FERRITIN SYNTHESIS IN INFLAMMATION .2. MECHANISM OF INCREASED FERRITIN SYNTHESIS
FERRITIN SYNTHESIS IN INFLAMMATION .2. MECHANISM OF INCREASED FERRITIN SYNTHESIS
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DOI：
10.1111/j.1365-2141.1981.tb07238.x
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发表时间：
1981-01-01
影响因子：
6.5
通讯作者：
HERSHKO, C
中科院分区：
文献类型：
--
作者：
KONIJN, AM;CARMEL, N;HERSHKO, C
研究了注射松节油后0 ~ 48 h大鼠肝脏中铁蛋白合成增加的机制。采用亚细胞蛋白合成系统，研究正常动物和治疗动物的细胞液因子和多体各自的作用。发现两波铁蛋白合成增加，第一波在炎症发生后6小时达到峰值，第二波在大约7点开始。24小时。铁蛋白合成增强的早期波与细胞液因子活性增加有关。铁蛋白合成的后期增强表现为多体活性增加和细胞液活性增加。这些观察结果表明，炎症中铁蛋白合成增强的早期阶段存在转录后控制机制，而铁蛋白合成增强的后期阶段存在转录和转录后控制机制。
The mechanism of increased ferritin synthesis in inflammation was studied in rat livers 0-48 h after turpentine injection. A subcellular protein synthesizing system was employed in which the respective roles of cell sap factors and polysomes from normal and treated animals could be studied. Two waves of increased ferritin synthesis were found, an early wave with peak activity at 6 h of inflammation and a 2nd wave starting at .apprx. 24 h. The early wave of enhanced ferritin synthesis was associated with increased activity of cell sap factors. The late enhancement of ferritin synthesis was characterized by increased polysomal activity and increased cell sap activity. These observations suggest a post-transcriptional control mechanism for the early phase of enhanced ferritin synthesis in inflammation, and a transcriptional and post-transcriptional control for the late phase of enhanced ferritin synthesis.