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Citations to this article

Transplanted endothelial cells repopulate the liver endothelium and correct the phenotype of hemophilia A mice
Antonia Follenzi, … , Sanj Raut, Sanjeev Gupta
Antonia Follenzi, … , Sanj Raut, Sanjeev Gupta
Published February 14, 2008
Citation Information: J Clin Invest. 2008;118(3):935-945. https://doi.org/10.1172/JCI32748.
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Research Article Hematology Article has an altmetric score of 8

Transplanted endothelial cells repopulate the liver endothelium and correct the phenotype of hemophilia A mice

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Abstract

Transplantation of healthy cells to repair organ damage or replace deficient functions constitutes a major goal of cell therapy. However, the mechanisms by which transplanted cells engraft, proliferate, and function remain unknown. To investigate whether host liver sinusoidal endothelium could be replaced with transplanted liver sinusoidal endothelial cells, we developed an animal model of tissue replacement that utilized a genetic system to identify transplanted cells and induced host-cell perturbations to confer a proliferative advantage to transplanted cells. Under these experimental conditions, transplanted cells engrafted efficiently and proliferated to replace substantial portions of the liver endothelium. Tissue studies demonstrated that transplanted cells became integral to the liver structure and reacquired characteristic endothelial morphology. Characterization of transplanted endothelial cells by membrane markers and studies of cellular function, including synthesis and release of coagulation factor VIII, demonstrated that transplanted cells were functionally intact. Further analysis showed that repopulation of the livers of mice that model hemophilia A with healthy endothelial cells restored plasma factor VIII activity and corrected their bleeding phenotype. Our studies therefore suggest that transplantation of healthy endothelial cells should be considered for cell therapy of relevant disorders and that endothelial reconstitution with transplanted cells may offer an excellent paradigm for defining organ-specific pathophysiological mechanisms.

Authors

Antonia Follenzi, Daniel Benten, Phyllis Novikoff, Louisa Faulkner, Sanj Raut, Sanjeev Gupta

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Total citations by year

Year: 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 Total
Citations: 4 4 4 6 8 4 7 5 9 4 4 6 5 2 7 7 86
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Citations to this article in year 2011 (2)

Title and authors Publication Year
Storage of Factor VIII Variants with Impaired von Willebrand Factor Binding in Weibel-Palade Bodies in Endothelial Cells
M Biggelaar, EA Bouwens, J Voorberg, K Mertens
PloS one 2011
Aquaporin-1 promotes angiogenesis, fibrosis, and portal hypertension through mechanisms dependent on osmotically sensitive microRNAs
RC Huebert, K Jagavelu, HI Hendrickson, MM Vasdev, JP Arab, PL Splinter, CE Trussoni, NF Larusso, VH Shah
The American Journal of Pathology 2011

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Referenced in 5 patents
Mentioned by 1 peer review sites
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