Assessment of endothelial apoptosis in the pulmonary arteries of rats with monocrotaline-induced pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a severe, rapidly progressing disease. Apoptosis of endothelial cells (EC) and their resistance to programmed death play a decisive role in the pathogenesis of PAH. It is assumed that the ratio of Bcl-2 and Bax proteins may be the main determinant of cellular ability to apoptosis. The article presents the results of a study of pulmonary artery EC apoptosis in the dynamics of monocrotaline-induced PAH development.Apoptosis is an important factor in arterial remodeling in PAH. With the development of PAH, activation of apoptotic death of EC reaches its maximum values 1 month after the beginning of the experiment; 2 months after the introduction of monocrotaline (MCT) to rats, apoptosis transitions to necrosis and a decrease in the apoptotic index is observed.Inhibition of anti-apoptotic mechanisms in the early stages of PAH leads to impaired permeability of the EC barrier and the risk of thrombosis. Apoptosis of EC is characterized by a decrease in the expression of the anti-apoptotic factor Bcl-2 with a fairly high expression value of the pro-apoptotic protein Baх.Thus, the ratio of pro- and anti-apoptotic proteins of the Bcl-2 family plays a significant role in the development of pathological changes in the pulmonary arteries in rats with PAH.