From integrative signalling to metabolic disorders
From integrative signalling to metabolic disorders
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DOI：
10.1016/j.jsbmb.2008.03.010
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发表时间：
2008-04-01
影响因子：
4.1
通讯作者：
Gallo-Payet, Nicole
中科院分区：
文献类型：
--
作者：
Otis, Melissa;Battista, Marie-Claude;Gallo-Payet, Nicole
肾上腺皮质经历持续的动态结构变化，这是确保腺体综合功能的关键因素。研究表明，细胞环境可以调节细胞功能，如增殖和类固醇分泌。例如，当在纤连蛋白上培养时，用血管紧张素II处理3天促进蛋白质合成，伴随着肾小球细胞增殖的减少，而不是在胶原IV或层粘连蛋白上培养。这些作用涉及细胞凋亡相关蛋白之间的密切相互作用和p42/p44（mapk）和p38 MAPK通路的激活。另一方面，促肾上腺皮质激素（ACTH），这显然是最有力的刺激束状细胞，诱导特定的调制靶蛋白，当细胞培养在胶原IV，但不是在纤连蛋白或层粘连蛋白。特别地，ACTH处理导致Seladin-1的表达增加，并诱导Seladin-1从细胞质到细胞核的再定位，在体内和培养条件下，在成年大鼠和人胎儿肾上腺中。总的来说，这些结果表明Seladin-1与胶原IV一起能够调节ACTH反应性。因此，Seladin-1可能参与调节类固醇生成时，定位在细胞质中，而反过来保护细胞免受氧化应激时，大量定位在细胞核中的强烈ACTH刺激。(C)2008爱思唯尔有限公司保留所有权利。
The adrenal cortex undergoes constant dynamic structural changes, a key element in ensuring integrative functionality of the gland. Studies have shown that the cellular environment can modulate cell functions such as proliferation and steroid secretion. For example, 3-day treatment with angiotensin II promotes protein synthesis with a concomitant decrease in proliferation of glomerulosa cells, when cultured on fibronectin, but not on collagen IV or laminin. These effects involve close interaction between cytoskeleton-associated proteins and activation of p42/p44(mapk) and p38 MAPK pathways. On the other hand, adrenocorticotropin hormone (ACTH), which is clearly the most potent stimulus of fasciculata cells, induces specific modulation of targeted proteins, when cells are cultured on collagen IV, but not on fibronectin or laminin. In particular, ACTH treatment leads to increased expression of Seladin-1 and induces the relocalization of Seladin-1 from the cytoplasm to the nucleus, both in vivo and in culture conditions, in adult rats and in human fetal adrenal glands. As a whole, these results indicate that Seladin-1, together with collagen IV, is able to modulate ACTH responsiveness. Hence, Seladin-1 may participate in the regulation of steroidogenesis when localized in the cytoplasm, while conversely protecting cells against oxidative stress generated by intense ACTH stimulation when massively localized in the nucleus. (C) 2008 Elsevier Ltd. All rights reserved.