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MPSV诱导的骨髓增殖性疾病中的异常脾巨核细胞生成。

Abnormal splenic megakaryopoiesis in MPSV-induced myeloproliferative disease.

作者信息

Le Bousse-Kerdiles M C, Fernandez-Delgado R, Smadja-Joffe F, Massier E, Degiorgis V, Bertoli A M, Paulus J M, Prenant M, Jasmin C

机构信息

INSERM U 268, Hôpital Paul Brousse, Villejuif, France.

出版信息

Leuk Res. 1987;11(9):781-7. doi: 10.1016/0145-2126(87)90062-2.

Abstract

The myeloproliferative sarcoma virus (MPSV) induces a murine myeloproliferative syndrome characterized by an erythromyelemia, an anemia, a thrombocytopenia associated with a myeloproliferation in the spleen and a splenic and medullar fibrosis. We have used the in-vitro plasma clot technique to measure megakaryocytic precursors in the spleen and bone-marrow of MPSV-infected mice. We report that megakaryocytic colonies are increased, in number (X75), in concentration (X9) and in size, in the spleen but not in the bone-marrow of neoplastic mice. Furthermore, these splenic precursors are hypersensitive to growth factors present in the anemic mouse serum used in the culture system. These data show that the thrombocytopenia observed in the MPSV-induced neoplasia does not result from a lack of megakaryocyte precursors, but rather from an excess of megakaryocyte destruction. This ineffective splenic megakaryopoiesis associated with the presence of a massive splenic fibrosis make the MPS-induced neoplasia a suitable model for studying the perturbation of megakaryopoiesis in myeloproliferative syndrome associated with fibrosis.

摘要

骨髓增殖性肉瘤病毒(MPSV)可诱发一种小鼠骨髓增殖综合征,其特征为红白血病、贫血、血小板减少,并伴有脾脏骨髓增殖以及脾脏和骨髓纤维化。我们运用体外血浆凝块技术来检测MPSV感染小鼠脾脏和骨髓中的巨核细胞前体。我们报告称,在肿瘤小鼠的脾脏中,巨核细胞集落的数量(增加75倍)、浓度(增加9倍)和大小均有所增加,而在骨髓中则没有。此外,这些脾脏前体对培养系统中使用的贫血小鼠血清中的生长因子高度敏感。这些数据表明,在MPSV诱发的肿瘤中观察到的血小板减少并非源于巨核细胞前体的缺乏,而是由于巨核细胞过度破坏所致。这种与大量脾脏纤维化相关的无效脾脏巨核细胞生成,使得MPS诱导的肿瘤成为研究与纤维化相关的骨髓增殖综合征中巨核细胞生成紊乱的合适模型。

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