Lipoprotein lipase-mediated uptake and degradation of low density lipoproteins by fibroblasts and macrophages.
Lipoprotein lipase-mediated uptake and degradation of low density lipoproteins by fibroblasts and macrophages.
复制标题
脂蛋白脂肪酶介导的成纤维细胞和巨噬细胞对低密度脂蛋白的摄取和降解。
DOI：
10.1172/jci116018
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Goldberg,IJ
中科院分区：
文献类型：
--
作者：
Rumsey,SC;Obunike,JC;Arad,Y;Deckelbaum,RJ;Goldberg,IJ
Lipoprotein lipase (LPL), the rate limiting enzyme for hydrolysis of lipoprotein triglyceride, also mediates nonenzymatic interactions between lipoproteins and heparan sulfate proteoglycans. To determine whether cell surface LPL increases LDL binding to cells, bovine milk LPL was added to upregulated and nonupregulated human fibroblasts along with media containing LDL. LDL binding to cells was increased 2-10-fold, in a dose-dependent manner, by the addition of 0.5-10 micrograms/ml of LPL. The amount of LDL bound to the cells in the presence of LPL far exceeded the capacity for LDL binding via the LDL receptor. Treatment of fibroblasts with heparinase and heparitinase resulted in a 64% decrease in LPL-mediated LDL binding. Compared to studies performed without LPL, more LDL was internalized and degraded in the presence of LPL, but the time course was slower than that of classical lipoprotein receptor mediated pathways. In LDL receptor negative fibroblasts, LPL increased surface bound LDL > 140-fold, intracellular LDL > 40-fold, and LDL degradation > 6-fold. These effects were almost completely inhibited by heparin and anti-LPL monoclonal antibody. LPL also increased the binding and uptake by fibroblasts of apolipoprotein-free triglyceride emulsions; binding was increased > 8-fold and cellular uptake was increased > 40-fold with LPL. LPL increased LDL binding to THP-1 monocytes, and increased LDL uptake (4.5-fold) and LDL degradation (2.5-fold) by THP-1 macrophages. In the absence of added LPL, heparin and anti-LPL monoclonal antibodies decreased LDL degradation by > 40%, and triglyceride emulsion uptake by > 50%, suggesting that endogenously produced LPL mediated lipid particle uptake and degradation. We conclude that LPL increases lipid and lipoprotein uptake by cells via a pathway not involving the LDL receptor. This pathway may be important for lipid accumulation in LPL synthesizing cells.
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DOI：
10.1016/0005-2760(72)90034-3
发表时间：
1972-01-01
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA
影响因子：
--
作者：
BILHEIMER, DW;LEVY, RI;EISENBERG, S
通讯作者：
EISENBERG, S
影响因子：
64.5
作者：
GOLDSTEIN, JL;BASU, SK;BROWN, MS
通讯作者：
BROWN, MS
培养物中巨噬细胞分泌脂蛋白脂肪酶。
DOI：
--
发表时间：
1981
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Khoo,JC;Mahoney,EM;Witztum,JL
通讯作者：
Witztum,JL
影响因子：
--
作者：
J. Goldstein;S. Basu;Michael S. Brown
通讯作者：
J. Goldstein;S. Basu;Michael S. Brown
均匀且稳定形式的牛乳脂蛋白脂肪酶的制备。
DOI：
10.1080/10826068508062267
发表时间：
1985
期刊：
Preparative biochemistry
影响因子：
--
作者：
Socorro,L;Green,CC;Jackson,RL
通讯作者：
Jackson,RL