Nurses should recognize that CINV occurs at all points of chemotherapy treatment. Nurses can assist children in developing active coping strategies to manage their CINV.

At the time of implantation, uterine luminal epithelial cells undergo a dramatic change in all plasma membrane domains. Changes in the basolateral plasma membrane at the time of implantation include progression from smooth to highly tortuous, as well as a loss of integrin-based focal adhesions. Another aspect of the basolateral plasma membrane that has not been studied in uterine epithelial cells are caveolae, which are omega-shaped invaginations of the plasma membrane known to be involved in endocytosis and contribute to membrane curvature. The current study investigated caveolin, a major protein of caveolae, to explore the possible roles that they play in the remodelling of the basolateral plasma membrane of uterine epithelial cells during early pregnancy in the rat. Morphological caveolae were found at the time of implantation and were significantly increased compared to day 1 of pregnancy. Caveolins 1 and 2 were found to shift to the basolateral plasma membrane of uterine epithelial cells at the time of implantation as well as when treated with progesterone alone, and in combination with oestrogen. A statistically significant increase in the amount of caveolin-1 and a decrease in caveolin-2 protein in uterine epithelial cells was observed at the time of implantation. Caveolin-1 also co-immunoprecipitated with integrin β1 on day 1 of pregnancy, which is a protein that has been reported to be found in integrin-based focal adhesions at the basolateral membrane on day 1 of pregnancy. The localisation and expression of caveolin-1 at the time of implantation is consistent with the presence and increase of morphological caveolae seen at this time. The localisation and expression of caveolins 1 and 2 in luminal uterine epithelium at the time of implantation suggest a role in trafficking proteins and the maintenance of a polarised epithelium.

In preparation for uterine receptivity, the uterine epithelial cells (UECs) exhibit a loss of microvilli and glycocalyx and a restructuring of the actin cytoskeleton. The prominin-1 protein contains large, heavily glycosylated extracellular loops and is usually restricted to apical plasma membrane (APM) protrusions. The present study examined rat UECs during early pregnancy using immunofluorescence, western blotting and deglycosylation analyses. Ovariectomised rats were injected with oestrogen and progesterone to examine how these hormones affect prominin-1. At the time of fertilisation, prominin-1 was located diffusely in the apical domain of UECs and 147- and 120-kDa glycoforms of prominin-1 were identified, along with the 97-kDa core protein. At the time of implantation, prominin-1 concentrates towards the APM and densitometry revealed that the 120-kDa glycoform decreased (P<0.05), but there was an increase in the 97-kDa core protein (P<0.05). Progesterone treatment of ovariectomised rats resulted in prominin-1 becoming concentrated towards the APM. The 120-kDa glycoform was increased after oestrogen treatment (P<0.0001), whereas the 97-kDa core protein was increased after progesterone treatment (P<0.05). Endoglycosidase H analysis demonstrated that the 120-kDa glycoform is in the endoplasmic reticulum, undergoing protein synthesis. These results indicate that oestrogen stimulates prominin-1 production, whereas progesterone stimulates the deglycosylation and concentration of prominin-1 to the apical region of the UECs. This likely presents the deglycosylated extracellular loops of prominin-1 to the extracellular space, where they may interact with the implanting blastocyst.

The non-receptive uterine luminal epithelium forms an intact polarised epithelial barrier that is refractory to blastocyst invasion. During implantation, organised dismantling of this barrier leads to a receptive state promoting blastocyst attachment. Claudins are tight junction proteins that increase in the uterine epithelium at the time of implantation. Claudin 7 is a member of this family but demonstrates a basolateral localisation pattern that is distinct from other claudins. The present study investigated the localisation, abundance and hormonal regulation of claudin 7 to elucidate a role for the protein during implantation. The results showed that claudin 7 demonstrates a distinct basal and lateral localisation in the uterine luminal and glandular epithelium throughout early pregnancy. On day 1, claudin 7 is abundantly present in response to ovarian estrogen. At the time of implantation, claudin 7 decreases in abundance. This decrease is not dependent on blastocyst presence, as shown by results in pseudopregnant animals. We propose that claudin 7 mediates intercellular adhesions in the uterine epithelium and also may be responsible for stabilising adhesion proteins at the basolateral cell surface. Thus, claudin 7 may function under the maintenance of the uterine luminal epithelial barrier, in the non-receptive state preventing implantation from occurring.

The glycocalyx of the uterine luminal epithelium in the rat undergoes considerable reduction before implantation. In particular, the reduction of some mucins is necessary to facilitate blastocyst adhesion and subsequent implantation. The present study investigated the localisation, abundance and hormonal control of two mucin proteins, Muc13 and Muc15, in rat uterine epithelial cells during early pregnancy to determine whether they are likely to play a role in uterine receptivity for implantation. Muc13 and Muc15 are localised to the uterine luminal epithelium but show a presence and an absence, respectively, at the apical cell surface at the time of implantation. This localisation corresponds to changes in the molecular weights of Muc13 and Muc15, as shown with western blotting analysis. Furthermore, the localisation of Muc13 and Muc15 was shown to be controlled by the ovarian hormones, oestrogen and progesterone, and they were also localised in preimplantation rat blastocysts. Our results suggest that Muc15 may operate in an anti-adhesive capacity to prevent implantation while Muc13 potentially functions in either an adhesive or cell-signalling role in the events of implantation.