A pregnancy defect in the osteopetrotic (op/op) mouse demonstrates the requirement for CSF-1 in female fertility.

A pregnancy defect in the osteopetrotic (op/op) mouse demonstrates the requirement for CSF-1 in female fertility.
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DOI:
10.1016/0012-1606(91)90336-2
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发表时间:
1991-11
影响因子:
2.7
通讯作者:
J. Pollard;J. Hunt;W. Wiktor-Jedrzejczak;E. Stanley
J. Pollard;J. Hunt;W. Wiktor-Jedrzejczak;E. Stanley
中科院分区:
生物学3区
文献类型:
--
作者:
J. Pollard;J. Hunt;W. Wiktor-Jedrzejczak;E. Stanley

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相似文献

相关证据表明,母体产生的单核吞噬细胞生长因子集落刺激因子-1 (CSF-1) 可调节胎盘发育。为了研究CSF-1在妊娠中的作用,对无CSF-1的骨硬化(op op)突变小鼠的生育能力进行了研究。纯合突变体杂交(op op×op op)始终不育。正如预期的那样,op op 雄性在与杂合雌性杂交时几乎完全具有生育能力。令人惊讶的是,op op 雌性与杂合子雄性交配时具有生育能力,尽管其生育率是 + op 雌性 × op op 雄性的 46%。这些数据表明 CSF-1 是妊娠所必需的。然而,母体 CSF-1 来源并不是绝对必要的,因为涉及 + op 父亲的妊娠得到了部分挽救,这表明 + op 胎儿和/或 + op 精液提供了 CSF-1 或 CSF-1 诱导因子,可补偿母体产生的 CSF-1 的缺失。尽管op op小鼠的子宫和胎盘中完全缺乏CSF-1,但胎盘重量正常,这表明蜕膜细胞和滋养层细胞(两者均表达CSF-1受体)的增殖可能不仅仅由CSF-1调节。 F4 80 抗原的组织化学染色用于鉴定子宫和胎盘中的巨噬细胞。尽管在子宫内大量存在子宫巨噬细胞,但在处女 op op 小鼠中无法检测到子宫巨噬细胞。有趣的是,在妊娠早期,可以在 op op uteri 中检测到巨噬细胞,作为异常圆形的细胞,然而,在 op op 小鼠中,它们没有得到维持,并且在妊娠第 14 天之后没有明显的巨噬细胞。对骨石小鼠的进一步研究将有助于描述受 CSF-1 调节的妊娠所需功能。
Correlative evidence suggests that maternal production of the mononuclear phagocyte growth factor colony stimulating factor-1 (CSF-1) regulates placental development. In order to study the role of CSF-1 in pregnancy the fertility of CSF-1-less osteopetrotic (op op) mutant mice was investigated. Homozygous mutant crosses (op op× op op) were consistently infertile. As expected, op op males were almost completely fertile when crossed with heterozygous females. Surprisingly, op op females when mated to heterozygote males were fertile, although at a rate that was 46% of the rate for+ op females× op op males. These data suggest that CSF-1 is required for pregnancy. However, a maternal CSF-1 source is not absolutely necessary in that pregnancies involving+ op fathers were partially rescued, suggesting that+ op fetuses and/or+ op seminal fluid provides CSF-1 or CSF-1-induced factors which compensate for the absence of maternally produced CSF-1. Despite the complete absence of CSF-1 in the uterus and placenta of op op mice placental weights were normal, suggesting that proliferation of decidual cells and trophoblasts, both of which express the CSF-1 receptor, may not be solely regulated by CSF-1. Histochemical staining for F4 80 antigen was used to identify macrophages in the uterus and placenta. Uterine macrophages could not be detected in virgin op op mice although they were abundant in+ op uteri. Interestingly, macrophages could be detected in op op uteri as uncharacteristically rounded cells in early gestation, however, they were not maintained and no macrophages were apparent beyond Day 14 of pregnancy in op op mice. Further studies in the osteopetrotic mouse will be useful in delineating those functions required for pregnancy that are regulated by CSF-1.