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首页> 外文期刊>Biochemistry >Insulin Promotes Shedding of Syndecan Ectodomains from 3T3-L1 Adipocytes:A Proposed Mechanism for Stabilization of Extracellular Lipoprotein Lipase
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Insulin Promotes Shedding of Syndecan Ectodomains from 3T3-L1 Adipocytes:A Proposed Mechanism for Stabilization of Extracellular Lipoprotein Lipase

机译：胰岛素促进3d3-L1脂肪细胞中Syndecan Ecdomains的脱落：一种稳定的细胞外脂蛋白脂肪酶的拟议机制。

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Syndecans are a family of four transmembrane heparan sulfate proteoglycans that act as coreceptors for a variety of cell-surface ligands and receptors.Receptor activation in several cell types leads to shedding of syndecan-1 and syndecan-4 ectodomains into the extracellular space by metallopro-teinase-mediated cleavage of the syndecan core protein.We have found that 3T3-L1 adipocytes express syndecan-1 and syndecan-4 and that their ectodomains are shed in response to insulin in a dose-,time-,and metalloproteinase-dependent manner.Insulin responsive shedding is not seen in 3T3-L1 fibroblasts.This shedding involves both Ras-MAP kinase and phosphatidylinositol 3-kinase pathways.In response to insulin,adipocytes are known to secrete active lipoprotein lipase,an enzyme that binds to heparan sulfate on the luminal surface of capillary endothelia.Lipoprotein lipase is transported as a stable enzyme from its site of synthesis to its site of action,but the transport mechanism is unknown.Our studies indicate that shed adipocyte syndecans associate with lipoprotein lipase.The shed syndecan ectodomain can stabilize active lipoprotein lipase.These data suggest that syndecan ectodomains,shed by adipocytes in response to insulin,are physiological extracellular chaperones for lipoprotein lipase as it translocates from its site of synthesis to its site of action.
机译：Syndecans是由四个跨膜硫酸乙酰肝素蛋白聚糖组成的家族，可作为多种细胞表面配体和受体的共受体。在几种细胞类型中，受体的激活导致syndecan-1和syndecan-4胞外域通过金属脯蛋白脱落到细胞外空间。 teinase介导的syndecan核心蛋白的裂解。我们发现3T3-L1脂肪细胞表达syndecan-1和syndecan-4，并且它们的胞外域在剂量，时间和金属蛋白酶依赖性的情况下响应胰岛素而脱落。在3T3-L1成纤维细胞中未见到胰岛素响应性脱落。该脱落涉及Ras-MAP激酶和磷脂酰肌醇3激酶途径。响应胰岛素，已知脂肪细胞分泌活性脂蛋白脂肪酶，该酶与硫酸乙酰肝素结合。脂蛋白脂肪酶作为一种稳定的酶从其合成位点转运至其作用位点，但其转运机理尚不清楚。死亡表明，脱落的己二糖胞外结合蛋白与脂蛋白脂肪酶相关。脱落的己二糖胞外域可以稳定活性脂蛋白脂肪酶。这些数据表明，脂肪细胞在胰岛素的作用下脱落，其多糖外结构域是脂蛋白脂肪酶的生理性细胞外伴侣，因为它从脂蛋白脂肪酶的位点转移出来。合成其作用部位。

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