Association of the estrogen receptor-β gene RsaI and AluI polymorphisms with human idiopathic thin endometrium

Le, Aiwen; Wang, Z H; Yuan, Ruixia; Shan, Lili; Xiao, Tian; Zhuo, Ren‐Xi; Shen, Yi

doi:10.4238/2013.november.26.7

Cited by 6 publications

(4 citation statements)

References 21 publications

(19 reference statements)

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“…Not only does it occur after uterine cavity manipulation and infection (Shufaro et al, 2008), but it is also related to endocrine disorder, aging, and drug induction (Kumbak and Sahin et al, 2009;Le et al, 2013). The pathological and physiological characteristics of a thin endometrium were first described by Miwa et al (2009) as slow growth of the glandular epithelium, high resistance of the uterine artery blood flow, vascular dysplasia, and low expression of vascular endothelial growth factor (VEGF).…”

Section: Introductionmentioning

confidence: 99%

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

Le¹,

Shan²,

Wang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We explored the effects of icariin on the expression of estrogen receptor (ER), vascular endothelial growth factor (VEGF), and kinase insert domain receptor (KDR) in the endometrial cells of the thin endometrium. Primary endometrial cells were obtained and divided into a blank control group, a high-, a middle-, and a low-dose icariin groups, as well as an estrogen treatment group to undergo cellular identification by immunocytochemistry. The expression levels of ER, VEGF, and its receptor were estimated by western blotting. The expression levels of ER, VEGF, and KDR gradually increased from the control group to the estrogen (E2) treatment and icariin treatment groups; the differences were statistically significant. However, the differences were not statistically significant among the different icariin dose groups. The endometrium may be thickened by icariin treatment by increasing the expression levels of ER, VEGF, and KDR in endometrial cells.

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Section: Introductionmentioning

confidence: 99%

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

Le¹,

Shan²,

Wang³

et al. 2015

Genet. Mol. Res.

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“…Causes of a "thin" endometrium include damage to the basal layer of the endometrium, hypoestrogenic conditions, prolonged use of oral contraceptives, stimulation of ovulation with clomiphene citrate, radiation therapy [53][54][55], impaired estrogen signaling due to estrogen receptor dysfunction (Erα-and β-polymorphisms) [56,57], while in some cases, the causes remain unknown.…”

Section: "Thin" Endometriummentioning

confidence: 99%

The Therapeutic Potential of Multipotent Mesenchymal Stromal Cell—Derived Extracellular Vesicles in Endometrial Regeneration

Tabeeva

Silachev

Vishnyakova

et al. 2023

IJMS

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Disruption of endometrial regeneration, fibrosis formation, and intrauterine adhesions underlie the development of “thin” endometrium and/or Asherman’s syndrome (AS) and are a common cause of infertility and a high risk for adverse obstetric outcomes. The methods used (surgical adhesiolysis, anti-adhesive agents, and hormonal therapy) do not allow restoration of the regenerative properties of the endometrium. The experience gained today with cell therapy using multipotent mesenchymal stromal cells (MMSCs) proves their high regenerative and proliferative properties in tissue damage. Their contribution to regenerative processes is still poorly understood. One of these mechanisms is based on the paracrine effects of MMSCs associated with the stimulation of cells of the microenvironment by secreting extracellular vesicles (EVs) into the extracellular space. EVs, whose source is MMSCs, are able to stimulate progenitor cells and stem cells in damaged tissues and exert cytoprotective, antiapoptotic, and angiogenic effects. This review described the regulatory mechanisms of endometrial regeneration, pathological conditions associated with a decrease in endometrial regeneration, and it presented the available data from studies on the effect of MMSCs and their EVs on endometrial repair processes, and the involvement of EVs in human reproductive processes at the level of implantation and embryogenesis.

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“…Proposed causes of a thin endometrium include Asherman's syndrome and previous intrauterine surgery including sharp curettage, radiation to the pelvis, genetics, impaired uterine blood flow, and acute or chronic endometrial infection. Moreover, it is linked to the use of medications such as clomiphene citrate as well as low estrogen levels or impaired estrogen signaling as a result of dysfunctional estrogen receptors [7][8][9][10][11]. A recent single-cell RNA sequencing study suggested that cellular senescence in the stroma and epithelium together with collagen overdeposition around the blood vessel is involved in endometrial thinness [12].…”

Section: Introductionmentioning

confidence: 99%

An Update on Experimental Therapeutic Strategies for Thin Endometrium

Tang,

Frisendahl,

Lalitkumar

et al. 2023

Endocrines

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Infertility caused by a thin endometrium remains a significant challenge in assisted reproduction and is often associated with a low success rate after treatment with assisted reproductive technology. There is a lack of consensus in the field concerning both its diagnostic criteria and clinical management. The currently available treatment options are few with limited efficacy. Recent advances in cell therapy and bioengineering have, however, shown promising results for the treatment of a thin endometrium. Notably, these novel interventions have demonstrated the ability to increase endometrial thickness, restore endometrial function, and improve reproductive outcomes. In this comprehensive review, we focus on a critical evaluation of these emerging therapeutic strategies for a thin endometrium including platelet-rich plasma, exosomes derived from stem cells, and bioengineering-based techniques. By synthesizing the findings from available clinical trials, we highlight the promising outcomes achieved so far and underscore the importance of robust clinical trials in assessing the safety and efficacy of these interventions in the future. Continued research efforts to unravel the intricate mechanisms involved in endometrial repair and regeneration will also be essential to enhance our understanding of this multifactorial condition and to identify novel treatment targets for future therapeutic interventions.

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Association of the estrogen receptor-β gene RsaI and AluI polymorphisms with human idiopathic thin endometrium

Cited by 6 publications

References 21 publications

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

The Therapeutic Potential of Multipotent Mesenchymal Stromal Cell—Derived Extracellular Vesicles in Endometrial Regeneration

An Update on Experimental Therapeutic Strategies for Thin Endometrium

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