PASMCPulmonary Artery Smooth Muscle Cell
PASMCPorcine Aortic Smooth Muscle Cell
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Abnormal pulmonary vascular reorganization, including excessive vascular proliferation and resistance to apoptosis of pulmonary artery smooth muscle cells (PASMCs) within the vascular wall, contributes to reduction of arterial compliance and increased vascular resistance and blood pressure, resulting in right-side heart failure and premature death.
Several underlying mechanisms leading to excessive proliferative and reduced apoptosis in PASMCs have been previously elucidated.
Development of PH involves various molecular pathways that include several cell types especially pulmonary arterial smooth muscle cells (PASMCs) and pulmonary arterial ECs (PAECs) [17].
It has been suggested that the miRNA/PPAR[gamma] regulatory axis might contribute greatly to PH pathogenesis by regulating proliferation/apoptosis, communication, and normal function of PAECs and PASMCs.
Also, the specific KO of EC-SOD in PASMC shows increased PH in the hypoxia model mouse model of PH [67].
In the context of PH, activation of this receptor has been shown to modulate the development of PH by mediating the release of hyaluronan [76-78], from the PASMC and macrophages.
In PAH, PASMCs proliferation maximizes the usage of methionine for protein synthesis which might reduce the methionine level (choline dehydrogenase: CHDH; methylene tetrahydrofolate dehydrogenase: MTHFD), although methionine is the metabolic production of betaine.
First, Lipofectamine delivery of pEGFP plasmid DNA into the PASMCs was successful.
Previous studies have shown that hypoxia induced the proliferation of PASMCs which plays a principal role in the pathogenesis of PAH [21].
On a cellular level, the remodeling of the small vessels is caused by increased proliferation and migration and decreased apoptosis of PASMC (Figure 1) [16], and the affected cells seem to comprise a specific subpopulation of PASMC that are not well differentiated.
In the present study, we evaluated the effects of ADM and ADT on PASMC proliferation, as well as collagen I, collagen III, and phosphorylated (p)-ERK1/2 expression, to determine if the ERK1/2 signal transduction pathway was activated during the response.
Primary cultured PASMCs were prepared from 24 male Sprague-Dawley rats (125250 g) as described previously [20].