Endothelial-like Cells in Chronic Thromboembolic Pulmonary Hypertension
Author Information
Author(s): Sakao Seiichiro, Hao Hiroyuki, Tanabe Nobuhiro, Kasahara Yasunori, Kurosu Katsushi, Tatsumi Koichiro
Primary Institution: Chiba University
Hypothesis
Myofibroblast-like cells in the microenvironment created by the unresolved clot may promote endothelial cell dysfunction.
Conclusion
The microenvironment created by the stabilized clot may induce endothelial cell alterations.
Supporting Evidence
- Endothelial-like cells exhibited altered morphology and lost the ability to form autophagosomes.
- Myofibroblast-like cells promoted endothelial cell dysfunction through inactivation of autophagy.
- Rapamycin treatment reversed phenotypic alterations in endothelial cells co-cultured with myofibroblast-like cells.
- Decreased expression of superoxide dismutase was observed in endothelial cells co-cultured with myofibroblast-like cells.
- Transitional cells co-expressing endothelial and smooth muscle markers were identified in the neointimal lesions.
Takeaway
In a study of patients with a lung condition, certain cells in their blood vessels were found to change and cause problems for other cells, which could make their condition worse.
Methodology
Cells were isolated from endarterectomized tissues and identified as myofibroblast-like cells and endothelial-like cells, followed by in vitro experiments to assess their effects on endothelial cells.
Potential Biases
Potential bias due to the small sample size and reliance on in vitro findings.
Limitations
The study is based on in vitro experiments and does not provide strong evidence for the mechanisms involved in endothelial cell dysfunction in vivo.
Participant Demographics
Patients with chronic thromboembolic pulmonary hypertension undergoing pulmonary endarterectomy.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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