Role of Differentiation of Liver Sinusoidal Endothelial Cells in Progression and Regression of Hepatic Fibrosis in Rats
Open accessAbstract
Background & aims Capillarization, characterized by loss of differentiation of liver sinusoidal endothelial cells (LSECs), precedes the onset of hepatic fibrosis. We investigated whether restoration of LSEC differentiation would normalize crosstalk with activated hepatic stellate cells (HSC) and thereby promote quiescence of HSC and regression of fibrosis. Methods Rat LSECs were cultured with inhibitors and/or agonists and examined by scanning electron microscopy for fenestrae in sieve plates. Cirrhosis was induced in rats using thioacetamide, followed by administration of BAY 60-2770, an activator of soluble guanylate cyclase (sGC). Fibrosis was assessed by Sirius red staining; expression of α-smooth muscle actin was measured by immunoblot analysis. Results Maintenance of LSEC differentiation requires vascular endothelial growth factor-A stimulation of nitric oxide-dependent signaling (via sGC and cyclic guanosine monophosphate) and nitric oxide-independent signaling. In rats with thioacetamide-induced cirrhosis, BAY 60-2770 accelerated the complete reversal of capillarization (restored differentiation of LSECs) without directly affecting activation of HSCs or fibrosis. Restoration of differentiation to LSECs led to quiescence of HSCs and regression of fibrosis in the absence of further exposure to BAY 60-2770. Activation of sGC with BAY 60-2770 prevented progression of cirrhosis, despite continued administration of thioacetamide. Conclusions The state of LSEC differentiation plays a pivotal role in HSC activation and the fibrotic process.
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LSEC activation involves VCAM-1 expression, which recruits pro-inflammatory and pro-fibrogenic immune cells and disrupts the quiescent state of HSCs.
“This activation involves the expression of adhesion proteins such as vascular cell adhesion molecule 1 (VCAM-1), which directly recruits pro-inflammatory and pro-fibrogenic immune cells into the liver, while also disrupting the quiescent state of HSCs (104) (105-109).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [106]
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- Authors
- Xie, G., Wang, X., Wang, L., Wang, L., Atkinson, R. D., Kanel, G. C., Gaarde, W. A., & DeLeve, L. D.
- Affiliations
- University of Southern California (US)
- Ionis Pharmaceuticals (United States) (US)
- Corresponding author
- DeLeve, Laurie D.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 142
- Issue
- 4
- Pages
- 918-927.e6
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC3618963
- OpenAlex
- W2111858134
- Cited by
- 410
- References
- 44
- Citations by year
- 2026: 23 · 2025: 37 · 2024: 49 · 2023: 40 · 2022: 26 · 2021: 36 · 2020: 43 · 2019: 25 · 2018: 31 · 2017: 34 · 2016: 19 · 2015: 14 · 2014: 12 · 2013: 10 · 2012: 9
- FWCI
- 5.96
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01-DK66423)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- liver sinusoidal endothelial cells, liver fibrosis, capillarization, hepatic stellate cells, soluble guanylate cyclase, BAY 60-2770, nitric oxide signaling, VEGF-A, thioacetamide-induced cirrhosis, fibrosis regression, endothelial differentiation, alpha-smooth muscle actin
- MeSH terms
- Soluble Guanylyl Cyclase, Actins, Animals, Benzoates, Biphenyl Compounds, Capillaries, Cell Differentiation, Cells, Cultured, Enzyme Activation, Cyclic GMP, Guanylate Cyclase, Hydrocarbons, Fluorinated, Liver, Liver Cirrhosis, Experimental, Male, Microscopy, Electron, Scanning, Nitric Oxide, Phenotype, Thioacetamide, Blotting, Western, Signal Transduction, Rats, Sprague-Dawley, Receptors, Cytoplasmic and Nuclear, Disease Progression, Paracrine Communication, Enzyme Activators, Vascular Endothelial Growth Factor A, Endothelial Cells, Cell Proliferation, Rats, Hepatic Stellate Cells
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