期刊
PLOS ONE
卷 9, 期 3, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0092925
关键词
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资金
- Herbert S. Coe Foundation
- American College of Surgeons Louis C. Argenta Fellowship
- American Surgical Association Foundation Fellowship
- Howard Hughes Medical Institute program in Molecular Medicine
- [R01CA127228]
- [T32HL007312]
Chronic liver injury leads to fibrosis, cirrhosis, and loss of liver function. Liver cirrhosis is the 12th leading cause of death in the United States, and it is the primary risk factor for developing liver cancer. Fibrosis and cirrhosis result from activation of hepatic stellate cells (HSCs), which are the primary collagen producing cell type in the liver. Here, we show that platelet-derived growth factor receptor alpha (PDGFR alpha) is expressed by human HSCs, and PDGFR alpha expression is elevated in human liver disease. Using a green fluorescent protein (GFP) reporter mouse strain, we evaluated the role of PDGFR alpha in liver disease in mice and found that mouse HSCs express PDGFR alpha and expression is upregulated during carbon tetrachloride (CCl4) induced liver injury and fibrosis injection. This fibrotic response is reduced in Pdgfr alpha heterozygous mice, consistent with the hypothesis that liver fibrosis requires upregulation and activation of PDGFR alpha. These results indicate that Pdgfr alpha expression is important in the fibrotic response to liver injury in humans and mice, and suggest that blocking PDGFR alpha-specific signaling pathways in HSCs may provide therapeutic benefit for patients with chronic liver disease.
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