Endothelial cell injury is an early event in systemic sclerosis (SSc) pathogenesis and several studies indicate oxidative stress as the trigger of SSc-associated vasculopathy. Here, we show that circulating factors present in sera of SSc patients increased reactive oxygen species (ROS) production and collagen synthesis in human pulmonary microvascular endothelial cells (HPMECs). In addition, the possibility that iloprost, a drug commonly used in SSc therapy, might modulate the above-mentioned biological phenomena has been also investigated. In this regard, as compared to sera of SSc patients, sera of iloprost-treated SSc patients failed to increased ROS levels and collagen synthesis in HPMEC, suggesting a potential antioxidant mechanism of this drug.
Iloprost attenuates oxidative stress-dependent activation of collagen synthesis induced by sera from scleroderma patients in human pulmonary microvascular endothelial cells / Giordo, R.; Thuan, D. T. B.; Posadino, A. M.; Cossu, A.; Zinellu, A.; Erre, G. L.; Pintus, G.. - In: MOLECULES. - ISSN 1420-3049. - 26:16(2021), p. 4729. [10.3390/molecules26164729]
Iloprost attenuates oxidative stress-dependent activation of collagen synthesis induced by sera from scleroderma patients in human pulmonary microvascular endothelial cells
Giordo R.;Posadino A. M.;Zinellu A.;Erre G. L.;Pintus G.
2021-01-01
Abstract
Endothelial cell injury is an early event in systemic sclerosis (SSc) pathogenesis and several studies indicate oxidative stress as the trigger of SSc-associated vasculopathy. Here, we show that circulating factors present in sera of SSc patients increased reactive oxygen species (ROS) production and collagen synthesis in human pulmonary microvascular endothelial cells (HPMECs). In addition, the possibility that iloprost, a drug commonly used in SSc therapy, might modulate the above-mentioned biological phenomena has been also investigated. In this regard, as compared to sera of SSc patients, sera of iloprost-treated SSc patients failed to increased ROS levels and collagen synthesis in HPMEC, suggesting a potential antioxidant mechanism of this drug.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.