Simple Summary
This study provides a basis concerning the distribution of heat shock proteins (HSPs) inside the pregnant canine uterus. In dogs, the establishment of pregnancy requires a balance between proliferative mechanisms, initiated by the embryo, and apoptosis inside maternal tissue, both enabling invasive growth. HSP60 and -70 contribute to the regulation of invasive cell growth and were detected in canine uterine and embryo tissue and in serum. As a next step, the distribution of these cellular stress proteins, together with further indicators of proliferation and apoptosis (Ki67 and caspase 3), was examined inside the pregnant uterus and ovaries during the pre- and postimplantation stages and compared with that in tissue from non-pregnant dogs. Importantly, HSP70 expression in superficial cells was significantly decreased in comparison with that in non-pregnant animals. In pregnant animals, while the number of HSP60-positive cells stayed equal, the number of cells positive for HSP70 further decreased during the postimplantation stage in almost all cell types; this might mirror the previous need for regulatory anti-apoptotic mechanisms during implantation, no longer needed after decidualization.
Abstract
Heat shock proteins (HSPs) fulfil protective tasks in the whole organism; in pregnant dogs, they are expressed in the ovary, placenta and preimplantation embryo. Our objective was to compare the expression of HSP60 and -70, along with indicators of proliferation and apoptosis, in the non-pregnant and pregnant uterus/placenta and ovaries. Tissues were obtained after ovariohysterectomy and examined by means of immunohistochemistry. There were differences between pregnant and non-pregnant tissues: the expression level of HSP70 during preimplantation in superficial cells was significantly lower than that in early diestrus, with similar results observed for Ki67. The immunosignal for HSP70 was significantly decreased during the postimplantation stage in almost all cell types, whilst the number of HSP60-positive cells did not change. In pregnant animals, the number of Ki67-positive cells significantly increased until the postimplantation stage. In the placenta and trophoblast, the expression of HSP60 and -70 was strong, while no HSP70 signal was detected in endometrial epithelial cells. The caspase 3 immunosignal in the uterus and placenta was generally weak. In the corpora lutea, HSP60, HSP70 and caspase 3 were mainly detected in theca lutein cells, while no signal for KI67 was seen. In follicles, caspase 3 and KI67 expression was low, except in granulosa cells of tertiary follicles and oocytes. We conclude that the different expression of HSPs in pregnant and non-pregnant animals may point towards different regulatory and/or protective tasks.