Masuno H, Okuda H
Department of Medical Laboratory Technology, Ehime College of Health Science, Japan.
J Atheroscler Thromb. 1995;2(1):46-52. doi: 10.5551/jat1994.2.46.
Time courses of synthesis and secretion of lipoprotein lipase (LPL) were examined in 3T3-L1 adipocytes. LPL was glycosylated in the endoplasmic reticulum (ER) within 10 min after synthesis, and was transported after 20-30 min to the trans Golgi where it was converted to the mature form with M(r) = 55,000-58,000, which was resistant to endoglycosidase H (endo H). LPL subunits with M(r) = 55,000-58,000 appeared in the medium within 30 min after synthesis. The effects of brefeldin A (BFA), which inhibits transport of glycoproteins in various types of cells, on secretion and glycosylation of LPL were also examined. BFA completely blocked release of LPL activity into the medium, causing accumulation of the activity in cells. The suppressive effect of BFA on release of LPL activity was reversible. BFA-treated cells synthesized LPL with M(r) = 53,000-55,000 consisting of 2 types of subunits, the main type being totally endo H-sensitive and the other partially endo H-sensitive. No LPL were secreted into the medium by BFA-treated cells.
在3T3-L1脂肪细胞中检测了脂蛋白脂肪酶（LPL）的合成和分泌的时间进程。LPL在合成后10分钟内在内质网（ER）中进行糖基化，并在20 - 30分钟后转运至反式高尔基体，在那里它被转化为成熟形式，分子量（M(r)）为55,000 - 58,000，对内切糖苷酶H（endo H）具有抗性。分子量为55,000 - 58,000的LPL亚基在合成后30分钟内出现在培养基中。还研究了布雷菲德菌素A（BFA）对LPL分泌和糖基化的影响，BFA可抑制多种类型细胞中糖蛋白的转运。BFA完全阻断了LPL活性释放到培养基中，导致细胞内活性积累。BFA对LPL活性释放的抑制作用是可逆的。经BFA处理的细胞合成的LPL分子量为53,000 - 55,000，由2种亚基组成，主要类型完全对内切糖苷酶H敏感，另一种部分对内切糖苷酶H敏感。经BFA处理的细胞没有将LPL分泌到培养基中。
