Prokineticin 1 induces Dickkopf 1 expression and regulates cell proliferation and decidualization in the human endometrium

Macdonald, Linsay J.; Sales, Kurt J.; Grant, Vivien; Brown, Pamela; Jabbour, Henry N.; Catalano, Rob D.

doi:10.1093/molehr/gar031

Cited by 45 publications

(38 citation statements)

References 51 publications

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“…EG-VEGF and PKRs were reported to exert their biological functions by phosphorylation of their downstream target ERK1/2, through cross talk with the EGFR system (Evans et al 2008), or by activation of the PI3 kinase/Akt pathway (Lin et al 2002) and calcium/cAMP mobilization (Brouillet et al 2012). EG-VEGF also modulates IL8, IL11, and DKK1 expression via the calcineurin/ NFAT signaling pathway (Cook et al 2010, Macdonald et al 2011. Most of the above cytokines and pathways were closely related to endometrial decidualization and embryo implantation (Evans et al 2008, Macdonald et al 2011, Brouillet et al 2012.…”

Section: Discussionmentioning

confidence: 99%

Prokineticin receptor variants (PKR1-I379V and PKR2-V331M) are protective genotypes in human early pregnancy

Su¹,

Lin²,

Chen³

et al. 2013

Reproduction

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Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) and its receptor genes (PROKR1 (PKR1) and PROKR2 (PKR2)) play an important role in human early pregnancy. We have previously shown that PROKR1 and PROKR2 are associated with recurrent miscarriage (RM) using the tag-SNP method. In this study, we aimed to identify PROKR1 and PROKR2 variants in idiopathic RM patients by genotyping of the entire coding regions. Peripheral blood DNA samples of 100 RM women and 100 controls were subjected to sequence the entire exons of PROKR1 and PROKR2. Significant non-synonymous variant genotypes present in the original 200 samples were further confirmed in the extended samples of 144 RM patients and 153 controls. Genetic variants that were over-or underrepresented in the patients were ectopically expressed in HEK293 and JAR cells to investigate their effects on intracellular calcium influx, cell proliferation, cell invasion, cell-cell adhesion, and tube organization. We found that the allele and genotype frequencies of PROKR1 (I379V) and PROKR2 (V331M) were significantly increased in the normal control groups compared with idiopathic RM women (P!0.05). PROKR1 (I379V) and PROKR2 (V331M) decreased intracellular calcium influx but increased cell invasiveness (P!0.05), whereas cell proliferation, cell-cell adhesion, and tube organization were not significantly affected. In conclusion, PROKR1 (I379V) and PROKR2 (V331M) variants conferred lower risk for RM and may play protective roles in early pregnancy by altering calcium signaling and facilitating cell invasiveness.

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Section: Discussionmentioning

confidence: 99%

Prokineticin receptor variants (PKR1-I379V and PKR2-V331M) are protective genotypes in human early pregnancy

Su¹,

Lin²,

Chen³

et al. 2013

Reproduction

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“…β-catenin) was shown to be compensated by Wnt3a addition [83]. Dkk1 decreased the migration of SGHPL-5 cells in the absence of compensating Wnt ligand (Wnt3a) [37]. Wnt3a-induced migration in primary firsttrimester villous explant cultures was also decreased in the presence of either Dkk1 or the PI3K inhibitor [83].…”

Section: Trophoblast Cell Proliferation Migration and Differentiationmentioning

confidence: 96%

“…In a recent study it was determined that, Dkk1 mRNA expression was significantly elevated in the mid-secretory phase of the menstrual cycle in human endometrium [37]. Dkk1 expression was also found to be increased in response to decidualization in vitro [28].…”

Section: Wnt Signaling In Uterine Receptivitymentioning

confidence: 98%

“…Both in vitro studies with cell lines and also with human endometrial primary cells reveal that, secreted protein prokineticin1 (PROK1) increased Dkk1 mRNA expression and this increase was provided via the calcineurinnuclear factor of activated T-cells (NFAT) pathway. Though PROK1-mediated Dkk1 expression via the NFAT pathway had an inhibitory effect on prokineticin receptor 1 (PROKR1) Ishikawa cell proliferation, PROK1 and Dkk1 expressions were shown to influence decidualization in human primary endometrial stromal cells [37].…”

Section: Uterus In Implantation Period: Decidualizationmentioning

confidence: 99%

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The role of Wnt signaling members in the uterus and embryo during pre-implantation and implantation

Tepekoy

Akkoyunlu

Demir

2014

J Assist Reprod Genet

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Wnt family members are best known for their roles in cell fate determination, differentiation, proliferation and apoptosis during embryonic development. Wnt signaling becomes effective during these cellular processes through the proper interaction between its ligands, receptors, effectors and inhibitors. Here we review Wnt signaling in terms of embryonic development to the blastocyst stage implantation with emphasis on endometrial changes that are critical for receptivity in the uterus. The relationship between Wnt signaling and implantation clearly reveals that, Wnt family members are critical for both early embryonic development and changing of the endometrium before implantation. Specific Wnt signaling pathway members are demonstrated to be critical for endometrial events such as decidualization and endometrial gland formation in addition to cyclic changes in the endometrium controlled by reproductive hormones. In conclusion, specific roles of Wnt members and associated factors for both uterine function and embryonic development should be further investigated with respect to the efficiency of human ARTs.

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“…expression of adhesion molecules (von Lukowicz et al 2008), transcriptional regulation of cyclooxygenase-2 (Lin et al 2011), transforming growth factor-b1 (TGF-b1) receptor (Sterling et al 2006), syndecan-4 (Lacal et al 2009), NF-kB (Kauppinen et al 2013), SMAD3 (Huang et al 2011), sex determining region Y-Box-2 (Musard et al 2001) and E-cadherin (McPhee et al 2008), which are essential during embryo implantation (Nakamura et al 2004, San et al 2004, Jha et al 2006, Lin et al 2006, St-Louis et al 2010. Furthermore, cell differentiation, cell proliferation (Lei et al 2009, Kaloglu & Onarlioglu 2010, Macdonald et al 2011, Afshar et al 2012) and the tissue remodelling process also take place in the uterus (Fazleabas & Strakova 2002, Rosario et al 2003, Kaloglu & Onarlioglu 2010, and can be influenced by PARP1 (Pagano et al 2007, Kobayashi 2011. In endometrial carcinoma, PARP1 can regulate the progesterone receptor (PR; Ghabreau et al 2004), suggesting the involvement of PARP1 in ovarian steroid signalling.…”

Section: Introductionmentioning

confidence: 99%

PARP1 during embryo implantation and its upregulation by oestradiol in mice

Joshi¹,

Mahfooz²,

Maurya³

et al. 2014

Reproduction

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Pregnancy requires successful implantation of an embryo, which occurs during a restricted period defined as 'receptivity of the endometrium' and is influenced by the ovarian steroids progesterone and oestradiol. The role of poly(ADP-ribose)polymerase-1 (PARP1) in apoptosis is well established. However, it is also involved in cell differentiation, proliferation and tissue remodelling. Previous studies have described the presence of PARP in the uterus, but its exact role in embryo implantation is not yet elucidated. Hence, in this study, we studied the expression of PARP1 in the uterus during embryo implantation and decidualisation, and its regulation by ovarian steroids. Our results show upregulation of the native form of PARP1 (w116 kDa) in the cytosolic and nuclear compartments of implantation and non-implantation sites at day 5 (0500 h), followed by downregulation at day 5 (1000 h), during the embryo implantation period. The transcript level of Parp1 was also augmented during day 5 (0500 h). Inhibition of PARP1 activity by the drug EB-47 decreased the number of embryo implantation sites and blastocysts at day 5 (1000 h). Further, cleavage of native PARP1 was due to the activity of caspase-3 during the peri-implantation stage (day 5 (0500 h)), and is also required for embryo implantation, as inhibition of its activity compromised blastocyst implantation. The native (w116 kDa) and cleaved (w89 kDa) forms of PARP1 were both elevated during decidualisation of the uterus. Furthermore, the expression level of PARP1 in the uterus was found to be under the control of the hormone oestrogen. Our results clearly demonstrate that PARP1 participates in the process of embryo implantation.

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Prokineticin 1 induces Dickkopf 1 expression and regulates cell proliferation and decidualization in the human endometrium

Cited by 45 publications

References 51 publications

Prokineticin receptor variants (PKR1-I379V and PKR2-V331M) are protective genotypes in human early pregnancy

Prokineticin receptor variants (PKR1-I379V and PKR2-V331M) are protective genotypes in human early pregnancy

The role of Wnt signaling members in the uterus and embryo during pre-implantation and implantation

PARP1 during embryo implantation and its upregulation by oestradiol in mice

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