Dysregulated endometrial podocalyxin and LIF expression in women with ovarian endometrioma

Objective To investigate whether ovarian endometrioma is associated with disruption of the endocrine-regulated transition between the anti-adhesive modulator podocalyxin (PCX) and the adhesive modulator leukemia inhibitory factor (LIF) in the endometrium.

This cross-sectional study included 42 women (32 infertile, 10 fertile controls). Among infertile participants, 17 had ovarian endometrioma (EOC), seven had non-endometriotic cysts, and eight had prior infertility treatment failure. Endometrial tissue obtained via laparoscopy or hysteroscopy was analyzed in 30 women with mid- or late-luteal endometrium. PCX mRNA, PCX protein, and LIF mRNA levels were assessed using qRT-PCR and ELISA.

LIF mRNA expression was significantly lower in the EOC group compared to all other groups (p < 0.001), while PCX mRNA and protein levels were higher (p < 0.001). Progesterone levels negatively correlated with PCX mRNA (r = −0.48, p = 0.007) and protein (r = −0.45, p = 0.012). LIF expression showed strong negative correlations with PCX mRNA (r = −0.81) and protein (r = −0.82) (p < 0.001). No associations were found with cyst characteristics.

Ovarian endometrioma is associated with disruption of the PCX–LIF transition, suggesting impaired endometrial progesterone responsiveness.

Endometriosis is a chronic inflammatory, heritable, and hormone-dependent disease characterised by pelvic pain and infertility, resulting from the ectopic presence of endometrial tissue in the peritoneum and ovaries [Citation1]. Clinically, it manifests as superficial peritoneal lesions, deep infiltrative disease, and ovarian endometriomas [Citation2]. Although the mechanisms underlying endometriosis-associated infertility are multifactorial, pathological endometrial inflammation, pelvic adhesions, reduced ovarian reserve, and impaired endometrial receptivity are considered key contributors [Citation3,Citation4]. Successful implantation requires a precisely regulated endocrine and molecular environment within the endometrium. The window of implantation (WOI) defines a limited post-ovulatory period during which the endometrium becomes receptive to embryo attachment [Citation5]. Clinical and experimental evidence indicates that women with endometriosis exhibit reduced implantation rates and impaired decidualization capacity, suggesting compromised endometrial receptivity [Citation6,Citation7]. This hormonally regulated process occurs approximately 3–6 days after ovulation and allows embryo adhesion and invasion during a narrow temporal interval [Citation8]. Despite its central role in reproduction, the molecular mechanisms governing the transition from a non-receptive to a receptive endometrial state remain incompletely understood. Podocalyxin (PCX), a barrier-protective transmembrane protein, has recently been identified as a key negative regulator of endometrial receptivity [Citation9–11]. PCX is abundantly expressed in the luminal and glandular epithelium of the non-receptive endometrium and is physiologically downregulated during the receptive phase [Citation9,Citation11]. This downregulation is essential for the transition from a non-adhesive to an adhesive endometrial surface. Although ovarian endometriomas are confined to the ovary, increasing evidence suggests that they exert systemic endocrine and inflammatory effects on the eutopic endometrium, beyond mechanical disruption of ovarian function, including enhanced inflammatory signalling and suppression of adhesive receptivity markers [Citation7,Citation12]. Implantation timing is governed by a tightly regulated balance between anti-adhesive and adhesive receptivity modulators [Citation10]. During the follicular phase, PCX suppresses adhesion-related gene expression and reinforces epithelial barrier integrity, preventing premature implantation [Citation9]. Following ovulation, progesterone-mediated downregulation of PCX enables the upregulation of adhesive genes, including leukaemia inhibitory factor (LIF), while reducing tight junction and barrier-associated proteins [Citation10,Citation11]. LIF, a pleiotropic cytokine of the interleukin-6 family, plays a critical role in endometrial receptivity through its interaction with the LIF receptor (LIFR) and gp130 [Citation13–15]. Although reduced expression of adhesive homeobox genes has been consistently reported in women with endometriosis, data regarding endometrial LIF expression remain heterogeneous [Citation7,Citation16,Citation17]. Importantly, PCX suppresses multiple adhesive genes, including LIF, until its physiological downregulation during the mid-luteal phase [Citation9,Citation11]. Coordinated PCX downregulation and LIF upregulation are therefore essential for timely opening of the implantation window [Citation10,Citation11]. While altered temporal patterns of PCX expression have been described in the eutopic endometrium of women with endometriosis [Citation18], the impact of ovarian endometriomas on the endocrine-regulated PCX–LIF transition during implantation has not been clinically investigated. Therefore, this study aimed to evaluate the expression of the anti-adhesive modulator podocalyxin and the adhesive modulator leukaemia inhibitory factor in endometrial samples obtained from women with ovarian endometrioma, to provide insight into endocrine-related endometrial dysfunction associated with this condition.

Patient selection Based on the study by Margioula-Siarkou et al. [Citation19], sample size calculation was performed using an effect size of f = 1.072, α = 0.05, and power (1 − β) = 90%, yielding a minimum of five participants per group. Sample size estimation was conducted using G*Power version 3.1.9.7 (Heinrich-Heine-Universität Düsseldorf, Germany). This prospective cross-sectional observational study included 42 women (32 infertile and 10 fertile). Among infertile participants, 17 had ovarian endometrioma cysts (EOC), seven had non-endometriotic benign ovarian cysts (non-EOC), and eight had no ovarian cysts but underwent hysteroscopy (H/S) for endometrial evaluation following infertility treatment failure. Participant distribution and endometrial histology are presented in Supplementary Figure S1. Patients in the failed IVF group had normal ovarian reserve and no endometrial pathology affecting receptivity. Inclusion criteria were infertility in women aged < 40 years, planned laparoscopy (L/S) for endometrioma or benign ovarian cysts or H/S for failed IVF evaluation, and mid- or late-luteal phase endometrial histology. Exclusion criteria included age ≥40 years, out-of-phase endometrial histology, premalignant or malignant endometrial pathology, and borderline or malignant ovarian cysts. Patients with polycystic ovary syndrome, prior mechanical endometrial injury, submucous fibroids, endometrial synechiae, or recent use of insulin sensitisers or hormonal medications were excluded. EOC and non-EOC diagnoses were established by transvaginal ultrasonography. Endometriomas were defined as cysts with diffuse low-level internal echoes persisting for at least three menstrual cycles. Cysts lacking characteristic sonographic features of endometrioma were classified as non-EOC. Endometrial thickness was measured by transvaginal ultrasonography prior to L/S or H/S with an empty bladder. Ten fertile women with proven fertility undergoing hysteroscopy for benign gynaecological indications were included as controls. Only cases with benign pathology and mid- or late-luteal phase histology were included. Basal venous blood samples were obtained on menstrual cycle days 2–5 following overnight fasting. To evaluate endocrine regulation of PCX expression, serum progesterone levels were additionally measured at the time of endometrial sampling. Serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), and progesterone levels were measured using electrochemiluminescence (Cobas e 601, Roche Diagnostics, Germany). Endometrial sampling The study was approved by the Institutional Ethics Committee, and written informed consent was obtained from all participants (Approval No: E-10840098-202.3.02-4879, July 2025). Patient recruitment and sample collection were conducted between July 2025 and December 2025. Endometrial tissue was obtained using a Pipelle cannula (Medbar, Turkey) during laparoscopic cystectomy or hysteroscopy. To minimise procedural bias, endometrial sampling was performed prior to cystectomy in patients with ovarian cysts. Samples were collected until adequate tissue including the fundal region was obtained. Endometrial tissue was divided into two portions: one preserved in RNA stabilisation buffer (Qiagen, Germany) for qRT-PCR analysis and the other stored at −20 °C for ELISA analysis. Menstrual cycle phase was determined using Noyes histological criteria [Citation20]. Only samples with mid- or late-luteal phase histology were included in molecular analyses; out-of-phase samples were excluded. qRT-PCR analysis of endometrial PCX and LIF mRNA Total RNA was isolated using the PureLink Total RNA Mini Kit (Invitrogen). RNA concentration was quantified using the Qubit RNA HS Assay Kit, and cDNA was synthesised from 500 ng RNA using ABCScript III RT Master Mix. Quantitative real-time PCR was performed using SYBR Green chemistry on the Applied Biosystems StepOnePlus® system. Primer sequences for PCX and LIF are provided in Supplementary Table S1. Gene expression levels were normalised to glyceraldehyde-3-phosphate dehydrogenase, and relative expression was calculated using the 2−ΔΔCt method [Citation10]. All reactions were performed in triplicate. ELISA analysis of PCX PCX protein concentrations were measured using a quantitative sandwich ELISA kit (Sunred Biotechnology Company, China) according to the manufacturer’s instructions. The assay detection range was 0.2–60 ng/mL, with intra- and inter-assay coefficients of variation < 10% and < 12%, respectively. Absorbance was measured at 450 nm using a CLARIOstar PLUS microplate reader (BMG Labtech, Germany). Statistical analysis Statistical analyses were performed using IBM SPSS Statistics version 27.0. Data distribution was assessed using the Shapiro–Wilk test, and variance homogeneity was evaluated using Levene’s test. Continuous variables are presented as mean ± standard deviation or median (interquartile range), and categorical variables as frequency (percentage). Appropriate parametric or non-parametric tests were applied according to data distribution. Correlations were assessed using Spearman’s correlation analysis. A correlation heat map was generated using R Studio version 4.3.3 with the ‘Metan’ package [Citation21]. Statistical significance was defined as p < 0.05.

Demographic characteristics, laboratory parameters, and adhesive and anti-adhesive receptivity marker expressions of all groups are summarised in . No significant differences were observed among the groups with respect to age, BMI, infertility duration, endometrial thickness, or serum FSH, LH, and progesterone levels. Cyst diameters were comparable between the EOC and non-EOC groups (p = 0.602). In the EOC group, cysts were unilateral in 10 patients (58.8%) and bilateral in seven (41.1%), whereas in the non-EOC group, five cysts (71.4%) were unilateral and two (28.5%) were bilateral. Relative LIF mRNA expression was significantly lower in the EOC group compared with the non-EOC, failed IVF, and control groups (p < 0.001 for all). LIF mRNA expression did not differ between the non-EOC, failed IVF, and control groups. Conversely, relative PCX mRNA expression and PCX protein levels were significantly higher in the EOC group than in all other groups (p < 0.001 for all comparisons), while no differences were observed among the non-EOC, failed IVF, and control groups (, , ). No significant differences in PCX mRNA, LIF mRNA, or PCX protein levels were detected between unilateral and bilateral endometrioma cases (Supplementary Table S2, Supplementary Figure S2). Serum progesterone levels were negatively correlated with PCX mRNA (r = −0.482, p = 0.007) and PCX protein levels (r = −0.451, p = 0.012). In addition, strong negative correlations were observed between LIF mRNA expression and both PCX mRNA (r = −0.807, p < 0.001) and PCX protein levels (r = −0.816, p < 0.001). No significant associations were identified between cyst diameter and adhesive or anti-adhesive gene expression (Supplementary Table S3, Supplementary Figure S3). Histological evaluation revealed out-of-phase endometrium in 16 patients, who were excluded from molecular analyses. Following exclusions due to cycle phase incompatibility and lack of histological confirmation of endometrioma, a total of 30 endometrial samples with mid- or late-luteal phase histology were included in the final PCR analysis.

Endometriosis is well recognised to be associated with reduced implantation rates in both natural and assisted reproductive cycles [Citation6,22–24]. However, the mechanisms underlying endometriosis-associated implantation failure remain debated. While some studies emphasise impaired oocyte or embryo quality [Citation23,Citation25,Citation26], others indicate that altered endometrial receptivity plays a central role [Citation27,Citation28]. Given the multifactorial nature of implantation, it is likely that both endometrial and ovarian factors contribute to reduced reproductive potential in affected women. In this context, the present study provides novel insight by demonstrating disruption of the physiological balance between anti-adhesive and adhesive receptivity modulators in the eutopic endometrium of women with ovarian endometrioma. The principal finding of this study was significantly increased expression of the anti-adhesive marker podocalyxin alongside reduced expression of the adhesive marker leukaemia inhibitory factor in women with ovarian endometrioma compared with both non-endometriotic ovarian cysts and fertile controls. Inclusion of a non-endometriotic cyst group allowed evaluation of whether a space-occupying ovarian lesion alone could influence endometrial receptivity. The comparable PCX and LIF expression profiles between the non-endometriotic cyst group and fertile controls suggest that the observed imbalance is unlikely to be attributable to mechanical or mass effects. Furthermore, the lack of association between cyst size or laterality and receptivity marker expression supports the hypothesis that ovarian endometriomas exert systemic endocrine and inflammatory effects on the eutopic endometrium. Under physiological conditions, rising mid-luteal progesterone levels suppress PCX expression in luminal epithelial cells, facilitating transition to a receptive endometrial state. In contrast, persistently elevated PCX expression despite normal circulating progesterone levels was observed in women with endometrioma, suggesting a possible impairment in progesterone-mediated regulation. Altered progesterone signalling, frequently reported in endometriosis, may represent a plausible mechanism underlying this finding [Citation29,Citation30]. Previous human and experimental studies have demonstrated reduced progesterone receptor expression—particularly the PR-B isoform—together with increased oestrogen receptor activity in endometriosis [Citation31–34]. Although progesterone receptor expression was not assessed in the present study, the observed failure of PCX downregulation despite adequate luteal progesterone levels is consistent with altered progesterone responsiveness. In this context, the persistence of PCX expression despite adequate hormonal conditions may reflect impaired progesterone-mediated regulation. However, this interpretation remains indirect due to the absence of receptor-level or functional data. Therefore, the proposed relationship between progesterone signalling, PCX persistence, and LIF suppression should be interpreted as hypothesis-generating rather than mechanistic evidence. Reduced LIF expression in the endometrioma group may further reflect the inflammatory and endocrine milieu characteristic of endometriosis. Chronic inflammation, oestrogen dominance, and dysregulated steroid signalling have all been implicated in impaired endometrial gene expression [Citation22,Citation31,Citation33]. Importantly, persistent PCX expression may directly suppress LIF and other adhesive genes, maintaining a non-receptive endometrial phenotype. The strong negative correlations observed between PCX mRNA, PCX protein, and LIF expression support this hypothesis. Consistent with previous studies, PCX has been shown to suppress multiple pro-receptive genes, including HOXA10, HOXA11, and LIF, while promoting expression of barrier-associated proteins that impair embryo adhesion [Citation10,Citation11]. Physiological opening of the implantation window requires coordinated progesterone-mediated downregulation of PCX and upregulation of adhesive factors such as LIF [Citation9–11]. In fertile women, LIF and its receptors are maximally expressed during the implantation window under combined oestrogen and progesterone signalling [Citation15,Citation35]. In contrast, persistently low LIF expression observed in women with endometrioma may result from both continued PCX-mediated suppression and impaired progesterone signalling [Citation36,Citation37]. Supporting this concept, previous studies have demonstrated that key adhesive genes fail to exhibit their normal mid-luteal upregulation in endometriosis, potentially due to epigenetic dysregulation [Citation38–40]. Restoration of adhesive gene expression following surgical resection of endometriomas further supports a systemic effect of ovarian endometriomas on endometrial function [Citation7,Citation27]. Although some investigators argue that implantation failure in endometriosis primarily reflects impaired embryo quality [Citation23,Citation25], substantial molecular and clinical evidence indicates altered endometrial receptivity in affected women [Citation3,Citation7,Citation18,Citation27,Citation28]. Reduced expression of adhesive genes during the implantation window and dysregulation of progesterone signalling pathways have been consistently reported and are associated with poorer reproductive outcomes [Citation7,Citation41]. Several limitations should be acknowledged. First, the relatively small sample size limits generalisability, and this study should be considered exploratory in nature. Second, the use of tissue homogenates precluded localisation of PCX and LIF expression to specific cell types (e.g. luminal epithelium) by immunohistochemistry. Third, LIF expression was assessed only at the mRNA level due to sample limitations, and functional protein deficits remain to be confirmed. Fourth, although a correlation with serum progesterone levels was observed, endometrial progesterone receptor (PR-A and PR-B) expression was not evaluated, precluding direct assessment of progesterone-related mechanisms. These limitations were primarily related to sample availability and the study design, which precluded additional molecular and histological analyses.

Limited data exist regarding alterations in podocalyxin, a negative regulator of endometrial receptivity, in women with endometriosis. Previous histological and in vitro studies suggested displacement of the receptive window but did not evaluate PCX at the molecular level or assess adhesive receptivity markers [Citation18]. The present study provides clinical and molecular evidence that ovarian endometrioma is associated with disruption of the physiological balance between anti-adhesive and adhesive endometrial receptivity modulators. Increased expression of podocalyxin accompanied by reduced leukaemia inhibitory factor expression suggests impaired endocrine regulation of the implantation window. Persistent PCX expression despite normal progesterone levels may reflect impaired progesterone responsiveness at the endometrial level, although this interpretation remains indirect in the absence of receptor-level or functional validation. Further studies integrating receptor-level and hormonal signalling analyses are warranted to clarify the clinical implications of these findings. Ethical approval This study was approved by the Clinical Research Ethics Committee of Istanbul Medipol University (Approval No: E-10840098-202.3.02-4879, July 2025). All participants provided written informed consent prior to inclusion. The study was conducted in accordance with the Declaration of Helsinki. Consent for publication Not applicable. No identifiable personal data or images are included in this manuscript. Supplemental material Supplementary Figure Caption Download MS Word (12 KB)Supplementary Figure CaptionSTROBE.doc Download MS Word (85 KB)STROBE.docSupplementary Figure S2 Download JPEG Image (23.8 KB)Supplementary Figure S2Supplementary Figure S3 Download JPEG Image (45.7 KB)Supplementary Figure S3Supplementary Table S3.docx Download MS Word (19 KB)Supplementary Table S3.docxSupplementary Figure S1 Download JPEG Image (79.1 KB)Supplementary Figure S1Supplementary Table S2.docx Download MS Word (16.7 KB)Supplementary Table S2.docxSupplementary Table S1.docx Download MS Word (14.5 KB)Supplementary Table S1.docxAcknowledgements Gökçenur Karakelleoğlu: Study conception and design, clinical procedures, data collection, analysis and interpretation, literature contribution, manuscript revision, manuscript draughting and critical revision, final approval of the version to be published, and agreement to be accountable for all aspects of the work. Cihan Karadağ: Laboratory supervision, ELISA and PCR methodology, data analysis, Primer design, PCR standardisation, gene expression analysis, manuscript revision, final approval, and agreement to be accountable for all aspects of the work. Disclosure statement The authors declare that they have no conflicts of interest. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Data availability statement The datasets supporting the conclusions of this article are included within the article. Due to ethical restrictions and patient privacy considerations, the raw data are not publicly available but are available from the corresponding author upon reasonable request. Supplemental material Supplemental data for this article can be accessed at https://doi.org/10.1080/09513590.2026.2662696.

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