Peroxisome proliferator-activated receptor-γ activation reduces cyclooxygenase-2 expression in vascular smooth muscle cells from hypertensive rats by interfering with oxidative stress

Abstract

PPARγ activation with pioglitazone reduces interleukin-1β-induced COX-2 expression by interference with the redox-sensitive transcription factor NF-κB.

Down-regulated Peroxisome Proliferator-activated Receptor γ (PPARγ) in Lung Epithelial Cells Promotes a PPARγ Agonist-reversible Proinflammatory Phenotype in Chronic Obstructive Pulmonary Disease (COPD)

“…Furthermore, treatment with either PPAR␥ agonist reversed the CSE-induced phosphorylation of IKK, thus blocking degradation of IB and consequent nuclear localization of NF-B (14). This extends to airway epithelial cells and an additional PPAR␥ agonist previous observations that the thiazolidinedione pioglitazone blocks IKK activation through a PPAR␥-dependent mechanism in IL-1␤-stimulated vascular smooth muscle cells (19). The agonist-induced reduction in IKK phosphorylation we see presumably reflects the accompanying decrease in activating phosphorylation of MSK1.…”

The Quest for Selective Nox Inhibitors and Therapeutics: Challenges, Triumphs and Pitfalls

“…In that regard, the popular mantra of ''more is better'' should be treated with healthy skepticism when it comes to both antioxidants and Nox inhibitors. Further, a growing body of evidence demonstrates a beneficial role for exogenously supplied catalase or the ROS scavenger Tempol in inhibiting the oxidative burden associated with ''feed-forward'' Nox activation and expression both in vitro and in vivo (42,111,112). This may include redox-sensitive pathways upstream or linking one Nox to another.…”

Pioglitazone, a PPARγ agonist, attenuates PDGF-induced vascular smooth muscle cell proliferation through AMPK-dependent and AMPK-independent inhibition of mTOR/p70S6K and ERK signaling

“…It is noteworthy that the basal ERK phosphorylation in vascular cells is mediated in part by reactive oxygen species (ROS), including superoxide (O 2 − ) [57, 58]. In addition, PIO has been shown to inhibit NADPH oxidase-mediated generation of ROS in aortic tissues and VSMCs [59, 60]. Thus, it is likely that PIO inhibits the basal ERK activation by suppressing ROS production in VSMCs.…”