Ultrastructural changes of bone marrow in canine cyclic hematopoiesis (CH dog). A sequential study.
Ultrastructural changes of bone marrow in canine cyclic hematopoiesis (CH dog). A sequential study.
复制标题
犬循环造血（CH狗）中骨髓超微结构的变化。
DOI：
10.1007/bf00443900
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Lange,RD
中科院分区：
文献类型：
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作者：
Machado,EA;Jones,JB;Aggio,MC;Chernoff,AI;Maxwell,PA;Lange,RD
灰色牧羊犬循环性造血（CH）的发病机制尚不清楚。已经提出，骨髓嗜中性粒细胞的周期性坏死的爆发将诱导干细胞分化的周期性停滞。本研究用电镜观察了CH犬骨髓红系和中性粒细胞系的动态变化。红系细胞呈定量周期振荡，但未成熟和成熟细胞的形态特征均正常。相反，在髓系中观察到非特异性坏死变化。这些异常在周期的第9天和第11天之间更为明显，主要涉及未成熟细胞，并且在较小程度上涉及成熟中性粒细胞。坏死细胞的数量在不同的周期中是可变的，但总是代表一小部分髓样细胞。此外，少数骨髓巨噬细胞显示出含有细胞碎片的吞噬活性迹象。髓系的超微结构变化伴随着过氧化物酶活性的异常降低和永久性的大型酸性磷酸酶阳性高尔基复合体在成熟的中性粒细胞，定义的形态学标准。在许多细胞中存在Döhle样的粗面内质网阵列。我们的研究结果表明，髓细胞的过度慢性发育是由于与骨髓先天性缺陷相关的调节异常而发生的，这种异常干扰了干细胞的分化和成熟。某些髓样细胞的坏死是一种继发现象，而不是先前提出的细胞成熟周期性停滞的原因。此外，坏死细胞群的小尺寸不能证明产生足够量的“抑制剂”以阻断骨髓干细胞池的正常进化是合理的。
The pathogenesis of cyclic hematopoiesis (CH) in the grey collie dog is still unknown. It has been proposed that periodic bursts of necrosis of the bone marrow neutrophils would induce cyclic arrests of the stem cell differentiation. In the present study, the sequential changes undergone by the erythroid and neutrophil series of the bone marrow of CH dogs were evaluated by electron microscopy. Erythroid cells presented quantitative periodic oscillations but the morphologic features of both immature and mature cells were normal. On the contrary, nonspecific necrotic changes were observed to occur in the myeloid series. Those abnormalities, which were more marked between days 9 and 11 of the cycle, mainly involved the immature cells and, to a lesser extent, the mature neutrophils. The number of necrotic cells was variable in different cycles, but always represented a small portion of the myeloid cells. In addition, few bone marrow macrophages displayed signs of phagocytic activity containing cell debris. The ultrastructural changes of the myeloid series were accompanied by an abnormal decrease of peroxidase activity and the permanence of large acid phosphatase-positive Golgi complexes in mature neutrophils, as defined by morphologic criteria. Döhle-like arrays of rough endoplasmic reticulum were present in many cells. Our findings suggest that an asynchronic development of myelocytes occurs as a result of regulatory abnormalities related to the congenital defect of the bone marrow which interferes with the differentiation and maturation of the stem cells. Necrosis in some myeloid cells would be a secondary phenomenon rather than a causal factor for the cyclic arrest of cell maturation as has been previously submitted. Furthermore, the small size of the necrotic cell population could not justify the production of “inhibitors” in sufficient amounts as to block the normal evolution of the bone marrow stem cell pool.