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醋酸视黄酯对汇合的C3H/10T1/2小鼠胚胎成纤维细胞纤连蛋白细胞外基质组装及纤连蛋白受体β亚基加工的影响。

Effect of retinyl acetate on the assembly of the fibronectin extracellular matrix and the processing of the fibronectin receptor beta subunit of confluent C3H/10T1/2 mouse embryo fibroblasts.

作者信息

Suzuki S S, Piette L H

机构信息

Department of Chemistry and Biochemistry, Utah State University, Logan 84322-0300.

出版信息

J Cell Biochem. 1993 Feb;51(2):181-9. doi: 10.1002/jcb.240510210.

Abstract

The mouse embryo fibroblast cell line, C3H/10T1/2, synthesized and deposited a large amount of fibronectin especially in the pericellular matrix. Confluent cultures of these cells cultured in the presence of 0.3 micrograms/ml of retinyl acetate released cell surface fibronectin and the extracellular matrix fibronectin fibrils were disorganized. The immunoblot analysis demonstrated that the number of the fibronectin receptor was decreased in the prolonged culturing of retinyl acetate-treated cells. Immunoprecipitation of 35S-methionine pulse-chase labeled cell extracts by antifibronectin receptor antibody indicated that about one-half of the pre-beta subunit was processed and converted to the mature form in control cells, and only about one-fourth of the pre-beta subunit was processed in the retinyl acetate-treated confluent cells. 1-deoxymannojirimycin (MNJ), which is an inhibitor of oligosaccharide processing, induced disorganization of the extracellular matrix fibronectin assembly similar to that observed with retinyl acetate. The results of this study suggest that a mechanism of action of retinyl acetate is inhibition of the glycosylation during processing of the fibronectin receptor, a step necessary for fibronectin binding and for assembly of the extracellular matrix.

摘要

小鼠胚胎成纤维细胞系C3H/10T1/2合成并沉积了大量纤连蛋白,尤其是在细胞周围基质中。在存在0.3微克/毫升视黄酸的情况下培养的这些细胞的汇合培养物释放细胞表面纤连蛋白,并且细胞外基质纤连蛋白原纤维变得紊乱。免疫印迹分析表明,视黄酸处理的细胞在延长培养后纤连蛋白受体的数量减少。用抗纤连蛋白受体抗体对35S-甲硫氨酸脉冲追踪标记的细胞提取物进行免疫沉淀表明,在对照细胞中约一半的前β亚基被加工并转化为成熟形式,而在视黄酸处理的汇合细胞中只有约四分之一的前β亚基被加工。1-脱氧甘露基野尻霉素(MNJ)是一种寡糖加工抑制剂,它诱导细胞外基质纤连蛋白组装紊乱,类似于视黄酸所观察到的情况。这项研究的结果表明,视黄酸的作用机制是抑制纤连蛋白受体加工过程中的糖基化,这是纤连蛋白结合和细胞外基质组装所必需的步骤。

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