Stefanović V, Djordjević V, Mitić M
Institute of Nephrology and Hemodialysis, Faculty of Medicine, Nis, Yugoslavia.
Arch Physiol Biochem. 1995 Aug;103(4):427-30. doi: 10.3109/13813459509047133.
Alkaline phosphodiesterase I was demonstrated in human glomerular mesangial cells (HGEC) as an ectoenzyme. Treatment of HGEC by dexamethasone increased surface phosphodiesterase I activity in a dose- and time-dependent manner. Maximal increase of phosphodiesterase I activity, about twice, occurred after treatment with 5 microM dexamethasone for 6 days. Cycloheximide prevented and RU 38486, a glucocorticoid receptor antagonist, suppressed the dexamethasone induced increase in phosphodiesterase I activity. This study shows that HGEC have a surface phosphodiesterase I controlled by glucocorticoids through a receptor-mediated mechanism.
碱性磷酸二酯酶I在人肾小球系膜细胞(HGEC)中作为一种外切酶被证实。地塞米松处理HGEC后,表面磷酸二酯酶I活性呈剂量和时间依赖性增加。用5 microM地塞米松处理6天后,磷酸二酯酶I活性最大增加约两倍。放线菌酮可阻止其增加,糖皮质激素受体拮抗剂RU 38486可抑制地塞米松诱导的磷酸二酯酶I活性增加。本研究表明,HGEC具有一种通过受体介导机制受糖皮质激素控制的表面磷酸二酯酶I。