Mattila P, Häyry P, Renkonen R
Transplantation Laboratory, University of Helsinki, Finland.
FEBS Lett. 1989 Jul 3;250(2):362-6. doi: 10.1016/0014-5793(89)80756-2.
We have demonstrated that IFN-gamma, a potent peptide mediator in inflammatory responses, operates via the protein kinase C dependent transduction pathway in the induction of class II MHC antigens on rat microvascular endothelial cells. Stimulators of protein kinase C, like PMA, replaced IFN-gamma in the induction of MHC class II on endothelial cells in a dose-dependent manner. Selective enzyme inhibitors of protein kinase C, H-7 as well as sphingosine down-regulated the IFN-gamma induced class II expression in a dose-dependent manner. Addition of cAMP or cGMP in the culture, had no effect on the class II expression on the endothelial cells. Transient rise of cytosolic Ca2+ by calcium ionophore A23187, or a calmodulin antagonist W-7, had no effect on the IFN-gamma induced class II expression.
我们已经证明，γ干扰素是炎症反应中一种有效的肽介质，它通过蛋白激酶C依赖性转导途径在大鼠微血管内皮细胞上诱导II类主要组织相容性复合体（MHC）抗原。蛋白激酶C的刺激剂，如佛波酯（PMA），能以剂量依赖的方式在内皮细胞上替代γ干扰素诱导MHC II类分子的表达。蛋白激酶C的选择性酶抑制剂H-7以及鞘氨醇以剂量依赖的方式下调γ干扰素诱导的II类分子表达。在培养物中添加环磷酸腺苷（cAMP）或环磷酸鸟苷（cGMP），对内皮细胞上II类分子的表达没有影响。钙离子载体A23187或钙调蛋白拮抗剂W-7引起的胞质钙离子（Ca2+）短暂升高，对γ干扰素诱导的II类分子表达没有影响。
