Loss of PPARγ in endothelial cells leads to impaired angiogenesis.

摘要: Tie2-promoter-mediated loss of peroxisome proliferator-activated receptor gamma (PPARγ, also known as PPARG) in mice leads to osteopetrosis and pulmonary arterial hypertension. Vascular disease is associated with PPARγ microvascular endothelial cells (PMVEC); we evaluated the role PMVEC functions, such angiogenesis migration. The was Tie2CrePPARγ(flox/flox) wild-type mice, mouse human PMVECs. RNA sequencing bioinformatic approaches were utilized reveal angiogenesis-associated targets for PPARγ. showed an impaired angiogenic capacity. Analysis progenitor-like using bone marrow transplantation combined evaluation isolated PMVECs revealed that attenuates migration capacity mature PPARγ-deficient a similar defect culture. Bioinformatic experimental analyses newly E2F1 target regulation Disruption PPARγ-E2F1 axis dysregulated Wnt pathway related GSK3B interacting protein (GSKIP). In conclusion, plays important sustaining potential through E2F1-mediated gene regulation.