Journal
FEBS LETTERS
Volume 590, Issue 1, Pages 101-109Publisher
WILEY
DOI: 10.1002/1873-3468.12038
Keywords
PDGF; pulmonary disease; pulmonary hypertension; smooth muscle cells; vascular remodeling; Wnt signaling
Funding
- Cardiovascular Medical Research and Education Fund
- Robert Wood Johnson Foundation, an NIH [K08 HL105884-01]
- Pulmonary Hypertension Association
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Pulmonary arterial hypertension (PAH) is characterized by excessive pulmonary arterial smooth muscle cells (PASMCs) growth, partially in response to PDGF-BB but whether this is dependent on -catenin (C) activation is unclear. Compared to healthy cells, PAH PASMCs demonstrate higher levels of proliferation both at baseline and with PDGF-BB that correlate with GSK3 dependent C activation. We show that C knockdown but not Wnt5a stimulation reduces PDGF-BB dependent growth and normalizes PAH PASMCs proliferation. These findings support that cross-talk between PDGF and Wnt signaling modulates PASMC proliferation and suggest that C targeted therapies could treat abnormal vascular remodeling in PAH.
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