Expression of kisspeptin/GPR54 and PIBF/PR in the first trimester trophoblast and decidua of women with recurrent spontaneous abortion

Wu, Shuang; Zhang, Hong; Tian, Jiwen; Liu, Lifen; Dong, Yi; Mao, Ting

doi:10.1016/j.prp.2013.09.017

Cited by 39 publications

(39 citation statements)

References 22 publications

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“…A number of studies in the literature have examined this with slight discrepancies in results. Most found that women with early bleeding in pregnancy [60], recurrent spontaneous abortion [61,62], metabolic conditions including diabetes and hypertension during pregnancy [63], development of pre-eclampsia, and intra-uterine growth restriction [64,65,66] had lower levels of circulating kisspeptin and decreased levels of kisspeptin receptor on placental immunohistochemistry. However, others found no difference in circulating levels of kisspeptin [67] and/or higher levels of placental expression of kisspeptin receptor at the time of pre-term labour [68].…”

Section: Potential Clinical Uses Of Kisspeptinmentioning

confidence: 99%

Potential Clinical Use of Kisspeptin

Prague

Dhillo

2015

Neuroendocrinology

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Over the last 10 years, kisspeptins - peptide products of varying lengths encoded by the KISS1 gene - have been found to be key regulators of normal reproductive function throughout life in animals and humans. By activating the kisspeptin receptor [previously known as orphan G protein-coupled receptor 54 (GPR54)], they elicit an effect on the central gonadotropin-releasing hormone neurons. Administration of kisspeptin by either the subcutaneous or intravenous route potently stimulates endogenous gonadotropin hormone release in healthy men and women as well as in animals. Kisspeptin also stimulates endogenous release of gonadotropins in subfertile as well as healthy volunteers, and therefore it has potential as a novel therapeutic agent in reproductive disorders. Further human studies have shown that chronic, high-dose administration of kisspeptin causes desensitisation with rapid subsequent suppression of the hypothalamic-pituitary-gonadal axis, and therefore high-dose long-acting analogues may have a clinical role in treating sex hormone-dependent malignancies. By further elucidating the intricacies and mechanisms of the kisspeptin signalling system, and the tissues it acts on during different phases of the reproductive timeline (including during puberty, fertility, pregnancy and menopause), pharmacologic analogues could become clinically useful.

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Section: Potential Clinical Uses Of Kisspeptinmentioning

confidence: 99%

Potential Clinical Use of Kisspeptin

Prague

Dhillo

2015

Neuroendocrinology

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“…Cartwright et al detected KP and GPR54 mainly in syncitiotrophoblast, and at a lower level also in the villous cytotrophoblast [20]. While, a recent study using immunohistochemistry, detected expression of kisspeptin and GPR54 in syncytiotrophoblasts and cytotrophoblasts [21].…”

Section: Introductionmentioning

confidence: 97%

Kisspeptin Regulation of Genes Involved in Cell Invasion and Angiogenesis in First Trimester Human Trophoblast Cells

et al. 2014

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The precise regulation of extravillous trophoblast invasion of the uterine wall is a key process in successful pregnancies. Kisspeptin (KP) has been shown to inhibit cancer cell metastasis and placental trophoblast cell migration. In this study primary cultures of first trimester human trophoblast cells have been utilized in order to study the regulation of invasion and angiogenesis-related genes by KP. Trophoblast cells were isolated from first trimester placenta and their identity was confirmed by immunostaining for cytokeratin-7. Real-time quantitative RT-PCR demonstrated that primary trophoblast cells express higher levels of GPR54 (KP receptor) and KP mRNA than the trophoblast cell line HTR8Svneo. Furthermore, trophoblast cells also expressed higher GPR54 and KP protein levels. Treating primary trophoblast cells with KP induced ERK1/2 phosphorylation, while co-treating the cells with a KP antagonist almost completely blocked the activation of ERK1/2 and demonstrated that KP through its cognate GPR54 receptor can activate ERK1/2 in trophoblast cells. KP reduced the migratory capability of trophoblast cells in a scratch-migration assay. Real-time quantitative RT-PCR demonstrated that KP treatment reduced the expression of matrix metalloproteinase 1, 2, 3, 7, 9, 10, 14 and VEGF-A, and increased the expression of tissue inhibitors of metalloproteinases 1 and 3. These results suggest that KP can inhibit first trimester trophoblast cells invasion via inhibition of cell migration and down regulation of the metalloproteinase system and VEGF-A.

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“…Recurrent spontaneous abortion (RSA) is defined as the miscarriage of two or more pregnancies before the 20th week of gestation and about a half of all cases are idiopathic. This led Wu et al 67 to investigate whether the expression of kisspeptin and KISS1R was altered in the decidua of women experiencing RSA. Using IHC, kisspeptin and KISS1R expression was assessed in the decidua from RSA patients (n ¼ 32) having pregnancy loss in the first trimester, and healthy women (n ¼ 35) undergoing an elective termination of their pregnancy during the first trimester.…”

Section: Expression Of Decidual Kisspeptin But Not Kiss1r Is Reducementioning

confidence: 99%

Regulation of Pregnancy: Evidence for Major Roles by the Uterine and Placental Kisspeptin/KISS1R Signaling Systems

Radovick

Babwah

2019

Semin Reprod Med

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Several studies provide strong evidence suggesting that in addition to central kisspeptin/KISS1R signaling, the peripheral uterine- and placental-based kisspeptin/KISS1R signaling systems are major regulators of pregnancy. Specifically, the evidence suggests that the uterine-based system regulates embryo implantation and decidualization, while both the uterine- and placental-based systems regulate placentation. Uterine kisspeptin and KISS1R regulate embryo implantation by controlling the availability of endometrial glandular secretions, like leukemia inhibitory factor, which are essential for embryo adhesion to the uterine epithelium. As for decidualization, the data suggest that decidualized stromal cells express KISS1R and secrete kisspeptin-inhibiting decidual cell motility and thereby indirectly regulate embryo and placental invasion of the uterus. Similarly, for placentation, placental kisspeptin and KISS1R negatively regulate extravillous trophoblast migration and invasion and thereby directly control placental invasion of the uterus. Having recognized a significant role for the uterine- and placental-based kisspeptin/KISS1R signaling systems regulating pregnancy, the future looks promising for the development of kisspeptin and KISS1R as prognostic and diagnostic markers of pregnancy disorders and the use of kisspeptin as a therapeutic agent in the prevention and treatment of conditions such as recurring implantation failure, recurrent pregnancy loss, and preeclampsia.

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Expression of kisspeptin/GPR54 and PIBF/PR in the first trimester trophoblast and decidua of women with recurrent spontaneous abortion

Cited by 39 publications

References 22 publications

Potential Clinical Use of Kisspeptin

Potential Clinical Use of Kisspeptin

Kisspeptin Regulation of Genes Involved in Cell Invasion and Angiogenesis in First Trimester Human Trophoblast Cells

Regulation of Pregnancy: Evidence for Major Roles by the Uterine and Placental Kisspeptin/KISS1R Signaling Systems

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