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[泡状和原核糖蛋白在胆固醇结石病发病机制中的作用]

[Vesicular and pronuclear glycoproteins in the pathogenesis of cholesterol lithiasis].

作者信息

Jirsa M, Smíd F, Marecek Z

机构信息

I. interní klinika 1, LF UK a VFN, Praha.

出版信息

Cas Lek Cesk. 1998 Jan 26;137(2):48-51.

PMID:9511266
Abstract

BACKGROUND

Several biliary proteins have been known to accelerate fusion of cholesterol rich phospholipid vesicles. Some of them are present in vesicular membrane, localisation of other proteins is unknown. Biliary glycoprotein has not been studied in consequence with pathogenesis of cholesterol lithiasis.

METHODS AND RESULTS

Low molecular extravesicular proteins were separated from vesicles by gel filtration on a 1200mm column of Sephacryl S-300 HR. Immunoglobulins IgM, IgA, haptoglobin, biliary glycoprotein I (BGP I) and nonspecific crossreactive antigen were eluted along with vesicles. Albumin and alpha 1-acid glycoprotein were eluted later and must be extravesicular.

CONCLUSIONS

Fact that BGP I (85 kDa membrane glycoprotein) eluted along with vesicles and not in albumin fraction suggests that it might be bound in vesicular membrane. As a known adhesion molecule it could thus play an important role in pathogenesis of cholesterol cholelithiasis.

摘要

背景

已知几种胆汁蛋白可加速富含胆固醇的磷脂囊泡的融合。其中一些存在于囊泡膜中,其他蛋白质的定位尚不清楚。胆汁糖蛋白尚未与胆固醇结石病的发病机制相关联进行研究。

方法与结果

通过在1200mm的Sephacryl S-300 HR柱上进行凝胶过滤,从囊泡中分离出低分子胞外蛋白。免疫球蛋白IgM、IgA、触珠蛋白、胆汁糖蛋白I(BGP I)和非特异性交叉反应抗原与囊泡一起洗脱。白蛋白和α1-酸性糖蛋白随后洗脱,必定位于胞外。

结论

BGP I(85kDa膜糖蛋白)与囊泡一起洗脱而不在白蛋白组分中洗脱,这一事实表明它可能结合在囊泡膜中。作为一种已知的黏附分子,它可能在胆固醇性胆结石的发病机制中起重要作用。

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