Abstract
C1q is the first recognition subcomponent of the complement classical pathway, which in addition to being synthesized in the liver, is also expressed by macrophages and dendritic cells (DCs). Trophoblast invasion during early placentation results in accumulation of debris that triggers the complement system. Hence, both early and late components of the classical pathway are widely distributed in the placenta and decidua. In addition, C1q has recently been shown to significantly contribute to feto-maternal tolerance, trophoblast migration, and spiral artery remodeling, although the exact mechanism remains unknown. Pregnancy in mice, genetically deficient in C1q, mirrors symptoms similar to that of human preeclampsia. Thus, regulated complement activation has been proposed as an essential requirement for normal successful pregnancy. Little is known about the molecular pathways that regulate C1q expression in pregnancy. PU.1, an Ets-family transcription factor, is required for the development of hematopoietic myeloid lineage immune cells, and its expression is tissue-specific. Recently, PU.1 has been shown to regulate C1q gene expression in DCs and macrophages. Here, we have examined if PU.1 transcription factor regulates decidual C1q expression. We used immune-histochemical analysis, PCR, and immunostaining to localize and study the gene expression of PU.1 transcription factor in early human decidua. PU.1 was highly expressed at gene and protein level in early human decidual cells including trophoblast and stromal cells. Surprisingly, nuclear as well as cytoplasmic PU.1 expression was observed. Decidual cells with predominantly nuclear PU.1 expression had higher C1q expression. It is likely that nuclear and cytoplasmic PU.1 localization has a role to play in early pregnancy via regulating C1q expression in the decidua during implantation.
Highlights
Decidua plays a critical role in accepting the semi-allogenic fetus and protecting it from the mother’s immune system during pregnancy [1]
We investigated the presence of PU.1 in paraffin-embedded decidual sections obtained from women who underwent elective termination of pregnancy
PU.1 expression was consistent between decidual samples, but varied field to field
Summary
Decidua plays a critical role in accepting the semi-allogenic fetus and protecting it from the mother’s immune system during pregnancy [1]. Immunological cross-talk between the mother (stromal cells) and the fetus (trophoblasts) takes place in the decidua [2]. Several immune and non-immune cells such as macrophages, dendritic cells (DCs), natural killer (NK) cells, T cells, stromal cells, and trophoblasts are involved in the maintenance of early pregnancy at the feto-maternal interface [3]. The process of lineage is tightly regulated by the transcription factors [8, 9]. PU., an Ets-family transcription factor, was originally shown to be transcriptionally up-regulated in murine erythroleukemia following proviral integration of “spleen focus forming virus” (SFFV) (known as SP11) in humans [10, 11]. PU. transcription factor has been shown to regulate C1q gene expression in macrophages and DCs [19]. The strong association between PU. and C1q expression raised the possibility that PU. may be responsible for C1q expression in the decidua during pregnancy
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
