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• W4293578701 abstract "Background and Aims : Endoglin (Eng), the TGF-β co-receptor, plays an important role in endothelial dysfunction and TRC105 is an antibody that blocks Eng and its signaling. Here we have investigated for the first time, the TRC105 effects on the Eng expression, signaling, and function in endothelial dysfunction induced by hypercholesterolemia (simulated by 7-ketocholesterol [7K], the most common oxysterol in plasma) and hyperglycemia (simulated by high glucose [HG]).Methods: In the hypercholesterolemia study, human aortic endothelial cells (HAECs), passage 5, were treated with TRC105 (300 μg/mL) for 1 hour, followed by the addition of 7K (10 μg/mL) for 12 hours. In the hyperglycemia study, HAECs were exposed to HG (45 mM) for 60 hours, followed by the addition of TRC105 (300 μg/mL) for 12 hours, and cells treated with 5mM glucose and 40 mM mannitol served as osmotic control. Protein levels, adhesion, and transmigration of monocytes were assessed by flow cytometry, mRNA expression was measured by qRT-PCR.Results: 7K and HG treatment increased protein levels of Eng and NF-κB, as well as adhesion and transmigration of monocytes through HAECs monolayer. TRC105 pretreatment reduced the 7K and HG induced Eng protein levels and Smad signaling. Despite increased protein levels of cell adhesion molecules (P-selectin and VCAM-1), TRC105 also prevented 7K and HG induced adhesion and transmigration of monocytes through endothelial monolayers.Conclusions: These results suggest that TRC105-mediated Eng blockage can counteract the 7K and HG induced endothelial dysfunction in HAECs, suggesting that Eng might be a potential therapeutic target in disorders associated with elevated cholesterol and glucose levels. Background and Aims : Endoglin (Eng), the TGF-β co-receptor, plays an important role in endothelial dysfunction and TRC105 is an antibody that blocks Eng and its signaling. Here we have investigated for the first time, the TRC105 effects on the Eng expression, signaling, and function in endothelial dysfunction induced by hypercholesterolemia (simulated by 7-ketocholesterol [7K], the most common oxysterol in plasma) and hyperglycemia (simulated by high glucose [HG]). Methods: In the hypercholesterolemia study, human aortic endothelial cells (HAECs), passage 5, were treated with TRC105 (300 μg/mL) for 1 hour, followed by the addition of 7K (10 μg/mL) for 12 hours. In the hyperglycemia study, HAECs were exposed to HG (45 mM) for 60 hours, followed by the addition of TRC105 (300 μg/mL) for 12 hours, and cells treated with 5mM glucose and 40 mM mannitol served as osmotic control. Protein levels, adhesion, and transmigration of monocytes were assessed by flow cytometry, mRNA expression was measured by qRT-PCR. Results: 7K and HG treatment increased protein levels of Eng and NF-κB, as well as adhesion and transmigration of monocytes through HAECs monolayer. TRC105 pretreatment reduced the 7K and HG induced Eng protein levels and Smad signaling. Despite increased protein levels of cell adhesion molecules (P-selectin and VCAM-1), TRC105 also prevented 7K and HG induced adhesion and transmigration of monocytes through endothelial monolayers. Conclusions: These results suggest that TRC105-mediated Eng blockage can counteract the 7K and HG induced endothelial dysfunction in HAECs, suggesting that Eng might be a potential therapeutic target in disorders associated with elevated cholesterol and glucose levels." @default.
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• W4293578701 date "2022-08-01" @default.
• W4293578701 modified "2023-09-28" @default.
• W4293578701 title "Critical impact of endoglin blockage in endothelial dysfunction induced by hypercholesterolemia and hyperglycemia in human aortic endothelial cells" @default.
• W4293578701 doi "https://doi.org/10.1016/j.atherosclerosis.2022.06.251" @default.
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