Borel J P, Maquart F X, Randoux A
Pathol Biol (Paris). 1984 Sep;32(7):795-812.
This paper summarizes the results of hormonal studies applying to collagen metabolism that were published during the last 10 years. This general review demonstrates that most of the hormones, when they act on this metabolism, either decrease the amount of synthesized collagen or increase its catabolism. This effect is demonstrated on whole living animals, in isolated organs, in pathological cases such as corticosteroid induced osteoporosis, and more directly in cell cultures. At physiological levels, some of the effects may be slight or biphasic but at pharmacological levels glucocorticoids and estrogens are strongly inhibiting. These inhibiting effects may be ascribed to various stages of collagen biosynthesis: transcription of the genes, translation of mRNA, post-translational reactions, that are particularly developed in the case of collagen and particularly sensitive to the hormone action. Intracellular degradation of collagen represents an important way of control for this biosynthesis and is noticeably activated by the system of cAMP and some prostaglandins. Finally, collagenases acting on the extracellular fibrils are stimulated by several groups of hormones such as thyroid hormone, testosterone, parathyroid hormone. This increase in catabolism acts in the sense of a fast decrease in the amount of collagen, confirming that most of the hormonal systems are aimed at decreasing both the synthesis of new collagen and the number of mature fibers existing in a given connective tissue. On the other hand, many growth factors and several hormones such as insulin and somatomedins are able to activate the mitoses in the cells that are know to produce collagen, and for this reason, indirectly stimulate the synthesis of this fibrous protein. It is of interest to point out that every time the organism needs depositing more collagen in any zone of the extracellular matrix, it has to send mobile cells from other tissues or to activate the divisions of the cells already present in the concerned tissue. This process is particularly conspicuous in the case of inflamed tissues. It is proposed as a general rule that decreases in the collagen amounts may be triggered by very fast hormonal mechanisms acting both to stop biosynthesis and to activate degradation, whereas the increase in collagen layering depends on indirect and slow mechanisms in which cell divisions represent the first event.
本文总结了过去十年发表的有关激素研究应用于胶原蛋白代谢的结果。这篇综述表明，大多数激素作用于这种代谢时，要么减少合成胶原蛋白的量，要么增加其分解代谢。这种作用在整个活体动物、离体器官、病理情况下如皮质类固醇诱导的骨质疏松症中得到证实，并且在细胞培养中更为直接地得到体现。在生理水平上，一些作用可能轻微或呈双相性，但在药理水平上，糖皮质激素和雌激素具有强烈的抑制作用。这些抑制作用可能归因于胶原蛋白生物合成的各个阶段：基因转录、mRNA翻译、翻译后反应，这些在胶原蛋白的情况下特别发达，并且对激素作用特别敏感。胶原蛋白的细胞内降解是这种生物合成控制的重要方式，并且明显地被cAMP系统和一些前列腺素激活。最后，作用于细胞外纤维的胶原酶受到几组激素的刺激，如甲状腺激素、睾酮、甲状旁腺激素。这种分解代谢的增加导致胶原蛋白量快速减少，证实大多数激素系统旨在减少新胶原蛋白的合成以及给定结缔组织中现有成熟纤维的数量。另一方面，许多生长因子和几种激素如胰岛素和生长调节素能够激活已知产生胶原蛋白的细胞中的有丝分裂，因此间接刺激这种纤维蛋白的合成。值得指出的是，每当生物体需要在细胞外基质的任何区域沉积更多胶原蛋白时，它必须从其他组织发送移动细胞或激活相关组织中已存在的细胞分裂。在炎症组织的情况下，这个过程特别明显。有人提出一条普遍规则，即胶原蛋白量的减少可能由非常快速的激素机制引发，这些机制既作用于停止生物合成又激活降解，而胶原蛋白分层的增加取决于间接和缓慢的机制，其中细胞分裂是首要事件。
