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蛋白激酶C激活剂对新鲜的终末分化静止巨噬细胞中c-fos mRNA表达的增强作用。

Augmentation of c-fos mRNA expression by activators of protein kinase C in fresh, terminally differentiated resting macrophages.

作者信息

Radzioch D, Bottazzi B, Varesio L

出版信息

Mol Cell Biol. 1987 Feb;7(2):595-9. doi: 10.1128/mcb.7.2.595-599.1987.

DOI:10.1128/mcb.7.2.595-599.1987
PMID:3029561
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC365113/
Abstract

Expression of c-fos mRNA was investigated in fresh, normal peritoneal macrophages (M phi), which are terminally differentiated, nonproliferating cells. The levels of c-fos mRNA were dramatically increased by stimulation with phorbol myristate acetate (PMA), calcium ionophore, or 1-oleoyl-2-acetoyl glycerol (OAG). Induction of c-fos mRNA by all the above agents followed similar kinetics, with a peak of mRNA 30 min after stimulation. These results demonstrate that c-fos mRNA can be augmented in fresh, terminally differentiated cells. Since the stimuli increasing c-fos mRNA are direct or indirect activators of protein kinase C, our data suggest that in M phi c-fos mRNA is controlled by protein kinase C activation. PMA, calcium ionophore, and OAG were biologically active in M phi. PMA and calcium ionophore induced respiratory burst and tumoricidal activity, respectively, whereas OAG and PMA were chemotactic for M phi. Interferons beta and gamma, potent M phi activators eliciting tumoricidal activity, did not alter the levels of c-fos mRNA. These results indicate that c-fos mRNA augmentation is a stimulus-specific rather than a function-specific response connected to activation of protein kinase C.

摘要

在新鲜的、正常的腹膜巨噬细胞(M phi)中研究了c-fos mRNA的表达,这些细胞是终末分化的、不增殖的细胞。佛波酯(PMA)、钙离子载体或1-油酰-2-乙酰甘油(OAG)刺激可使c-fos mRNA水平显著升高。上述所有试剂诱导c-fos mRNA的动力学相似,刺激后30分钟mRNA达到峰值。这些结果表明,在新鲜的终末分化细胞中c-fos mRNA可以增加。由于增加c-fos mRNA的刺激物是蛋白激酶C的直接或间接激活剂,我们的数据表明在M phi中c-fos mRNA受蛋白激酶C激活的控制。PMA、钙离子载体和OAG在M phi中具有生物学活性。PMA和钙离子载体分别诱导呼吸爆发和杀肿瘤活性,而OAG和PMA对M phi具有趋化作用。干扰素β和γ是引发杀肿瘤活性的强效M phi激活剂,它们不会改变c-fos mRNA的水平。这些结果表明,c-fos mRNA增加是一种与蛋白激酶C激活相关的刺激特异性而非功能特异性反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b52/365113/77d5db9b8d53/molcellb00074-0039-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b52/365113/ba6da8af28a9/molcellb00074-0038-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b52/365113/a60bdedc31ae/molcellb00074-0039-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b52/365113/77d5db9b8d53/molcellb00074-0039-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b52/365113/ba6da8af28a9/molcellb00074-0038-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b52/365113/a60bdedc31ae/molcellb00074-0039-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b52/365113/77d5db9b8d53/molcellb00074-0039-b.jpg

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