Key result
Endothelin-1 significantly increased lysyl oxidase expression in pulmonary artery smooth muscle cells from patients with pulmonary arterial hypertension, which was restored to basal levels by prostacyclin and trapidil.
Why the study?
Little was known about the details of internal elastic lamina formation in pulmonary arterial hypertension.
Does endothelin-1 stimulation increase lysyl oxidase expression in pulmonary artery smooth muscle cells from PAH patients?
Population
Human pulmonary artery smooth muscle cells from PAH patients and controls
Comparison
Endothelin-1 stimulation with or without prostacyclin or trapidil vs basal level
Design
In vitro laboratory study
Authors
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May link endothelin-1 to LOx-driven matrix remodeling in PAH; hypothesis-generating and requires in vivo confirmation before clinical consideration.
Does endothelin-1 stimulation increase lysyl oxidase expression in pulmonary artery smooth muscle cells from PAH patients?
p-value: p=<0.05
Endothelin-1 overexpression in PAH may drive ectopic matrix deposition by increasing lysyl oxidase expression, a process potentially mitigated by prostacyclin or trapidil.
Maruyama et al. (2020) studied Idiopathic pulmonary arterial hypertension (n=19). Endothelin-1 vs. Unstimulated cells was evaluated on Lysyl oxidase (LOx) mRNA expression (p=<0.05). Endothelin-1 significantly increased lysyl oxidase expression in pulmonary artery smooth muscle cells from patients with pulmonary arterial hypertension, which was restored to basal levels by prostacyclin and trapidil.
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