Hyperplastic Growth of Pulmonary Artery Smooth Muscle Cells from Subjects with Pulmonary Arterial Hypertension Is Activated through JNK and p38 MAPK

• Published in: PloS one Vol. 10; no. 4; p. e0123662
• Main Authors: Wilson, Jamie L., Yu, Jun, Taylor, Linda, Polgar, Peter
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 23.04.2015; Public Library of Science (PLoS)
• Subjects: Actin; Activation; Becaplermin; Biochemistry; Cell cycle; Cell Cycle - physiology; Cell growth; Cell proliferation; Cell Proliferation - physiology; Cells, Cultured; Etiology; Familial Primary Pulmonary Hypertension - metabolism; Familial Primary Pulmonary Hypertension - pathology; Fibroblast growth factor 2; Fibroblast Growth Factor 2 - metabolism; Fibroblast growth factors; Genotype & phenotype; Growth; Growth factors; Humans; Hyperplasia; Hypertension; Hypertension, Pulmonary - metabolism; Hypertension, Pulmonary - pathology; Hypoxia; JNK protein; Kinases; MAP kinase; MAP Kinase Kinase 4 - metabolism; Medicine; Muscle proteins; Muscles; Myocytes, Smooth Muscle - metabolism; Myocytes, Smooth Muscle - pathology; p38 Mitogen-Activated Protein Kinases - metabolism; Phosphotransferases; Platelet-derived growth factor; Platelet-derived growth factor BB; Protein-tyrosine kinase receptors; Proteins; Proto-Oncogene Proteins c-sis - metabolism; Pulmonary arteries; Pulmonary artery; Pulmonary Artery - metabolism; Pulmonary Artery - pathology; Pulmonary hypertension; Rodents; Signal transduction; Signal Transduction - physiology; Smooth muscle; TOR protein; TOR Serine-Threonine Kinases - metabolism; Transcription factors; Tyrosine; Veins & arteries

Smooth muscle in the pulmonary artery of PAH subjects, both idiopathic and hereditary, is characterized by hyperplasia. Smooth muscle cells (HPASMC) isolated from subjects with or without PAH retain their in vivo phenotype as illustrated by their expression of alpha-smooth muscle actin and expressio...