Triiodothyronine modulates interleukin-6 synthesis in osteoblasts: inhibitions in protein kinase A and C pathways.
Triiodothyronine modulates interleukin-6 synthesis in osteoblasts: inhibitions in protein kinase A and C pathways.
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Triiodothyronine 调节成骨细胞中 IL-6 的合成：抑制蛋白激酶 A 和 C 通路。
DOI：
10.1210/endo.139.3.5853
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发表时间：
1998
期刊：
影响因子：
4.8
通讯作者：
T. Uematsu
中科院分区：
文献类型：
--
作者：
H. Tokuda;O. Kozawa;A. Harada;K. Isobe;T. Uematsu
在成骨样MC 3 T3-E1细胞中，我们最近报道了PGE 1和PGF 2 α分别通过激活蛋白激酶A和蛋白激酶C诱导白细胞介素（IL）-6合成。此外，在IL-1诱导的IL-6合成的情况下，在这些细胞中，我们表明，蛋白激酶C激活IL-1限制了IL-6的合成。在本研究中，我们研究了T3对这些激动剂诱导的MC 3 T3-E1细胞IL-6合成的影响。T3本身对IL-6合成几乎没有影响，但在10 pM和10 nM之间的范围内以剂量依赖性方式显著降低PGE 1诱导的IL-6合成。T3还降低了PGE 1诱导的蛋白激酶A的激活。T3抑制由霍乱毒素（Gs的激活剂）或毛喉素（其直接激活腺苷酸环化酶）诱导的IL-6合成。然而，T3不影响（Bu）2cAMP诱导的IL-6合成。此外，T3在10 pM至10 nM范围内呈剂量依赖性降低PGF 2 α诱导的IL-6合成。T3还抑制由蛋白激酶C激活剂12-O-十四酰基佛波醇-13-乙酸酯诱导的IL-6合成。另一方面，T3显著增强IL-1诱导的IL-6合成。T3的这种增强作用在蛋白激酶C下调的细胞中得到加强。T3几乎不影响PGF 2 α或IL-1诱导的蛋白激酶C活化。这些结果强烈表明，T3调节IL-6的合成在两个点在成骨细胞如下;一个是施加在腺苷酸环化酶和蛋白激酶A之间的点，另一个是在一个点下游的蛋白激酶C激活。
In osteoblast-like MC3T3-E1 cells, we recently reported that PGE1 and PGF2alpha induce interleukin (IL)-6 synthesis via activation of protein kinase A and protein kinase C, respectively. Moreover, in the case of IL-1-induced IL-6 synthesis in these cells, we showed that protein kinase C activation by IL-1 limits the IL-6 synthesis. In the present study, we investigated the effect of T3 on IL-6 synthesis induced by these agonists in MC3T3-E1 cells. T3, which by itself had little effect on IL-6 synthesis, significantly reduced the IL-6 synthesis induced by PGE1 in a dose-dependent manner in the range between 10 pM and 10 nM. T3 also reduced PGE1-induced activation of protein kinase A. T3 inhibited the IL-6 synthesis induced by cholera toxin, an activator of Gs, or forskolin, which directly activates adenylate cyclase. However, T3 did not affect (Bu)2cAMP-induced IL-6 synthesis. In addition, T3 reduced PGF2alpha-induced IL-6 synthesis dose dependently in the range between 10 pM and 10 nM. T3 also inhibited IL-6 synthesis induced by 12-O-tetradecanoylphorbol-13-acetate, an activator of protein kinase C. On the other hand, T3 markedly enhanced IL-1-induced IL-6 synthesis. This enhancement by T3 was potentiated in protein kinase C down-regulated cells. T3 hardly affected the protein kinase C activation induced by PGF2alpha or IL-1. These results strongly suggest that T3 modulates IL-6 synthesis at two points in osteoblasts as follows; one is exerted at the point between adenylate cyclase and protein kinase A, and the other is at a point downstream from protein kinase C activation.
血小板衍生生长因子刺激成骨细胞谱系细胞中白细胞介素 6 的合成。
DOI：
10.1210/endo.136.12.7588297
发表时间：
1995
期刊：
Endocrinology.
影响因子：
--
作者：
Franchimont,N;Canalis,E
通讯作者：
Canalis,E