Activation of Thromboxane Receptor Upregulates Interleukin (IL)-1β–Induced VCAM-1 Expression Through JNK Signaling

Adiponectin Promotes Revascularization of Ischemic Muscle through a Cyclooxygenase 2-Dependent Mechanism

“…An adenoviral construct Ad-NF-B-luc containing the luciferase reporter gene driven by four tandem copies of the NF-B consensus sequence was used in the luciferase assay as previously described (6). Luciferase activity was measured with a luciferase assay kit (Promega) and a luminometer.…”

Enhanced airway smooth muscle cell thromboxane receptor signaling via activation of JNK MAPK and extracellular calcium influx

“…The best-characterized of the mammalian MAPKs are 1) the 3 42-and 44-kDa extracellular signal-regulated kinases (ERKs) ERK2 and ERK1; 2) the c-Jun amino-terminal kinase (JNK) or stress-activated protein kinase (SAPK); and 3) p38 MAPK. Among them, the JNK signaling is demonstrated to tightly regulate the TP receptor related inflammation (Bayat et al, 2008;Kumar et al, 2005) in vasculature and the JNK inhibitor SP600125 exerts effects on allergen-induced airway inflammation and remodeling (Eynott et al, 2004;Nath et al, 2005). A common feature associated with the regulation of airway smooth muscle contraction is a change in intracellular Ca Previously, we have demonstrated that organ culture induced airway hyperresponsiveness to bradykinin occurs via the up-regulated bradykinin receptors (Lei et al, 2010).…”

Map Kinase Phosphatase-1 Suppresses Endothelial Activation in Regions of the Arterial Tree That Are Resistant to Atherosclerosis

“…Pro-inflammatory mediators activate p38 and JNK which play an essential role in VCAM-1 expression by activating ATF-2 and c-jun transcription factors and by regulating VCAM-1 mRNA stability 11,12,14 . Here we demonstrate that activation of p38 and JNK in EC occurs constitutively and can be enhanced by LPS treatment in the lesser curvature of the aortic arch, a region that is exposed to low shear and is pre-disposed to vascular inflammation and atherosclerosis.…”

“…They are activated in EC in response to pro-inflammatory stimuli by dual phosphorylation of Thr-X-Tyr motifs within the phosphorylation loop 10 . Active forms of JNK and p38 phosphorylate transcription factors belonging to the AP-1 superfamily (including c-Jun, ATF2, c-fos) which subsequently form complexes with NF-κB at the promoters of pro-inflammatory genes including VCAM-1 [11][12][13] . Activation of p38 also regulates VCAM-1 at a post-transcriptional level by enhancing message stability 14 .…”