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缺乏集落刺激因子-1的骨石化(op/op)小鼠子宫、胎盘和胚胎中肿瘤坏死因子-α信使核糖核酸和蛋白质的正态分布

Normal distribution of tumor necrosis factor-alpha messenger ribonucleic acid and protein in the uteri, placentas, and embryos of osteopetrotic (op/op) mice lacking colony-stimulating factor-1.

作者信息

Hunt J S, Chen H L, Hu X L, Pollard J W

机构信息

Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City 66160-7400.

出版信息

Biol Reprod. 1993 Sep;49(3):441-52. doi: 10.1095/biolreprod49.3.441.

Abstract

In order to map mouse tumor necrosis factor-alpha (TNF) gene expression in detail and to determine whether transcription or translation of the TNF gene is regulated by uterine colony stimulating factor-1 (CSF-1), preimplantation embryos, oviducts, uteri, and uteroplacental units were studied in various strains of mice. These included homozygous osteopetrotic (op/op) female mice, which completely lack CSF-1, and heterozygous (+/op) females, which have normal levels of CSF-1. TNF mRNA was identified in all samples except preimplantation embryos by use of Northern blot hybridization or reverse transcriptase polymerase chain reaction. In situ hybridization and immunocytochemical experiments showed that the TNF gene was expressed in mouse oviduct and uterine epithelial cells, decidual cells, macrophage-like cells, placental trophoblast, and embryos. Despite an absence of CSF-1, TNF gene expression in the uteri, placentas, and embryos of op/op mothers did not differ in any major respect from expression in +/op or other strains of mice. The results of this study therefore indicate that the TNF gene is transcribed and translated in an ordered sequence through mouse gestation, and that maternal CSF-1 is not essential to expression of this cytokine gene. Collectively, these findings are consistent with a major role for TNF in mouse reproduction and development and with a potential compensatory function for this potent polypeptide factor in CSF-1 deficiency.

摘要

为了详细绘制小鼠肿瘤坏死因子-α(TNF)基因的表达图谱,并确定TNF基因的转录或翻译是否受子宫集落刺激因子-1(CSF-1)调控,我们在多种品系的小鼠中研究了植入前胚胎、输卵管、子宫和子宫胎盘单位。这些小鼠包括完全缺乏CSF-1的纯合性骨硬化症(op/op)雌性小鼠,以及CSF-1水平正常的杂合子(+/op)雌性小鼠。通过Northern印迹杂交或逆转录聚合酶链反应,在除植入前胚胎外的所有样本中均鉴定出了TNF mRNA。原位杂交和免疫细胞化学实验表明,TNF基因在小鼠输卵管和子宫上皮细胞、蜕膜细胞、巨噬细胞样细胞、胎盘滋养层细胞和胚胎中表达。尽管缺乏CSF-1,但op/op母鼠的子宫、胎盘和胚胎中的TNF基因表达与+/op或其他品系小鼠的表达在任何主要方面均无差异。因此,本研究结果表明,TNF基因在小鼠妊娠期按有序序列进行转录和翻译,并且母体CSF-1对于该细胞因子基因的表达并非必不可少。总体而言,这些发现与TNF在小鼠生殖和发育中的主要作用以及该强效多肽因子在CSF-1缺乏时的潜在补偿功能一致。

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