Brockbank K G, Piersma A H, Ploemacher R E, Voerman J S
Acta Haematol. 1985;74(2):75-80. doi: 10.1159/000206860.
Mice of the Sl/Sld genotype have an approximately 3-fold higher number of fibroblastoid progenitors (CFU-F) in their spleens than their normal +/+ littermates. Experiments were performed to determine whether the elevated Sl/Sld splenic CFU-F numbers were due to compensatory mechanisms acting in the presence of a functionally abnormal CFU-F population or to a nonspecific response to chronic anemia. Comparison of the functional ability of Sl/Sld splenic fibroblasts to produce granulocyte/macrophage colony-stimulating activity with +/+ splenic fibroblasts demonstrated that there was no difference. Similar results were obtained for Sl/Sld and +/+ femoral fibroblasts. Analysis of CFU-F in W/Wv mice revealed an approximately 3-fold higher number of splenic CFU-F than in either +/+ or heterozygous (W/+ and Wv/+) littermates. Since the anemia in W/Wv mice is attributed to a hemopoietic stem cell defect and that of the Sl/Sld mice is attributed to a microenvironmental defect, we suggest that the increased splenic CFU-F number in Sl/Sld mice is not specifically due to the microenvironmental defect, but is part of a general response to hemopoietic stress.
Sl/Sld基因型小鼠脾脏中的成纤维细胞样祖细胞（CFU-F）数量比其正常的+/+同窝小鼠大约高3倍。进行实验以确定Sl/Sld脾脏中CFU-F数量的增加是由于在功能异常的CFU-F群体存在时起作用的补偿机制，还是对慢性贫血的非特异性反应。将Sl/Sld脾脏成纤维细胞产生粒细胞/巨噬细胞集落刺激活性的功能能力与+/+脾脏成纤维细胞进行比较，结果表明没有差异。Sl/Sld和+/+股骨成纤维细胞也得到了类似的结果。对W/Wv小鼠的CFU-F分析显示，其脾脏CFU-F数量比+/+或杂合子（W/+和Wv/+）同窝小鼠大约高3倍。由于W/Wv小鼠的贫血归因于造血干细胞缺陷，而Sl/Sld小鼠的贫血归因于微环境缺陷，我们认为Sl/Sld小鼠脾脏中CFU-F数量的增加并非特别由于微环境缺陷，而是造血应激的一般反应的一部分。
