Key result
Quercetin effectively inhibited TGF-β1-induced proliferation and transdifferentiation of pulmonary arterial endothelial cells and activation of the Akt/Erk1/2 cascade.
Hypothesis-generating for quercetin in pulmonary hypertension; leaves open clinical translation pending in vivo validation.
This study aimed to investigate the effects and mechanisms of quercetin on pulmonary arterial endothelial cell (PAEC) transdifferentiation into smooth muscle-like cells. TGF-β1-induced PAEC transdifferentiation models were applied to evaluate the pharmacological actions of quercetin. PAEC proliferation was detected with CCK8 method and BurdU immunocytochemistry. Meanwhile, the identification and transdifferentiation of PAECs were determined by FVIII immunofluorescence staining andα-SMA protein expression. The related mechanism was elucidated based on the levels of Akt and Erk1/2 signal pathways. As a result, quercetin effectively inhibited the TGF-β1-induced proliferation and transdifferentiation of the PAECs and activation of Akt/Erk1/2 cascade in the cells. In conclusion, quercetin is demonstrated to be effective for pulmonary arterial hypertension (PAH) probably by inhibiting endothelial transdifferentiation possibly via modulating Akt and Erk1/2 expressions.
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Huang et al. (2017) studied Pulmonary arterial hypertension. Quercetin vs. TGF-β1-induced PAEC transdifferentiation models without quercetin was evaluated on PAEC proliferation and transdifferentiation. Quercetin effectively inhibited TGF-β1-induced proliferation and transdifferentiation of pulmonary arterial endothelial cells and activation of the Akt/Erk1/2 cascade.
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