters post-reperfusion, may have a protective effect on IRI. In summary, our study provides the first dynamic transcriptome map of intrahepatic cell clusters during liver transplantation at single-cell resolution.
Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transcriptional profile of intrahepatic cells during liver transplantation is still unclear. We performed a single-cell transcriptome analysis of 14,313 cells from liver tissues collected from pre-procurement, at the end of preservation and 2 h post-reperfusion. We made detailed annotations of mononuclear phagocyte, endothelial cell, NK/T, B and plasma cell clusters, and we described the dynamic changes of the transcriptome of these clusters during IRI and the interaction between mononuclear phagocyte clusters and other cell clusters. In addition, we found that TNFAIP3 interacting protein 3 (TNIP3), specifically and highly expressed in Kupffer cell clusters post-reperfusion, may have a protective effect on IRI. In summary, our study provides the first dynamic transcriptome map of intrahepatic cell clusters during liver transplantation at single-cell resolution.
Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transcriptional profile of intrahepatic cells during liver transplantation is still unclear. We performed a single-cell transcriptome analysis of 14,313 cells from liver tissues collected from pre-procurement, at the end of preservation and 2 h post-reperfusion. We made detailed annotations of mononuclear phagocyte, endothelial cell, NK/T, B and plasma cell clusters, and we described the dynamic changes of the transcriptome of these clusters during IRI and the interaction between mononuclear phagocyte clusters and other cell clusters. In addition, we found that TNFAIP3 interacting protein 3 ( TNIP3) , specifically and highly expressed in Kupffer cell clusters post-reperfusion, may have a protective effect on IRI. In summary, our study provides the first dynamic transcriptome map of intrahepatic cell clusters during liver transplantation at single-cell resolution.
Ischemia-reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transcriptional profile of intrahepatic cells during liver transplantation is still unclear. We performed a single-cell transcriptome analysis of 14,313 cells from liver tissues collected from pre-procurement, at the end of preservation and 2 h post-reperfusion. We made detailed annotations of mononuclear phagocyte, endothelial cell, NK/T, B and plasma cell clusters, and we described the dynamic changes of the transcriptome of these clusters during IRI and the interaction between mononuclear phagocyte clusters and other cell clusters. In addition, we found that TNFAIP3 interacting protein 3 (TNIP3), specifically and highly expressed in Kupffer cell clusters post-reperfusion, may have a protective effect on IRI. In summary, our study provides the first dynamic transcriptome map of intrahepatic cell clusters during liver transplantation at single-cell resolution.Ischemia-reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transcriptional profile of intrahepatic cells during liver transplantation is still unclear. We performed a single-cell transcriptome analysis of 14,313 cells from liver tissues collected from pre-procurement, at the end of preservation and 2 h post-reperfusion. We made detailed annotations of mononuclear phagocyte, endothelial cell, NK/T, B and plasma cell clusters, and we described the dynamic changes of the transcriptome of these clusters during IRI and the interaction between mononuclear phagocyte clusters and other cell clusters. In addition, we found that TNFAIP3 interacting protein 3 (TNIP3), specifically and highly expressed in Kupffer cell clusters post-reperfusion, may have a protective effect on IRI. In summary, our study provides the first dynamic transcriptome map of intrahepatic cell clusters during liver transplantation at single-cell resolution.
ArticleNumber 589
Author Guo, Zhiyong
Huang, Shunwei
Yu, Xinyu
Chen, Shirui
Wan, Xuesi
He, Shujiao
Liu, Yang
Zou, Dawei
Wang, Linhe
Luo, Tao
He, Shuai
He, Xiaoshun
Li, Jie
Chen, Haitian
Yin, Meixian
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34103479$$D View this record in MEDLINE/PubMed
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crossref_primary_10_1038_s41419_021_03878_3
springer_journals_10_1038_s41419_021_03878_3
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PublicationDate 2021-06-08
PublicationDateYYYYMMDD 2021-06-08
PublicationDate_xml – month: 06
  year: 2021
  text: 2021-06-08
  day: 08
PublicationDecade 2020
PublicationPlace London
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PublicationTitle Cell death & disease
PublicationTitleAbbrev Cell Death Dis
PublicationTitleAlternate Cell Death Dis
PublicationYear 2021
Publisher Nature Publishing Group UK
Springer Nature B.V
Nature Publishing Group
Publisher_xml – name: Nature Publishing Group UK
– name: Springer Nature B.V
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SSID ssj0000330256
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Snippet Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism...
Ischemia-reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism...
Abstract Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The...
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StartPage 589
SubjectTerms 38/39
38/47
38/91
631/80/304
631/80/86
Adult
Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Endothelial cells
Gene expression
Gene Expression Profiling - methods
Hepatocytes
Hepatocytes - metabolism
Hepatocytes - pathology
Humans
Immunology
Ischemia
Kupffer Cells - metabolism
Kupffer Cells - pathology
Life Sciences
Liver
Liver - blood supply
Liver - metabolism
Liver - pathology
Liver - physiopathology
Liver transplantation
Liver Transplantation - adverse effects
Liver transplants
Male
Middle Aged
Primary Graft Dysfunction - etiology
Primary Graft Dysfunction - genetics
Primary Graft Dysfunction - physiopathology
Reperfusion
Reperfusion Injury - genetics
Reperfusion Injury - physiopathology
RNA-Seq - methods
Single-Cell Analysis - methods
Transcription
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Title Resolving the graft ischemia-reperfusion injury during liver transplantation at the single cell resolution
URI https://link.springer.com/article/10.1038/s41419-021-03878-3
https://www.ncbi.nlm.nih.gov/pubmed/34103479
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https://pubmed.ncbi.nlm.nih.gov/PMC8187624
https://doaj.org/article/86ba605e8dd14dd6a0969bc23f2cdb3f
Volume 12
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