The Effects of Sirolimus and Magnesium on Primary Human Coronary Endothelial Cells: An In Vitro Study.
Giorgia FedeleSara CastiglioniJeanette A M MaierLaura LocatelliPublished in: International journal of molecular sciences (2023)
Drug eluting magnesium (Mg) bioresorbable scaffolds represent a novel paradigm in percutaneous coronary intervention because Mg-based alloys are biocompatible, have adequate mechanical properties and can be resorbed without adverse events. Importantly, Mg is fundamental in many biological processes, mitigates the inflammatory response and is beneficial for the endothelium. Sirolimus is widely used as an antiproliferative agent in drug eluting stents to inhibit the proliferation of smooth muscle cells, thus reducing the occurrence of stent restenosis. Little is known about the potential interplay between sirolimus and Mg in cultured human coronary artery endothelial cells (hCAEC). Therefore, the cells were treated with sirolimus in the presence of different concentrations of extracellular Mg. Cell viability, migration, barrier function, adhesivity and nitric oxide synthesis were assessed. Sirolimus impairs the viability of subconfluent, but not of confluent cells independently from the concentration of Mg in the culture medium. In confluent cells, sirolimus inhibits migration, while it cooperates with Mg in exerting an anti-inflammatory action that might have a role in preventing restenosis and thrombosis.
Keyphrases
- endothelial cells
- induced apoptosis
- coronary artery
- nitric oxide
- inflammatory response
- cell cycle arrest
- percutaneous coronary intervention
- coronary artery disease
- high glucose
- signaling pathway
- anti inflammatory
- endoplasmic reticulum stress
- pulmonary artery
- acute coronary syndrome
- oxidative stress
- risk assessment
- vascular endothelial growth factor
- drug delivery
- induced pluripotent stem cells
- toll like receptor
- left ventricular
- pulmonary hypertension
- pi k akt
- lipopolysaccharide induced
- coronary artery bypass grafting
- st elevation myocardial infarction
- drug release
- nitric oxide synthase