Cellular sources of fibrotic collagen.
Cellular sources of fibrotic collagen.
复制标题
纤维化胶原蛋白的细胞来源。
DOI：
10.1016/0272-0590(85)90070-3
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Lindblad,WJ
中科院分区：
文献类型：
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作者：
Diegelmann,RF;Lindblad,WJ
纤维化胶原蛋白的细胞来源。林德布莱德和狄格曼(1985).北京：北京.APPL托昔康。5,219-227。脊椎动物物种中的每个体细胞都包含遗传信息，因此有可能合成胶原蛋白。通常，当损伤后需要新的结缔组织时，中胚层起源的细胞被激活以满足这一需求，并提供足够数量的胶原蛋白，以恢复受损组织或器官的结构和功能。在这种情况下，非结缔组织细胞要么不合成胶原蛋白，要么可能只产生极少量的胶原蛋白，这是我们最敏感的技术几乎无法检测到的。然而，当这些非中胚层细胞暴露在异常或有毒的环境中时，胶原蛋白的表达可能会大大增强。例如，当肝细胞被从其正常的活体环境中移出并置于细胞培养中时，它们显示出其产生胶原的潜力显著增加。当肝细胞暴露在体内的毒素或损伤中时，它们也可能表达这种产生大量胶原的能力。近年来，产生胶原或含有与胶原生物合成相关的酶的细胞的名单已经扩大，现在包括肾小球系膜细胞、脂肪细胞、主动脉内皮细胞、平滑肌细胞、雪旺细胞和淋巴细胞等多样化和专门化的细胞。因此，纤维化导致的组织或器官的结构和功能的丧失可能是由于非中胚层来源和结缔组织细胞中的胶原过度沉积所致。
Cellular Sources of Fibrotic Collagen. DIEGELMANN, R. F., AND LINDBLAD, W. J. (1985).Fundam. Appl. Toxicol. 5, 219–227. Every somatic cell within vertebrate species contains genetic information and therefore the potential to synthesize collagen. Normally, when there is a requirement for new connective tissue following injury, cells of mesodermal origin are activated to meet that demand and supply sufficient amounts of collagen to return structure and function to the damaged tissue or organ. Under these conditions, nonconnective tissue cells either do not synthesize collagen or may produce only minute quantities which are barely detectable by our most sensitive techniques. However, when these nonmesodermal cells are exposed to an abnormal or toxic environment, collagen expression may become greatly enhanced. For example, when hepatocytes are removed from their normalin vivoenvironment and placed in cell culture, they demonstrate a dramatic increase in their potential to produce collagen. Hepatocytes may also express this ability to produce significant quantities of collagen when they are exposed to toxins or injuryin vivo. The list of cells shown to produce collagen or contain enzymes related to collagen biosynthesis has expanded in recent years and now includes such diverse and specialized cells as glomerular mesangial, adipocytes, aortic endothelial, smooth muscle, Schwann cells, and lymphocytes. Therefore, the loss of structure and function in a tissue or organ due to fibrosis may result from excessive deposition of collagen from nonmesodermal sources as well as from connective tissue cells.