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Enhanced expression of pluripotency gene Oct‐4 in pulmonary artery smooth muscle cells from patients with idiopathic pulmonary arterial hypertension
Author(s) -
Yao Weijuan,
Firth Amy L.,
Ogawa Aiko,
Yuan Jason X.J.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1209.15
Subject(s) - homeobox protein nanog , cd34 , progenitor cell , embryonic stem cell , pulmonary artery , medicine , vascular smooth muscle , pulmonary hypertension , muscle hypertrophy , stem cell , downregulation and upregulation , pathology , biology , cancer research , microbiology and biotechnology , induced pluripotent stem cell , gene , smooth muscle , biochemistry
Pulmonary vascular remodeling is a major cause for the elevated pulmonary vascular resistance in patients with idiopathic pulmonary arterial hypertension (IPAH). This study aimed at testing the hypothesis that the vascular medial hypertrophy may partially result from the de‐differentiation of pulmonary artery smooth muscle cells (PASMCs). RT‐PCR was performed to determine transcripts of pluripotency genes (Oct‐4/Nanog) and progenitor cell markers (CD34/Flk‐1) in PASMCs from normal subjects (n=3) and IPAH patients (n=3). The mRNA level of Oct‐4 in IPAH PASMCs was significantly higher than in normal PASMC, whereas Nanog was not detectable in IPAH and normal cells. The mRNA level of CD34/Flk‐1 was very low and no difference was found between IPAH and normal cells. Oct‐4 is a transcription factor highly expressed in undifferentiated cells (e.g., embryonic stem cells and multipotent adult progenitor cells). The upregulation of Oct‐4 indicates that PASMCs from IPAH patients are in the de‐differentiated state, and the transition from a differentiated (contractile and synthetic) phenotype to a de‐differentiated (proliferative) phenotype may serve as an important cause for vascular medial hypertrophy in IPAH. Founding source: NIH grants (HL064945, HL054043, HL066012)