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CorrigendumHepatology Free access | 10.1172/JCI23486C1

TWEAK induces liver progenitor cell proliferation

Aniela Jakubowski, Christine Ambrose, Michael Parr, John M. Lincecum, Monica Z. Wang, Timothy S. Zheng, Beth Browning, Jennifer S. Michaelson, Manfred Baetscher, Bruce Wang, D. Montgomery Bissell, and Linda C. Burkly

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Published October 1, 2005 - More info

Published in Volume 115, Issue 10 on October 3, 2005
J Clin Invest. 2005;115(10):2955–2955. https://doi.org/10.1172/JCI23486C1.
© 2005 The American Society for Clinical Investigation
Published October 1, 2005 - Version history
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TWEAK induces liver progenitor cell proliferation
Aniela Jakubowski, … , D. Montgomery Bissell, Linda C. Burkly
Aniela Jakubowski, … , D. Montgomery Bissell, Linda C. Burkly
Research Article Hepatology

TWEAK induces liver progenitor cell proliferation

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Abstract

Progenitor (“oval”) cell expansion accompanies many forms of liver injury, including alcohol toxicity and submassive parenchymal necrosis as well as experimental injury models featuring blocked hepatocyte replication. Oval cells can potentially become either hepatocytes or biliary epithelial cells and may be critical to liver regeneration, particularly when hepatocyte replication is impaired. The regulation of oval cell proliferation is incompletely understood. Herein we present evidence that a TNF family member called TWEAK (TNF-like weak inducer of apoptosis) stimulates oval cell proliferation in mouse liver through its receptor Fn14. TWEAK has no effect on mature hepatocytes and thus appears to be selective for oval cells. Transgenic mice overexpressing TWEAK in hepatocytes exhibit periportal oval cell hyperplasia. A similar phenotype was obtained in adult wild-type mice, but not Fn14-null mice, by administering TWEAK-expressing adenovirus. Oval cell expansion induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) was significantly reduced in Fn14-null mice as well as in adult wild-type mice with a blocking anti-TWEAK mAb. Importantly, TWEAK stimulated the proliferation of an oval cell culture model. Finally, we show increased Fn14 expression in chronic hepatitis C and other human liver diseases relative to its expression in normal liver, which suggests a role for the TWEAK/Fn14 pathway in human liver injury. We conclude that TWEAK has a selective mitogenic effect for liver oval cells that distinguishes it from other previously described growth factors.

Authors

Aniela Jakubowski, Christine Ambrose, Michael Parr, John M. Lincecum, Monica Z. Wang, Timothy S. Zheng, Beth Browning, Jennifer S. Michaelson, Manfred Baestcher, Bruce Wang, D. Montgomery Bissell, Linda C. Burkly

×

Original citation: J. Clin. Invest.115:2330–2340 (2005). doi:10.1172/JCI23486

Citation for this corrigendum: J. Clin. Invest.115:2955 (2005). doi:10.1172/JCI23486C1

The name of one of the authors, Manfred Baetscher, was misspelled. The corrected author list is shown above.

The authors regret this error.

Version history
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