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首页> 外文期刊>American Journal of Physiology >Liver sinusoidal endothelial cells are the principal site for elimination of unfractionated heparin from the circulation
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Liver sinusoidal endothelial cells are the principal site for elimination of unfractionated heparin from the circulation

机译：肝窦窦内皮细胞是从循环中消除普通肝素的主要部位

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First published December 6, 2007; doi:10.1152/ajpgi.00489.2007.-The mechanism of elimination of blood bome heparin was studied. To this end unfractionated heparin (UFH) was tagged with FTTC, which served as both a visual marker and a site of labeling with ~(125)I-iodine. UFH labeled in this manner did not alter the anticoagulant activity or binding specificity of the glycosaminoglycan. Labeled heparin administered intravenously to rats (0.1 IU/kg) had a circulatory t_(-/2) of 1.7 min, which was increased to 16 min upon coinjection with unlabeled UFH (100 IU/kg). At 15 min after injection, 71 % of recovered radioactivity was found in liver. Liver cell separation revealed the following relative uptake capacity, expressed per cell: liver sinusoidal endothelial cell (LSEC)-parenchymal cell-Kupffer cell = 15:3.6:1. Fluorescence microscopy on liver sections showed accumulation of FITC-UFH only in cells lining the liver sinusoids. No fluorescence was detected in parenchymal cells or endothelial cells lining the central vein. Fluorescence microscopy of cultured LSECs following binding of FITC-UFH at 4degC and chasing at 37degC, showed accumulation of the probe in vesicles located at the periphery of the cells after 10 min, with transfer to large, evenly stained vesicles in the perinuclear region after 2 h. Immunogold electron microscopy of LSECs to probe the presence of FITC following injection of FITC-UFH along with BSAgold to mark lysosomes demonstrated colocalization of the probe with the gold particles in the lysosomal compartment. Receptor-ligand competition experiments in primary cultures of LSECs indicated the presence of a specific heparin receptor, functionally distinct from the hyaluronan/scavenger receptor (Stabilin2). The results suggest a major role for LSECs in heparin elimination.
机译：首次发布于2007年12月6日; doi：10.1152 / ajpgi.00489.2007.-研究了消除血红素肝素的机制。为此，将普通肝素（UFH）用FTTC标记，FTTC既用作视觉标记，又用作〜（125）I-碘的标记位点。以这种方式标记的UFH不会改变糖胺聚糖的抗凝活性或结合特异性。静脉给予大鼠的标记肝素（0.1 IU / kg）的循环t _（-/ 2）为1.7分钟，与未标记的UFH（100 IU / kg）共注射后，循环t _（-/ 2）增加至16分钟。注射后15分钟，在肝脏中发现71％的回收放射性。肝细胞分离显示每个细胞表达以下相对吸收能力：肝窦内皮细胞（LSEC）-实质细胞-库普弗细胞= 15：3.6：1。肝切片上的荧光显微镜检查显示，FITC-UFH仅在肝窦内衬的细胞中蓄积。在中心静脉内的实质细胞或内皮细胞中未检测到荧光。 FITC-UFH在4degC结合并在37degC追逐之后，培养的LSEC的荧光显微镜显示，探针在10分钟后在细胞外围的囊泡中积累，并在2周后转移到大的，染色均匀的核周区域中H。在注射FITC-UFH和BSAgold标记溶酶体后，LSEC的免疫金电子显微镜检查了FITC的存在，证明了探针与溶酶体区室中的金颗粒共定位。 LSECs原代培养物中的受体-配体竞争实验表明，存在一种特定的肝素受体，功能上不同于透明质酸/清道夫受体（Stabilin2）。结果表明LSEC在肝素清除中起主要作用。

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