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Updated: Aug 27, 2025
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Protocol for Isolation of Primary Human Hepatocytes and Corresponding Major Populations of Non-parenchymal Liver Cells
Published on: March 30, 2016
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Hepatic factor may not originate from hepatocytes.
Monica Merbach1, Ramani Ramchandran2,3, Andrew D Spearman1,2
1Division of Cardiology, Department of Pediatrics, Medical College of Wisconsin, Children's Wisconsin, Herma Heart Institute, Milwaukee, WI, United States.
Frontiers in Cardiovascular Medicine
|September 23, 2022
Summary
Pulmonary arteriovenous malformations (PAVMs) in congenital heart disease may not be caused by a factor from liver cells. Research suggests soluble vascular endothelial growth factor receptor 1 (sVEGFR1) originates from non-parenchymal liver cells, not hepatocytes.
Area of Science:
- Cardiovascular Research
- Hepatology
- Vascular Biology
Background:
- Pulmonary arteriovenous malformations (PAVMs) are common in univentricular congenital heart disease (CHD).
- PAVMs are hypothesized to result from a deficiency in a hepatic factor essential for lung vascular homeostasis.
- The precise origin and identity of this hepatic factor remain unknown.
Purpose of the Study:
- To investigate the origin of soluble vascular endothelial growth factor receptor 1 (sVEGFR1), a potential hepatic factor candidate.
- To determine if sVEGFR1 is produced by hepatocytes in the liver.
Main Methods:
- Utilized imaging and molecular approaches in wild-type mice.
- Analyzed sVEGFR1 expression within different liver cell populations.
Main Results:
- Identified negligible sVEGFR1 expression in hepatocytes.
- Demonstrated robust sVEGFR1 expression in the non-parenchymal cell population of the liver.
Conclusions:
- The hepatic factor involved in preventing PAVMs may not originate from hepatocytes.
- Alternative hypotheses regarding the source of hepatic factor should be explored.
- Further research is needed to identify hepatic factor for targeted CHD-associated PAVM therapies.
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