作者: Tülay Yucel-Lindberg , Harri Ahola , Jan Carlstedt-Duke , Thomas Modéer
关键词: Pathogenesis 、 Biology 、 Protein kinase C 、 Tumor necrosis factor alpha 、 Activator (genetics) 、 Downregulation and upregulation 、 Phospholipase A2 、 Molecular biology 、 Phorbol 、 Messenger RNA
摘要: The involvement of phospholipase A2 (PLA2) enzymes, the 85 kDa cytosolic PLA2 (cPLA2) and 14 secretory (sPLA2), on PGE2 production in human gingival fibroblasts was investigated. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that inflammatory mediators interleukin-1β (IL-1β) tumor necrosis factor α (TNFα) induce mRNA expression cPLA2 fibroblasts. In addition, treatment cells with calcium ionophore, A23187, or protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA), also induced expression, accompanied by enhanced production. anti-inflammatory steroid dexamethasone (DEX) reduced basal as well blocked induction IL-1β TNFα contrast to cPLA2, sPLA2 not detected either untreated treated study demonstrates is upregulated suggesting an important role for enzyme cytokine-induced Furthermore, rather than sPLA2, may be involved pathogenesis periodontal disease mediating