van der Westhuyzen D R, Gevers W, Coetzee G A
Eur J Biochem. 1980 Nov;112(1):153-60. doi: 10.1111/j.1432-1033.1980.tb04996.x.
The degradation of 135I-apoprotein B of human low-density lipoprotein by cell extracts of cultured bovine aortic smooth muscle cells was determined by measuring the formation of acid-soluble products and by analyzing the electrophoretic patterns of digested apoprotein in gels containing sodium dodecyl sulfate. Degradation resulted in an initial rapid accumulation of a limited number of distinct smaller fragments. Two products with apparent molecular weights of 220,000 and 200,000 predominated. Pepstatin inhibited proteolysis almost completely, as measured by either assay. Leupeptin decreased hydrolysis to acid-soluble products by approximately 50%, but had no effect on the initial cleavage of intact apoprotein B. Similar results were found in the case of extracts from cultured human skin fibroblasts and from adult bovine arterial smooth muscle. Leupeptin inhibited intracellular degradation of 125I-apoprotein B in cultured cells by approximately 50%. It is concluded that the intralysosomal degradation of apoprotein B involves an initial limited endoproteolytic attack at susceptible sites by cathepsin D. This and other enzymes, including cathepsin B, then act synergistically to bring degradation to completion.
通过测量酸溶性产物的形成以及分析含十二烷基硫酸钠的凝胶中消化的载脂蛋白的电泳图谱,来测定培养的牛主动脉平滑肌细胞提取物对人低密度脂蛋白中135I-载脂蛋白B的降解情况。降解导致最初迅速积累有限数量的不同较小片段。两种表观分子量分别为220,000和200,000的产物占主导。通过任何一种测定方法测量,胃蛋白酶抑制剂几乎完全抑制了蛋白水解。亮抑蛋白酶肽使水解为酸溶性产物的程度降低了约50%,但对完整载脂蛋白B的初始裂解没有影响。在培养的人皮肤成纤维细胞和成年牛动脉平滑肌提取物的情况下也发现了类似结果。亮抑蛋白酶肽抑制培养细胞中125I-载脂蛋白B的细胞内降解约50%。得出的结论是,载脂蛋白B的溶酶体内降解涉及组织蛋白酶D在敏感位点的初始有限内切蛋白水解攻击。然后,这种酶和其他酶,包括组织蛋白酶B,协同作用使降解完成。