Research Papers: Pathology:
Galectin-1 is essential for efficient liver regeneration following hepatectomy
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Tamara Potikha1, Ezra Ella1, Juan P. Cerliani3, Lina Mizrahi1, Orit Pappo2, Gabriel A. Rabinovich3,4, Eithan Galun1 and Daniel S. Goldenberg1
1 The Goldyne Savad Institute of Gene Therapy, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
2 Department of Pathology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
3 Laboratory of Immunopathology, Institute of Biology and Experimental Medicine, CONICET, Buenos Aires, Argentina
4 Faculty of Exact and Natural Sciences, University of Buenos Aires, Buenos Aires, Argentina
Daniel S. Goldenberg, email:
Keywords: galectin-1, liver regeneration, hepatectomy, lipid metabolism, Pathology Section
Received: January 19, 2016 Accepted: April 19, 2016 Published: May 05, 2016
Galectin-1 (Gal1) is a known immune/inflammatory regulator which acts both extracellularly and intracellularly, modulating innate and adaptive immune responses. Here, we explored the role of Gal1 in liver regeneration using 70% partial hepatectomy (PHx) of C57BL/6 wild type and Gal1-knockout (Gal1-KO, Lgals1-/-) mice. Gene or protein expression, in liver samples collected at time intervals from 2 to 168 hours post-operation, was tested by either RT-PCR or by immunoblotting and immunohistochemistry, respectively. We demonstrated that Gal1 transcript and protein expression was induced in the liver tissue of wild type mice upon PHx. Liver regeneration following PHx was significantly delayed in the Gal1-KO compared to the control liver. This delay was accompanied by a decreased Akt phosphorylation, and accumulation of the hepatocyte nuclear p21 protein in the Gal1-KO versus control livers at 24 and 48 hours following PHx. Transcripts of several known regulators of inflammation, cell cycle and cell signaling, including some known PHx-induced genes, were aberrantly expressed (mainly down-regulated) in Gal1-KO compared to control livers at 2, 6 and 24 hours post-PHx. Transient steatosis, which is imperative for liver regeneration following PHx, was significantly delayed and decreased in the Gal1-KO compared to the control liver and was accompanied by a significantly decreased expression in the mutant liver of several genes encoding lipid metabolism regulators. Our results demonstrate that Gal1 protein is essential for efficient liver regeneration following PHx through the regulation of liver inflammation, hepatic cell proliferation, and the control of lipid storage in the regenerating liver.
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