The role of selectins in the first trimester pregnancy loss

Eskicioğlu, Fatma; Laçin, Selman; Özbilgin, Kemal; Köse, Can

doi:10.17772/gp/1725

Cited by 5 publications

(6 citation statements)

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“…L-selectin, E-selectin, and glycodelin-an E-selectin binding ligand-are downregulated in the placenta of miscarriage patients [121,122]. On the other hand, upregulation of Pselectin occurs in these placentae [122,123].…”

Section: Selectinsmentioning

confidence: 97%

The Involvement of Cell Adhesion Molecules, Tight Junctions, and Gap Junctions in Human Placentation

et al. 2020

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Placentation is a major determinant of the success of pregnancy. It is regulated by several factors such as cell adhesion molecules, tight junctions, and gap junctions. The cell adhesion molecules are integrins, cadherins, immunoglobulins, nectins, and selectins. The tight junctions are composed of claudins, occludin, and junction adhesion molecule proteins while the gap junctions are composed of connexins of varying molecular weights. During placentation, some of these molecules regulate trophoblast proliferation, trophoblast fusion, trophoblast migration, trophoblast invasion, trophoblastendothelium adhesion, glandular remodeling, and spiral artery remodeling. There is a dysregulated placental expression of some of these molecules during obstetric complications. We have, hereby, indicated the expression patterns of the subunits of each of these molecules in the various trophoblast subtypes and in the decidua, and have highlighted their involvement in physiological and pathological placentation. The available evidence points to the relevance of these molecules as distinguishing markers of the various trophoblast lineages and as potential therapeutic targets in the management of malplacentation-mediated diseases.

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Section: Selectinsmentioning

confidence: 97%

The Involvement of Cell Adhesion Molecules, Tight Junctions, and Gap Junctions in Human Placentation

et al. 2020

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“…Moreover, P-and E-selectins are also involved in immune recognition between maternal decidua and the embedded embryo, as well as trophoblast migration within decidual spiral arterioles (19). Reduced expression of all selectins has been reported in both decidual cells in uterine decidual stroma and in the placenta (cytotrophoblasts and syncytiotrophoblasts) of early miscarriages (6-11 weeks) compared to controls (terminations for social reasons) (20).…”

Section: Introductionmentioning

confidence: 99%

Maternal, Fetal, and Placental Selectins in Women With Pre-eclampsia; Association With the Renin-Angiotensin-System

et al. 2020

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Selectins [endothelial (E), platelet (P), and leucocytes (L)] are a class of cell adhesion molecules, stimulated in response to inflammation. Pre-eclampsia is characterized by inflammation, and angiotensin II is pro-inflammatory. We hypothesized that circulating maternal and fetal concentrations and placental expression of selectins would be increased in women with pre-eclampsia and would be associated with the angiotensin receptors (AT1R and AT2R). Maternal and fetal blood and placental tissue was collected at delivery from White European normotensive controls (n = 17) and women with pre-eclampsia (n = 17). Soluble (s) E-, P-and L-selectin protein concentrations were measured by ELISA and placental protein expression was examined by immunohistochemistry. Maternal sE-selectin concentrations were increased in pre-eclampsia (P < 0.001); conversely fetal sE-and sP-selectin levels were lower in pre-eclampsia (P < 0.05 for both). Staining was mainly localized to the syncytiotrophoblast for all selectins. E-selectin expression was increased, while P-selectin was decreased in placental from pre-eclampsia (P < 0.05 for both); no differences were observed for L-selectin expression. Both E-and L-selectin were positively correlated (P < 0.008; P < 0.02) with AT2R placental expression, whilst P-selectin was negatively associated with AT1R (P < 0.005), all only in the pre-eclampsia group. This novel study reports maternal, fetal and placental expression of selectins in pre-eclampsia. The increased E-selectins reflect the endothelial dysfunction, characteristic of pre-eclampsia. In contrast, the reduced P-selectins and the positive association of placental AT2Rs with both E-and L-selectin in pre-eclampsia could be a protective mechanism to limit the endothelial dysfunction.

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“…De-regulated genes including Prokineticin 1 were identified in the endometrium of women with idiopathic recurrent pregnancy loss [7,19]. A series of genes, including S100A8, S100A9, selectins, and interleukin-22, were found to be differentially expressed in human deciduas from women with pregnancy loss [8,[20][21][22]. Herein, we report significantly reduced expression of FABP4 in the deciduas of women with pregnancy loss, and we also revealed the inhibition or silence of FABP4 in mouse uterus significantly increased the embryo absorption.…”

Section: Discussionmentioning

confidence: 99%

Fatty Acid-Binding Protein 4 in Endometrial Epithelium Is Involved in Embryonic Implantation

Wang

Zhu

Peng

et al. 2017

Cell Physiol Biochem

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Aims: To clarify the role of fatty acid-binding protein 4 (FABP4) of endometrial epithelial cell in the establishment and maintenance of pregnancy and the involvement in the pathogenesis of pregnancy loss. Methods: The expression of FABP4 and uterine receptive factor (LIF, Integrin-β3 and Claudin 4) was determined by Western blotting or quantitative PCR. FABP4 siRNA was used to silence FABP4 while FABP4 inhibitor was used to inhibit the function of FABP4 in endometrial epithelial cell. ICR mice were raised to evaluate the effect of FABP4 silence or inhibition on embryo implantation in vivo after FABP4 siRNA mixture or inhibitor was injected into uterus, and an embryonic adhesion system using trophoblast spheroids mimicking embryos was set up to assess the effect of FABP4 silence or inhibition on embryonic adhesion onto endometrial cell in vitro. Results: The expression of FABP4 mRNA was significantly decreased in the deciduas of women with pregnancy loss compared with that of women with normal pregnancy. FABP4 siRNA significantly reduced the number of embryos implanted and FABP4 expression in ICR mice. FABP4 inhibition also significantly decreased the number of embryos implanted. Either silence or inhibition of FABP4 in endometrial epithelial cell abolished the expression of uterine receptive factors induced by the combination of estrogen and progesterone-induced, and reduced the number of trophoblast spheroids adhered onto endometrial cell. Conclusions: FABP4 regulates embryo implantation via altering uterine receptivity and decreased expression of FABP4 in endometrium may be linked with pregnancy loss, indicating FABP4 has biological role in the establishment and maintenance of pregnancy and subsequently is involved in pathogenesis of pregnancy loss.

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The role of selectins in the first trimester pregnancy loss

Cited by 5 publications

References 0 publications

The Involvement of Cell Adhesion Molecules, Tight Junctions, and Gap Junctions in Human Placentation

The Involvement of Cell Adhesion Molecules, Tight Junctions, and Gap Junctions in Human Placentation

Maternal, Fetal, and Placental Selectins in Women With Pre-eclampsia; Association With the Renin-Angiotensin-System

Fatty Acid-Binding Protein 4 in Endometrial Epithelium Is Involved in Embryonic Implantation

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