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移植物抗宿主病诱导的浦肯野细胞树突畸形

Malformation of Purkinje cell dendrites induced by graft-versus-host disease.

作者信息

Griffin W S, Eriksson M A, Crom E N, Head J R

出版信息

Brain Res Bull. 1980 Nov-Dec;5(6):673-8. doi: 10.1016/0361-9230(80)90204-x.

DOI:10.1016/0361-9230(80)90204-x
PMID:7470938
Abstract

Impairment of cerebral Purkinje cell growth was assessed in Golgi-Cox stained tissue in 14 day old (Fischer X DA)F1 hybrid rats subjected to graft versus host disease (GVHD). GVHD was induced by grafting parental strain lymph node cells (PSLNC) into the anterior facial vein on the day of birth. We have previously described GVHD induced changes in nucleotide and protein content [12] and RNA function [14] as well as alterations in cell numbers and areas of the external granular and molecular layers in diseased animals [13]. In this report some effects of GVHD on the gross morphology of Purkinje cells in 14 day old animals are enumerated. Most Purkinje cells (62%) from GVHD animals had a height to width ratio greater than 1, whereas most from control animals (71%) had ratios of less than 1. The majority of Purkinje cells (67%) from diseased animals had elongated main dendrites which were devoid of branches and often (13%) these elongated main dendrites were S-shaped. In addition, comparison of Purkinje cells from GVHD and control animals revealed a greater tendency (15%) toward retention of extrasomal process in GVHD animals. These findings suggest that GVHD affects nondividing, differentiating cell populations as well as those which are proliferating and migrating. Our evidence that, as a result of GVHD, the protein synthesizing capacity of the cerebellum is altered [14] and that Purkinje cells are more closely spaced at day 11 suggests that both intrinsic and extrinsic factors are involved in producing the changes in dendritic shape reported here.

摘要

在患有移植物抗宿主病(GVHD)的14日龄(Fischer×DA)F1杂交大鼠中,通过高尔基-考克斯染色组织评估大脑浦肯野细胞的生长受损情况。GVHD是通过在出生当天将亲代品系淋巴结细胞(PSLNC)移植到面静脉前部诱导产生的。我们之前已经描述了GVHD诱导的核苷酸和蛋白质含量变化[12]、RNA功能变化[14],以及患病动物中外颗粒层和分子层细胞数量和面积的改变[13]。在本报告中,列举了GVHD对14日龄动物浦肯野细胞大体形态的一些影响。来自GVHD动物的大多数浦肯野细胞(62%)的高宽比大于1,而来自对照动物的大多数浦肯野细胞(71%)的高宽比小于1。患病动物的大多数浦肯野细胞(67%)具有细长的主树突,且无分支,这些细长的主树突常常呈S形(13%)。此外,比较GVHD动物和对照动物的浦肯野细胞发现,GVHD动物中额外细胞突起保留的趋势更大(15%)。这些发现表明,GVHD会影响非分裂、分化的细胞群体以及增殖和迁移的细胞群体。我们有证据表明,由于GVHD,小脑的蛋白质合成能力发生了改变[14],并且在第11天时浦肯野细胞的间距更近,这表明内在和外在因素都参与了此处报道的树突形状变化的产生。

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Malformation of Purkinje cell dendrites induced by graft-versus-host disease.移植物抗宿主病诱导的浦肯野细胞树突畸形
Brain Res Bull. 1980 Nov-Dec;5(6):673-8. doi: 10.1016/0361-9230(80)90204-x.
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