The molecular mechanisms that promote platelet hyperactivity remain unclear but could be due to glycation-induced conformational changes of platelet membranes resulting in impaired aspirin entry or less-efficient acetylation/compensatory increase in COX-2 expression in newborn platelets.
Fibroblastic reticular cells of the lymphoid tissues modulate T cell activation threshold during homeostasis via hyperactivecyclooxygenase-2/prostaglandin E<sub>2</sub> axis.
In this study, we examined whether the hyper-methylation mediated transcriptional silencing of Cox-2 also occurred in human gastric carcinoma tissues and which portion of CpG island methylation is important in Cox-2 gene expression.
Hyper activation of COX-2 with abnormal prostaglandin generation is considered to contribute to the pathophysiology of endometriosis and disease progression.