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原发性(特发性)骨髓纤维化中的脾造血:红系增殖活性及巨核细胞内复制能力(增殖细胞核抗原和Ki-67染色)的免疫组织化学和形态计量学评估

Splenic haematopoiesis in primary (idiopathic) osteomyelofibrosis: immunohistochemical and morphometric evaluation of proliferative activity of erytro- and endoreduplicative capacity of megakaryopoiesis (PCNA- and Ki-67 staining).

作者信息

Thiele J, Bennewitz F G, Bertsch H P, Falk S, Fischer R, Stutte H J

机构信息

Institute of Pathology, University of Cologne, Germany.

出版信息

Virchows Arch B Cell Pathol Incl Mol Pathol. 1993;64(5):281-6. doi: 10.1007/BF02915123.

Abstract

Using monoclonal antibodies against proliferating cell nuclear antigen or PCNA (PC10) and the Ki-67 antigen (MIB1), an immunohistochemical and morphometric study was performed on routinely processed splenic tissue from ten patients with primary (idiopathic) osteomyelofibrosis (OMF). To determine the proliferation capacity of erythroid precursors and the endoreduplicative activity of megakaryocytes, corresponding antibodies (Ret40f and CD61) were applied in combination with the cell-cycle markers (sequential double-immunostaining). Morphometric analysis revealed no significant differences in PCNA or Ki-67 reactivity in either cell lineages. In comparison with previous studies on normal bone marrow, in splenic tissue showing myeloid metaplasia, the numbers of PCNA-labelled proerythroblasts, erythroblasts and megakaryocytes were conspicuously increased. Considering the ineffective erythropoiesis in OMF, there seemed to be a disproportional enhancement in PCNA and Ki-67 immunostaining of the red cell lineage. Similarly, the small size of megakaryocytes in advanced, OMF-associated myeloid metaplasia was in keeping with an impairment of endoreduplicative activity. In addition to various other contributory factors, anaemia in OMF may be partially caused by secondary folate (haematinic) deficiency. From experimental studies this defect is known to cause an abnormal arrest in the S-phase of the cell-cycle, comparable to that characterising pernicious anaemia. As a sequel of this pathomechanism, an undue overexpression of PCNA and Ki-67 has to be assumed, that is not necessarily associated with DNA synthesis or cell cycling.

摘要

使用抗增殖细胞核抗原(PCNA)(PC10)和Ki-67抗原(MIB1)的单克隆抗体,对10例原发性(特发性)骨髓纤维化(OMF)患者经常规处理的脾脏组织进行了免疫组织化学和形态计量学研究。为了确定红系前体细胞的增殖能力和巨核细胞的核内复制活性,将相应抗体(Ret40f和CD61)与细胞周期标记物联合应用(连续双重免疫染色)。形态计量学分析显示,两种细胞谱系中PCNA或Ki-67反应性均无显著差异。与先前对正常骨髓的研究相比,在显示髓外化生的脾脏组织中,PCNA标记的早幼红细胞、红细胞和巨核细胞数量明显增加。考虑到OMF中无效的红细胞生成,红细胞谱系的PCNA和Ki-67免疫染色似乎有不成比例的增强。同样,晚期OMF相关髓外化生中巨核细胞体积小与核内复制活性受损一致。除了各种其他促成因素外,OMF中的贫血可能部分由继发性叶酸(造血素)缺乏引起。从实验研究可知,这种缺陷会导致细胞周期S期异常停滞,类似于恶性贫血的特征。作为这种病理机制的结果,必须假定PCNA和Ki-67存在过度表达,这不一定与DNA合成或细胞周期有关。

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