Fibroblast growth factor modulates synthesis of collagen in cultured vascular endothelial cells.
Fibroblast growth factor modulates synthesis of collagen in cultured vascular endothelial cells.
复制标题
成纤维细胞生长因子调节培养的血管内皮细胞中胶原蛋白的合成。
DOI：
10.1111/j.1432-1033.1982.tb05888.x
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Gospodarowicz,D
中科院分区：
文献类型：
--
作者：
Tseng,SC;Savion,N;Stern,R;Gospodarowicz,D
来自成年牛主动脉弓的血管内皮细胞可以以两种方式生长，在存在或不存在成纤维细胞生长因子的情况下。比较了在这两种条件下培养产生的胶原类型。在存在成纤维细胞生长因子的情况下，细胞以有序的方式生长，表达其正常表型，并以10：1：3的比例主要合成III型胶原蛋白加上IV型和V型胶原蛋白。在缺乏该因子的情况下生长的培养物失去其有序的生长模式，失去极性和正常的表型表达。它们将总蛋白质合成能力的两倍用于胶原蛋白，现在除了其他类型的胶原蛋白外，还合成I型胶原蛋白。胶原蛋白I：III：IV：V的比例约为30：70：1：13。表达的V型胶原蛋白链的种类也改变。成纤维细胞生长因子似乎调节胶原合成，细胞外基质的主要成分，并间接调节培养的血管内皮细胞的表型表达。在动脉粥样硬化中，发现I型胶原与内膜层相关。在无成纤维细胞生长因子的情况下培养的这些血管内皮细胞的无序生长和I型胶原的异常产生是包括动脉粥样硬化斑块形成在内的许多病理情况的模型。
Vascular endothelial cells derived from adult bovine aortic arch can be grown in two ways, either in the presence or absence of fibroblast growth factor. The types of collagen produced by cultures under these two con‐ ditions have been compared. In the presence of fibroblast growth factor, cells grow in an orderly fashion, express their normal phenotype and synthesize primarily type III collagen plus collagens types IV and V at a ratio of 10: 1: 3. Cultures grown in the absence of the factor lose their orderly pattern of growth, lose polarity and normal phenotypic expression. They devote twice the proportion of total protein‐synthesizing capacity to collagen, and now synthesize type I in addition to the other collagen types. The ratio of collagen types I: III: IV: V is approxi‐ mately 30:70:1:13. The kinds of type V collagen chains expressed are also altered. Fibroblast growth factor appears to modulate collagen synthesis, the major component of the extracellular matrix, and indirectly modulates the phenotypic expression of cultured vascular endothelial cells. In atherosclerosis, type I collagen is found in association with the intimal layer. The disorderly growth and the abnormal production of type I collagen by these vascular endothelial cells cultured in the absence of fibroblast growth factor is a model for a number of pathological situations including atherosclerotic plaque formation.