ArticleResearch and practice in thrombosis and haemostasis2025
Identification of novel gene expression programs in thrombin-stimulated hepatic stellate cells.
Article in Research and practice in thrombosis and haemostasis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Activated protein C promotes hematopoietic stem and progenitor cell quiescence and engraftment.EMBO molecular medicine · 2026Article
- Hemostatic efficacy of a novel Ca/P/S-based bone graft material and its preliminary clinical evidence in sternum closure procedures.Frontiers in bioengineering and biotechnology · 2026Article
- Clinical and pathophysiological perspectives on haemostasis, inflammation, and thrombo-haemorrhagic risk in cirrhosis.EXCLI journal · 2026Review
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6 authors.
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Abstract
Background: Evidence suggests that the coagulation factor thrombin plays a pathologic role in liver fibrosis. Studies have proposed that thrombin signaling through protease-activated receptor-1 (PAR1) promotes activation of hepatic stellate cells (HSCs), the primary collagen-producing cells in the fibrotic liver. However, a comprehensive view of the effect of thrombin on HSCs is lacking. Objectives: This study tests the hypothesis that thrombin induces expression of fibrogenic mediators in HSCs via PAR1 activation. Methods: Immortalized human HSCs (LX-2) were cultured for 48 hours, then stimulated with human α-thrombin (0-10 U/mL). In some experiments, cells were pretreated with the PAR1 antagonist, vorapaxar (0.01-10 μM). PAR1 activation and gene and protein expression were assessed. Results: Rapid intracellular calcium mobilization was detected in thrombin-stimulated HSCs (0-10 U/mL) in a dose-dependent manner, which was blocked by vorapaxar pretreatment. Surprisingly, HSCs treated with thrombin for 24 to 48 hours did not affect gene or protein expression of fibrotic mediators. However, thrombin treatment for 4, 24, or 48 hours did provoke distinct transcriptomic changes. Pathway overrepresentation analysis revealed altered pathways associated with cell migration, inflammation, and metabolism, as well as enrichment for published gene signatures associated with HSC activation. Interestingly, several genes from altered pathways were shown to be regulated by PAR1 signaling. Conclusion: These results show that thrombin alters previously unidentified transcriptomic profiles, suggesting a program toward HSC activation. Thrombin activates complex signaling pathways for HSC preinitiation, which may drive HSC activation and hepatic fibrosis.
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