Detection of Math6-Expressing Cell Types in Murine Placenta

生物 胎盘 滋养层 电池类型 细胞生物学 转录因子 免疫组织化学 表位 转基因小鼠 单元格排序 转基因 胎儿 胚胎干细胞 抗体 细胞 免疫学 分子生物学 基因 遗传学 怀孕
作者
Maren Brendel,Marion Scharf,Urs Kindler,Satya Srirama Karthik Divvela,Beate Brand‐Saberi
出处
期刊:Biology [Multidisciplinary Digital Publishing Institute]
卷期号:12 (9): 1252-1252
标识
DOI:10.3390/biology12091252
摘要

The transcription factor Math6, mouse atonal homolog 6, belongs to the family of highly conserved basic helix-loop-helix transcription factors. It plays an important role in embryonic development and shows a wide expression pattern in murine tissues. The placenta, as a life-sustaining transient organ for the fetus, also depends on the expression of Math6. The adverse effects of deleting Math6 in mice, leading to deficient placental development and pregnancy loss, have already been demonstrated by us. Until now, detailed investigations regarding the specific mechanisms underlying the improper placental development in these murine mutants have failed, as the Math6 expression could not be confined to a specific cell type due to the lack of a highly specific Math6 antibody. To circumvent this problem, we used transgenic mice, where Math6 is marked with a Flag sequence that functions as a specific epitope. Tissues from these transgenic mice were used to establish immunohistochemical staining and fluorescence-activated cell sorting (FACS). The establishment of these methods yielded initial findings pertaining to the identification of Math6-expressing cell types and their localization. Our results reveal that Math6 shows a wide expression pattern in both maternal and fetal components of the murine placenta. It shows expression in various cell types, but predominantly in trophoblast giant cells, endothelial cells and macrophages. The largest subpopulation that we detected in the group of Math6-positive cells were identified as DBA+ uterine natural killer cells. These findings reveal information and a chance for further investigation on the involvement of Math6 in placental development and the molecular pathomechanisms of spontaneous abortion.

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