STUDIES INVITRO ON THE UPTAKE AND DEGRADATION OF SODIUM HYALURONATE IN RAT-LIVER ENDOTHELIAL-CELLS
STUDIES INVITRO ON THE UPTAKE AND DEGRADATION OF SODIUM HYALURONATE IN RAT-LIVER ENDOTHELIAL-CELLS
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DOI：
10.1042/bj2230617
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发表时间：
1984-01-01
影响因子：
4.1
通讯作者：
LAURENT, TC
中科院分区：
文献类型：
--
作者：
SMEDSROD, B;PERTOFT, H;LAURENT, TC
7℃原代培养物中的大鼠肝内皮细胞C 特异性地并以高亲和力 (Kd = 6 × 10-11 M) 结合放射性标记的透明质酸钠 (HA；MW，400,000)。最大结合能力约为 104 个分子/p 细胞。使用未标记的HA和来自HA的寡糖进行的抑制实验表明，每个分子都被多个协同作用的受体结合，并且单个受体识别多糖的四糖或六糖序列。 37度。 C 肝内皮细胞内吞HA。该过程结合了受体介导和液相内吞作用的特征。随着HA浓度的增加，内化速率并未表现出任何饱和，但与生理浓度或高于生理浓度的多糖浓度大致成正比。在50μg游离Ha/l时，每个肝内皮细胞每分钟积累0.1fg多糖。荧光 HA 在核周颗粒（可能是溶酶体）中积聚。将多糖添加到培养物中后约 30 分钟，HA 的降解产物出现在培养基中。来自糖环中含有N-[3H]乙酰基或14C的HA的放射性主要分别以[3H]乙酸盐和[14C]乙酸盐的形式回收。对肝内皮细胞体外内化和降解HA的能力的估计表明，这些细胞可能主要负责体内从人血液中清除HA。
Rat liver endothelial cells in primary cultures at 7.degree. C bind radioactively labeled sodium hyaluronate (HA; MW, 400,000) specifically and with high affinity (Kd = 6 .times. 10-11 M). Maximal binding capacity is .apprx.. 104 molecules/p cell. Inhibition experiments with unlabeled HA and oligosaccharides from HA indicate that each molecule is bound by several receptors acting co-operatively and that the single receptor recognizes a tetra- or hexa-saccharide sequence of the polysaccharide. At 37.degree. C the liver endothelial cells endocytose the HA. The process combines the features of a receptor-mediated and a fluid-phase endocytosis. The rate of internalization does not show any saturation with increasing HA concentration, but is approximately proportional to the polysaccharide concentration at and above the physiological concenration. At 50 .mu.g of free Ha/l each liver endothelial cell accumulates 0.1 fg of the polysaccharide/min. Fluorescent HA accumulates in perinuclear granules, presumably lysosomes. Degradation products from HA appear in the medium about 30 min after addition of the polysaccharide to the cultures. The radioactivity from HA containing N-[3H]acetyl groups or 14C in the sugar rings is recovered mainly as [3H]acetate and [14C]acetate respectively. Estimations of the capacity of liver endothelial cells to internalize and degrade HA in vitro indicate that these cells may be primarily responsible for the clearance of HA from human blood in vivo.