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Search All Journals. The changes of pro-inflammatory factors, oxidative stress, vasodilator, vasoconstrictor, contractile and synthetic genes, and the morphological changes of HPASMC were investigated.
Pulmonary arterial hypertension PAH is a vascular remodeling disease with a poor prognosis and limited therapeutic option. Pulmonary vascular remodeling is the key structural alteration in the normal architecture of the walls of pulmonary arteries. Vascular smooth muscle cells SMCs are involved in this process 1. Vascular SMCs exhibit phenotypic and functional plasticity in response to environment.
This processes plays a major role in the development of vascular remodeling 2 , and is accompanied by decrease in expression of SMCs-specific markers transgelin, SM a-actin responsible for SMCs contraction, increase in expression of synthetic SMC markers thrombospondin, epiregulin , and production of pro-inflammatory mediators that modulate induction of proliferation and chemotaxis 3. Inflammatory infiltrates into the lungs mediate phenotypic transition in pulmonary vascular SMCs, stimulate the structural remodeling in the vasculature 4 , lead to the activation of oxidative stress, cause a decrease in vasodilators nitric oxide, prostacyclins and an increase in vasoconstrictors endothelin ET -1 and thromboxanes 4.
Some studies suggest that nitric oxide NO has been shown to reduce inflammation, apoptosis 5 , and regulate the vascular SMCs proliferation, migration and differentiation 6. Therefore, it is important to maintain the functions of endothelial cells.
Mesenchymal stem cells MSCs have been proposed to the treatment of pulmonary hypertension to improve vascular endothelial functions of the monocrotaline MCT -injured lung. MCT is a pyrrolizidine alkaloid which selectively injures the pulmonary vascular endothelium and induces pulmonary vasculitis, can cause PAH in rats and is widely utilized to analyze the pathophysiology of PAH 9.