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Differential regulation of hepatic physiology and injury by the TAM receptors Axl and Mer

Anna Zagórska, Paqui G Través, Lidia Jiménez-García, View ORCID ProfileJenna D Strickland, Joanne Oh, View ORCID ProfileFrancisco J Tapia, View ORCID ProfileRafael Mayoral, Patrick Burrola, Bryan L Copple, View ORCID ProfileGreg Lemke  Correspondence email
Anna Zagórska
1Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA, USA
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Paqui G Través
1Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA, USA
2Instituto de Investigaciones Biomédicas Alberto Sols (CSIC-UAM), Madrid, Spain
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Lidia Jiménez-García
1Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA, USA
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Jenna D Strickland
3Department of Pharmacology & Toxicology, Michigan State University, East Lansing, MI, USA
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  • ORCID record for Jenna D Strickland
Joanne Oh
1Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA, USA
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Francisco J Tapia
1Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA, USA
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Rafael Mayoral
4Division of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA
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  • ORCID record for Rafael Mayoral
Patrick Burrola
1Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA, USA
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Bryan L Copple
3Department of Pharmacology & Toxicology, Michigan State University, East Lansing, MI, USA
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Greg Lemke
1Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, CA, USA
5Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute, La Jolla, CA, USA
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  • For correspondence: lemke@salk.edu
Published 22 June 2020. DOI: 10.26508/lsa.202000694
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Abstract

Genome-wide association studies have implicated the TAM receptor tyrosine kinase (RTK) Mer in liver disease, yet our understanding of the role that Mer and its related RTKs Tyro3 and Axl play in liver homeostasis and the response to acute injury is limited. We find that Mer and Axl are most prominently expressed in hepatic Kupffer and endothelial cells and that as mice lacking these RTKs age, they develop profound liver disease characterized by apoptotic cell accumulation and immune activation. We further find that Mer is critical to the phagocytosis of apoptotic hepatocytes generated in settings of acute hepatic injury, and that Mer and Axl act in concert to inhibit cytokine production in these settings. In contrast, we find that Axl is uniquely important in mitigating liver damage during acetaminophen intoxication. Although Mer and Axl are protective in acute injury models, we find that Axl exacerbates fibrosis in a model of chronic injury. These divergent effects have important implications for the design and implementation of TAM-directed therapeutics that might target these RTKs in the liver.

  • Received March 11, 2020.
  • Revision received May 28, 2020.
  • Accepted May 29, 2020.
  • © 2020 Zagórska et al.
Creative Commons logoCreative Commons logohttps://creativecommons.org/licenses/by/4.0/

This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

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TAM receptor signaling in the liver
Anna Zagórska, Paqui G Través, Lidia Jiménez-García, Jenna D Strickland, Joanne Oh, Francisco J Tapia, Rafael Mayoral, Patrick Burrola, Bryan L Copple, Greg Lemke
Life Science Alliance Jun 2020, 3 (8) e202000694; DOI: 10.26508/lsa.202000694

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TAM receptor signaling in the liver
Anna Zagórska, Paqui G Través, Lidia Jiménez-García, Jenna D Strickland, Joanne Oh, Francisco J Tapia, Rafael Mayoral, Patrick Burrola, Bryan L Copple, Greg Lemke
Life Science Alliance Jun 2020, 3 (8) e202000694; DOI: 10.26508/lsa.202000694
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Volume 3, No. 8
August 2020
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