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复发性流产和反复种植失败中子宫内膜容受性的评估。

Evaluation of endometrial receptivity in recurrent pregnancy loss and recurrent implantation failure.

作者信息

Canan Sultan, İnan Mehmet Arda, Erdem Ahmet, Demirdağ Erhan, Gündüz Mualla İlknur, Erdem Özlem, Erdem Mehmet

机构信息

Sakarya Training and Research Hospital, Clinic of Obstetrics and Gynecology, Sakarya, Turkey.

Gazi University Faculty of Medicine, Department of Pathology, Ankara, Turkey.

出版信息

Turk J Obstet Gynecol. 2024 Mar 4;21(1):22-27. doi: 10.4274/tjod.galenos.2024.42959.

DOI:10.4274/tjod.galenos.2024.42959
PMID:38440964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10920968/
Abstract

OBJECTIVE

The cause of implantation defects in patients with recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL) has not been clearly established. We aimed to evaluate the immunohistochemical changes in HOXA-11, β1 integrin, focal adhesion kinase (FAK), cluster of differentiation 44 (CD44), and extracellular matrix protein 1 (ECM1) molecules during the receptive endometrial period in patients with RIF and RPL.

MATERIALS AND METHODS

This study was retrospectively conducted at a university hospital. After the exclusion of cases with pathology that may cause a change in the level of receptors in the endometrium, biopsies performed during the receptive period were selected, and the patients were categorized into RPL (n=15), RIF (n=16), control (n=16) groups. All preparations were immunohistochemically stained for HOXA-11, β1 integrin, FAK, CD44, and ECM1.

RESULTS

HOXA-11 and β1 Integrin expression changes were similar between the RIF and control groups. However, FAK expression was significantly increased in the RIF group (p<0.01). Additionally, ECM1 and CD44 expressions were significantly decreased in the RIF group compared with the control group (p<0.01). There was no significant difference in the endometrial staining of HOXA-11, FAK, and ECM1 in patients with a history of RPL. However, β1 Integrin and CD44 levels were significantly decreased in the RPL group compared with the control group (p<0.05).

CONCLUSION

Implantation is a complex process, and altered adhesion mechanisms involved in endometrial receptivity may be related to defective implantation in patients with RIF and RPL. Among the adhesion molecules, the expression of CD44, β1 integrin, FAK, and ECM1 molecules varies in inappropriate implantation compared with the normal population.

摘要

目的

复发性植入失败(RIF)和复发性流产(RPL)患者植入缺陷的原因尚未明确。我们旨在评估RIF和RPL患者在子宫内膜容受期HOXA - 11、β1整合素、黏着斑激酶(FAK)、分化簇44(CD44)和细胞外基质蛋白1(ECM1)分子的免疫组化变化。

材料与方法

本研究在一家大学医院进行回顾性研究。排除可能导致子宫内膜受体水平变化的病理病例后,选取容受期进行的活检组织,将患者分为RPL组(n = 15)、RIF组(n = 16)、对照组(n = 16)。所有标本均进行HOXA - 11、β1整合素、FAK、CD44和ECM1的免疫组化染色。

结果

RIF组和对照组之间HOXA - 11和β1整合素表达变化相似。然而,RIF组FAK表达显著增加(p < 0.01)。此外,与对照组相比,RIF组ECM1和CD44表达显著降低(p < 0.01)。有RPL病史的患者,其子宫内膜HOXA - 11、FAK和ECM1染色无显著差异。然而,与对照组相比,RPL组β1整合素和CD44水平显著降低(p < 0.05)。

结论

植入是一个复杂的过程,子宫内膜容受性中涉及的黏附机制改变可能与RIF和RPL患者的植入缺陷有关。在黏附分子中,与正常人群相比,CD44、β1整合素、FAK和ECM1分子在不适当植入中的表达有所不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/10920968/b857a13d98e4/TJOG-21-22-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/10920968/f3eee42e88c2/TJOG-21-22-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/10920968/b857a13d98e4/TJOG-21-22-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/10920968/f3eee42e88c2/TJOG-21-22-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/10920968/b857a13d98e4/TJOG-21-22-g2.jpg

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Decreased CD44v3 expression impairs endometrial stromal cell proliferation and decidualization in women with recurrent implantation failure.CD44v3 表达降低可损害复发性种植失败患者的子宫内膜间质细胞增殖和蜕膜化。
Reprod Biol Endocrinol. 2022 Dec 16;20(1):170. doi: 10.1186/s12958-022-01042-w.
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Increased expression of HOXA11-AS attenuates endometrial decidualization in recurrent implantation failure patients.
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Mol Ther. 2022 Apr 6;30(4):1706-1720. doi: 10.1016/j.ymthe.2022.01.036. Epub 2022 Jan 31.
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Lichen Sclerosus: An autoimmunopathogenic and genomic enigma with emerging genetic and immune targets.硬化性苔藓:一种自身免疫性疾病,具有潜在的遗传和免疫靶点。
Int J Biol Sci. 2019 Jun 2;15(7):1429-1439. doi: 10.7150/ijbs.34613. eCollection 2019.
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