维生素A缺乏大鼠红系祖细胞表面N连接型糖链结构改变的机理研究

目的：阐明维生素Ａ缺乏（ＶＡＤ）引起大鼠红系祖细胞（ＥＰＣ）表面Ｎ连接型糖链结构改变从而导致ＥＰＣ增殖分化障碍的机理。方法：经３Ｈ－甘露糖掺入和结合外切糖苷酶的系列凝集素柱层析和凝胶过滤，研究ＶＡＤ大鼠骨髓基质细胞和脾细胞条件培养液（ＢＭＳＣＭ和ＳＣＭ）对正常大鼠ＥＰＣ表面Ｎ糖链结构的影响。结果：ＶＡＤ大鼠的ＢＭＳＣＭ和ＳＣＭ可致：３Ｈ－苷露糖掺入ＥＰＣ表面Ｎ糖肽的总量减少；高甘露糖型和杂合型糖链结构比例增大，复杂型的糖链结构比例下降；而在复杂型糖链中，二天线糖链的比例和不含分叉型Ｎ－乙酰基葡萄糖（Ｂ－Ｇｎ）和核心岩藻糖（Ｃ－Ｆｕｃ）的组分降低，含Ｂ－Ｇｎ或Ｃ－Ｆｕｃ或同时含Ｂ－Ｇｎ和Ｃ－Ｆｕｃ的组分增大。结论：ＶＡＤ可能影响造血生长因子（ＩＬ－３和ＧＭ－ＣＳＦ等）的表达／活性，因而导致ＥＰＣ表面糖链的异常以及ＥＰＣ增殖分化障碍。

STUDY ON THE MECHANISM OF CHANGES IN N LINKED SUGAR CHAIN STRUCTURE OF ERYTHROID PROGENITOR CELLS SURFACE IN VITAMIN A DEFICIENCY RATS

Objective: To clarify the mechanism of abnormality of N linked sugar chain structure of erythroid progenitor cells (EPC) caused by vitamin A deficiency (VAD). Method: Effects of bone marrow stromal cell media (BMSCM) and spleen cell media (SCM) from VAD rats on the N linked sugar chain structure of EPC surface in normal rats were investigated by 3H Mannose ( 3H Man) incorporation, serial lectin affinity chromatography and gelfiltration combined with exoglycosidase treatment. Results: The results showed that BMSCM and SCM from VAD rats: (1) decreased 3H Man incorporation into N glycopeptide on EPC surface; (2) decreased the percentage of complex type and increased the percentages of high mannose and hybrid type; (3) in complex type, declined the percentages of biantennary sugar chains and sugar chains which did not contain bisecting GlcNAC (B Gn) and core fucose (C Fuc), and increased the percentages of sugar chains which contained B Gn or C Fuc or B Gn and C Fuc. Conclusion: It is suggested that VAD can affect the expression/activity of hematopoietic growth factors, IL 3 and GM CSF, and therefore lead to abnormality of N sugar chains of EPC surface and proliferation of EPC.