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Wistar Furth大鼠的巨核细胞缺乏致密区室和细胞间斑块,后者是富含细胞骨架蛋白的膜性结构。

Wistar Furth rat megakaryocytes lack dense compartments and intercellular plaques, membranous structures rich in cytoskeletal proteins.

作者信息

Stenberg P E, Beckstead J H, Jackson C W

机构信息

Department of Pathology, Oregon Health Sciences University, Portland, USA.

出版信息

Cell Adhes Commun. 1998 Jul;5(5):397-407. doi: 10.3109/15419069809010784.

DOI:10.3109/15419069809010784
PMID:9789686
Abstract

Wistar Furth (WF) rats have an abnormal thrombopoietic phenotype with morphologically aberrant megakaryocytes, larger than normal mean platelet volume, and platelet alpha-granule protein deficiency. Here, ultrastructural comparisons of WF rat megakaryocytes to those of rats (Wistar) with normal platelet formation during stimulated megakaryocytopoiesis following 5-fluorouracil administration, have revealed a previously unrecognized membrane structure in normal rat megakaryocytes, and two additional abnormalities in WF megakaryocytes. The novel structures were zones of electron density on the cytoplasmic face of apposed plasma membranes of adjoining normal megakaryocytes. These modified focal adhesion-type contacts were distributed at intervals between adjacent megakaryocytes, and were spaced by deposits of extracellular material. These structures also were present between apposed plasma membranes of Wistar rat megakaryocytes in unperturbed marrows, but were absent between megakaryocytes of WF rats. The second WF rat megakaryocyte abnormality is the absence of cytoplasmic dense compartments, another specialized membranous structure that is continuous with the megakaryocyte demarcation membrane system. Both the intercellular plaques and dense compartments of Wistar rat megakaryocytes were found to be rich in cytoskeletal proteins including actin, alpha-actinin, talin, and vinculin as indicated by ultrastructural immunogold labeling. We hypothesize that an abnormality in cytoskeletal protein function may be responsible for the lack of these structures in the WF rat.

摘要

Wistar Furth(WF)大鼠具有异常的血小板生成表型,其巨核细胞形态异常,平均血小板体积大于正常,且血小板α颗粒蛋白缺乏。在此,对WF大鼠巨核细胞与5-氟尿嘧啶给药后刺激巨核细胞生成过程中血小板形成正常的大鼠(Wistar)巨核细胞进行超微结构比较,发现正常大鼠巨核细胞中有一种先前未被识别的膜结构,以及WF巨核细胞中的另外两种异常情况。这种新结构是相邻正常巨核细胞并列质膜胞质面的电子密度区。这些修饰的粘着斑样接触点间隔分布于相邻巨核细胞之间,并由细胞外物质沉积物隔开。这些结构在未受干扰的骨髓中Wistar大鼠巨核细胞的并列质膜之间也存在,但在WF大鼠的巨核细胞之间不存在。WF大鼠巨核细胞的第二个异常是缺乏细胞质致密区室,这是另一种与巨核细胞分界膜系统连续的特殊膜结构。超微结构免疫金标记显示,Wistar大鼠巨核细胞的细胞间斑块和致密区室富含包括肌动蛋白、α辅肌动蛋白、踝蛋白和纽蛋白在内的细胞骨架蛋白。我们推测细胞骨架蛋白功能异常可能是WF大鼠缺乏这些结构的原因。

相似文献

1
Wistar Furth rat megakaryocytes lack dense compartments and intercellular plaques, membranous structures rich in cytoskeletal proteins.Wistar Furth大鼠的巨核细胞缺乏致密区室和细胞间斑块,后者是富含细胞骨架蛋白的膜性结构。
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Disruption of microtubules in vivo by vincristine induces large membrane complexes and other cytoplasmic abnormalities in megakaryocytes and platelets of normal rats like those in human and Wistar Furth rat hereditary macrothrombocytopenias.长春新碱在体内破坏微管会在正常大鼠的巨核细胞和血小板中诱导出大的膜复合物和其他细胞质异常,类似于人类和威斯塔·富思大鼠遗传性大血小板减少症中的情况。
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Abnormal subcellular distribution of myosin and talin in Wistar Furth rat platelets.Wistar Furth大鼠血小板中肌球蛋白和踝蛋白的亚细胞分布异常。
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Platelets of the Wistar Furth rat have reduced levels of alpha-granule proteins. An animal model resembling gray platelet syndrome.Wistar Furth大鼠的血小板α-颗粒蛋白水平降低。一种类似灰色血小板综合征的动物模型。
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The Wistar Furth rat: an animal model of hereditary macrothrombocytopenia.威斯塔·弗思大鼠:一种遗传性巨血小板减少症的动物模型。
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Prolonged bleeding time with defective platelet filopodia formation in the Wistar Furth rat.Wistar Furth大鼠出现出血时间延长且血小板丝状伪足形成存在缺陷。
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Decreased serglycin proteoglycan size is associated with the platelet alpha granule storage defect in Wistar Furth hereditary macrothrombocytopenic rats. Serglycin binding affinity to type I collagen is unaltered.在Wistar Furth遗传性大血小板减少症大鼠中,丝甘素蛋白聚糖大小的降低与血小板α颗粒储存缺陷相关。丝甘素与I型胶原的结合亲和力未改变。
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Lipid and membrane fluidity abnormalities in platelets and megakaryocytes of the hereditary macrothrombocytopenic Wistar Furth rat.遗传性巨血小板减少性Wistar Furth大鼠血小板和巨核细胞中的脂质及膜流动性异常
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