Ectopic Epithelial Cells Research Articles

A method for isolating and culturing ectopic epithelial and stromal cells to study human adenomyosis.

Although adenomyosis is a common and benign gynecological disease, the specific pathogenesis of this condition is yet to be fully elucidated. It is difficult to culture primary cells of the ectopic endometrial epithelia and stroma from human adenomyosis lesions. Most of the previous of studies on adenomyosis were based on primary eutopic endometrium cells. However, as yet, no efficient protocols have been developed for the isolation, culture or purification of primary ectopic epithelial and stromal cells from human adenomyosis lesions. Therefore, the present study aimed to develop an efficient protocol for the isolation and culture of primary ectopic epithelial and stromal cells from human adenomyosis lesions. In the present study, we aimed to obtain ectopic endometrium tissue from human adenomyosis foci and use a simple and operable type I collagenase digestion method for primary culture. Cells were isolated by sterile cell strainer filtration and flow cytometry was performed to identify, purify, and evaluate the viability of isolated ectopic endometrial cells. Using our method, we successfully isolated and cultured highly purified and active ectopic endometrial epithelial and stromal cells from human adenomyosis foci. Ep-CAM was expressed in ectopic epithelial cells of human adenomyosis with a purity of 93.74% and a viability of 80.58%. In addition, CD10 were robustly expressed by ectopic stromal cells in human adenomyosis. Cellular purity and viability were determined to be 96.37 and 93.49%, respectively. Our method provides a new experimental model for studying the molecular pathogenesis of human adenomyosis.

The role of phoenixin in the proliferation and migration of ectopic epithelial cells in vitro

AimEndometriosis is one of the most common gynecologic diseases in women of reproductive age. The pathophysiology of endometriosis is still not fully understood. Phoenixin (PNX-14) is a newly discovered neuropeptide that regulates the hypothalamo–pituitary–gonadal (HPG) axis and reproductive functions. Recently, we reported that PNX-14, its precursor protein and receptor were expressed in human endometrium. Moreover, PNX-14 serum levels in endometriosis were reduced. This study aimed to evaluate the in vitro biological functions of physiological PNX-14 concentrations on the ectopic endometrium Z12 cells. MethodsThe proliferation and migration of Z12 cells were assessed using the xCELLigence® RTCA DP system following 72 h of stimulation with 0.05 and 0.2 nM of PNX-14. GPR173 and small integral membrane protein 20 (SMIM20) gene expression was evaluated using quantitative polymerase chain reaction (qPCR) and the protein levels of GPR173 were analyzed using Western blot analysis. ResultsPNX-14 at the concentration observed in the serum of patients with endometriosis (0.05 nM) reduced GPR173 and increased SMIM20 expression, while protein levels of GPR173 remained unchanged. Cell proliferation was increased by the 0.02 nM PNX-14— the concentration found in healthy subjects. The 0.2 nM of PNX-14 decreased SMIM20 expression with no change to GPR173 expression and reduced ectopic epithelial cell proliferation during the first 5 h after stimulation. However, at 72 h, the proliferation increased. ConclusionsThis study shows that PNX-14 at endometriosis specific concentration desensitized ectopic epithelium to PNX-14, and increased the expression of SMIM20 to restore the physiological levels of PNX-14.

Contribution of Trp63CreERT2-labeled cells to alveolar regeneration is independent of tuft cells.

Viral infection often causes severe damage to the lungs, leading to the appearance of ectopic basal cells (EBCs) and tuft cells in the lung parenchyma. Thus far, the roles of these ectopic epithelial cells in alveolar regeneration remain controversial. Here, we confirm that the ectopic tuft cells are originated from EBCs in mouse models and COVID-19 lungs. The differentiation of tuft cells from EBCs is promoted by Wnt inhibition while suppressed by Notch inhibition. Although progenitor functions have been suggested in other organs, pulmonary tuft cells don't proliferate or give rise to other cell lineages. Consistent with previous reports, Trp63CreERT2 and KRT5-CreERT2-labeled ectopic EBCs do not exhibit alveolar regeneration potential. Intriguingly, when tamoxifen was administrated post-viral infection, Trp63CreERT2 but not KRT5-CreERT2 labels islands of alveolar epithelial cells that are negative for EBC biomarkers. Furthermore, germline deletion of Trpm5 significantly increases the contribution of Trp63CreERT2-labeled cells to the alveolar epithelium. Although Trpm5 is known to regulate tuft cell development, complete ablation of tuft cell production fails to improve alveolar regeneration in Pou2f3-/- mice, implying that Trpm5 promotes alveolar epithelial regeneration through a mechanism independent of tuft cells.

Arf6 regulates endometriotic epithelial-mesenchymal transition and mitochondrial distribution

Objective: To investigate the role of adenosine diphosphate ribosylation factor 6 (Arf6) in the pathogenesis of endometriosis. Methods: Endometrial tissues were sampled from women who were hospitalized in the Affiliated Hospital of Medical School of Ningbo University and Ningbo Women and Children's Hospital from November 2020 to May 2021 with endometriosis (n=44, endometriosis group) and without endometriosis (n=17, control group). The expression of Arf6 protein in the endometrial tissues was detected by western blot. Endometrial epithelial cells from both groups were primary cultured and the distribution of intracellular mitochondria was detected by immunofluorescence. The expression of Arf6 protein was down-regulated by small interference RNA (siRNA), the distribution of mitochondria in cells with decreased Arf6 protein expression was observed, and the expression of mitochondria-related proteins development and differentiation enhancing factor 1 (DDEF1, also called AMAP1), reactive oxygen species 1 (ROS1) and epithelial-mesenchymal transition (EMT)-related proteins E-cadherin, vimentin were detected. Transwell assay was used to detect the changes in the migration ability of the cells. Results: Compared with the control group, ectopic endometrial tissue of endometriosis group showed high expression of Arf6 protein (0.174±0.019 vs 0.423±0.033; t=29.630, P<0.01); and in ectopic endometrial epithelial cells, mitochondria were distributed near the edge of the cell membrane. While Arf6 expression was down-regulated by siRNA, the distribution of mitochondria in ectopic cells returned to natural, close to the control level. In addition, the expression levels of AMAP1 and ROS1 in ectopic cells after Arf6 protein knockdown were significantly decreased. Transwell assay results indicated that knockdown of Arf6 could reduce the migration ability of ectopic epithelial cells [migration cell count: (34.3±7.5) cells]; and immunofluorescence verified low expression of E-cadherin but high expression of vimentin in ectopic epithelial cells, whereas knockdown of Arf6 protein E-cadherin expression increased but vimentin expression decreased. Conclusions: High expression of Arf6 protein in ectopic endometrial epithelial cells leads to the distribution of mitochondria tending to membrane marginalization, while inducing EMT, which are involved in the mechanism of endoheterosis pathogenesis.

Trophic and immunomodulatory effects of adipose tissue derived stem cells in a preclinical murine model of endometriosis

Endometriosis, which exhibits enigmatic pathological features such as stromal fibrosis and proliferation of ectopic epithelial cells, is known as a refractory disease. Mesenchymal stem cells modulate the fibrosis in stromal tissues through their trophic and immunomodulatory properties. To investigate the potential of stem cells in treating endometriosis, we examined the secondary morphology and molecular alterations in endometriosis-like lesions after the administration of adipose tissue-derived stem cells (ASCs) to an experimental murine model of endometriosis. The infused ASCs were found integrated in the endometriosis-like lesions. Accompanied by the suppression of stromal fibrosis and proliferation of endometriotic epithelial cells, the infusion of ASCs with stemness potential (early passage of ASCs) suppressed the growth of endometriosis-like lesions and inhibited the expression of pro-inflammatory and pro-fibrotic cytokines, whereas no significant attenuation of endometriosis-like lesions occurred after the infusion of ASCs without stemness potential (late passage of ASCs). Accordingly, the trophic and immunomodulatory properties of ASCs may regulate fibrosis in endometriosis-like lesions, suggesting that regenerative medicine could be recognized as an innovative treatment for patients with endometriosis through the accumulation of evidence of preclinical efficacy.

The History of the Discovery of Ectopic Epithelial Cells in Lower Peritoneal Organs: The So-Called Mucosal Invasion

Through microscopy, early researchers identified the epithelium on the inner surfaces of the uterus, cervix and Fallopian tubes. The identification of ectopic epithelium was gradual, starting from the gross pathology study of unusual cystic lesions. Towards the end of the nineteenth century, attention focused on the epithelium as a critical component. The term ‘adenomyoma’ was coined around eighteen eighty to designate the majority of mucosa-containing lesions. Several theories were advanced to explain its aetiology. In the main, lesions were considered to arise from invasion from uterine epithelium; implantation of endometrium through retrograde menstruation; hematogenous or lymphatic spread; or from embryonic remnants. Although initially widely rejected, around 1920, an almost unanimous consensus formed on the endometrial nature of epithelial invasions. During the following years, adenomyosis and endometriosis came to be used to distinguished lesions within or outside the uterus. Adenomyosis was attributed to direct infiltration of uterine mucosa into the myometrium, and endometriosis to the implantation of endometrial cells and stroma into the peritoneal cavity through retrograde menstruation. Around the same time, ovarian lesions, initially described as ovarian hematomas or chocolate cysts, were regarded as a form of endometriosis. Three variants of endometriosis were thus described: superficial peritoneal, deep nodular and ovarian endometriomas. Ectopic epithelium has long been recognised as having similarities to tubal, or cervical epithelium. Lesions containing mixed epithelium are often termed Müllerianosis. This article demonstrates the stepwise evolution of knowledge, the role of the pioneers and the difficulties that needed to be overcome. It also demonstrates the value of collaboration and the inter-connected nature of the scientific endeavour.

Biomimetic niches reveal the minimal cues to trigger apical lumen formation in single hepatocytes.

The symmetry breaking of protein distribution and cytoskeleton organization is an essential aspect for the development of apicobasal polarity. In embryonic cells this process is largely cell autonomous, while differentiated epithelial cells collectively polarize during epithelium formation. Here, we demonstrate that the de novo polarization of mature hepatocytes does not require the synchronized development of apical poles on neighbouring cells. De novo polarization at the single-cell level by mere contact with the extracellular matrix and immobilized cadherin defining a polarizing axis. The creation of these single-cell liver hemi-canaliculi allows unprecedented imaging resolution and control and over the lumenogenesis process. We show that the density and localization of cadherins along the initial cell-cell contact act as key triggers of the reorganization from lateral to apical actin cortex. The minimal cues necessary to trigger the polarization of hepatocytes enable them to develop asymmetric lumens with ectopic epithelial cells originating from the kidney, breast or colon.

Dietary inclusion of Antarctic krill meal during the finishing feed period improves health and fillet quality of Atlantic salmon (Salmo salar L.).

There is an urgent need to find alternative feed resources that can further substitute fishmeal in Atlantic salmon diets without compromising health and food quality, in particular during the finishing feeding period when the feed demand is highest and flesh quality effects are most significant. This study investigates efficacy of substituting a isoprotein (35 %) and isolipid (35 %) low fishmeal diet (FM, 15 %) with Antarctic krill meal (KM, 12 %) during 3 months with growing finishing 2·3 kg salmon (quadruplicate sea cages/diet). Final body weight (3·9 (se 0·04) kg) was similar in the dietary groups, but the KM group had more voluminous body shape, leaner hearts and improved fillet integrity, firmness and colour. Ectopic epithelial cells and focal Ca deposits in intestine were only detected in the FM group. Transcriptome profiling by microarray of livers showed dietary effects on several immune genes, and a panel of structural genes were up-regulated in the KM group, including cadherin and connexin. Up-regulation of genes encoding myosin heavy chain proteins was the main finding in skeletal muscle. Morphology examination by scanning electron microscopy and secondary structure by Fourier transform IR spectroscopy revealed more ordered and stable collagen architecture of the KM group. NEFA composition of skeletal muscle indicated altered metabolism of n-3, n-6 and SFA of the KM group. The results demonstrated that improved health and meat quality in Atlantic salmon fed krill meal were associated with up-regulation of immune genes, proteins defining muscle properties and genes involved in cell contacts and adhesion, altered fatty acid metabolism and fat deposition, and improved gut health and collagen structure.

Impaired Localization of Claudin-11 in Endometriotic Epithelial Cells Compared to Endometrial Cells.

Claudins are the major components of tight junctions and are often deregulated in human cancer, permitting escape of cancer cells along with the acquisition of invasive properties. Similarly, endometrial cells also show invasive capabilities; however, the role of tight junctions in endometriosis has only rarely been examined. In this study, we analyzed the protein expression and localization of claudin-7 and claudin-11 in human eutopic and ectopic endometrium and endometrial cell lines. We identified claudin-7 primarily at the basolateral junctions of the glandular epithelial cells in eutopic endometrium as well as in the ectopic lesions in nearly all glands and cysts. Quantification of claudin-7 localization by HSCORE showed a slight increase in peritoneal and deep infiltrating endometriosis (DIE) compared to eutopic endometrium. In contrast, claudin-11 was localized mainly in the apicolateral junctions in nearly all glandular epithelial cells of the eutopic endometrium. Interestingly, we observed a deregulation of claudin-11 localization to a basal or basolateral localization in ovarian (P < .001), peritoneal (P < .01), and DIE (P < .05) and a moderately decreased abundance in ovarian endometriosis. In endometrial cell lines, claudin-7 was only present in epithelial Ishikawa cells, and silencing by small-interfering RNA increased cell invasiveness. In contrast, claudin-11 could be demonstrated in Ishikawa and endometriotic 12Z and 49Z cells. Silencing of claudin-11 decreased invasiveness of 12Z slightly but significantly in 49Z. We suggest that although claudin-7 and claudin-11 can be found in nearly all eutopic and ectopic epithelial cells, the impaired localization of claudin-11 in ectopic endometrium might contribute to the pathogenesis of endometriosis.

Ectopic epithelial cell clusters in salmonid intestine are associated with inflammation.

An epizootic incidence of intestinal adenocarcinomas was reported in brood fish of Atlantic salmon (Salmo salar L.) in 2009. The condition was associated with a specific diet inducing enteritis and morphological changes. Here, two field trials of fish up to slaughter size were initiated. In Trial 1, two different feed recipes were used. Feed I was predominantly based on marine ingredients, whereas plant ingredients were limited to soy protein concentrate and wheat. Feed II was lower in fishmeal and without soya protein, which was substituted with plant proteins from other sources. In Trial 2, a commercial feed (Feed III) was included. No macroscopic tumours were observed in 300 fish (Trial 1). At the end of both trials, samples from five different segments of the gastrointestinal tract of a total of 39 fish were investigated with morphological methods. Here, we show the presence of ectopic proliferating epithelial cells only occurring in inflamed intestine and predominantly in the second segment of the mid-intestine. Presence of ectopic epithelial cells in submucosal inflammatory foci may indicate early stages in tumorigenesis, but other possibilities such as proliferative enteric disorders cannot be excluded. Together with inflammation, carcinogenesis should be a focus of investigation in future feed trials.

Local upregulation of transient receptor potential ankyrin 1 and transient receptor potential vanilloid 1 ion channels in rectosigmoid deep infiltrating endometriosis.

Transient Receptor Potential Vanilloid 1 (TRPV1) and Transient Receptor Potential Ankyrin 1 (TRPA1) expressed mainly by primary sensory neurons function as major nociceptive integrators. They are also present on the rat endometrium in an oestrogen-regulated manner. TRPV1 is upregulated in peritoneal and ovarian endometriosis patients, but there is no information about TRPA1 and their pathophysiological significances. In this study, patients undergoing laparoscopic surgery were investigated: severe dysmenorrhoea due to rectosigmoid deep infiltrating endometriosis (n = 15), uterine fibroid-induced moderate dysmenorrhoea (n = 7) and tubal infertility with no pain (n = 6). TRPA1 and TRPV1 mRNA and protein expressions were determined by quantitative polymerase chain reaction and semi-quantitative immunohistochemistry from the endometrium samples taken by curettage. Results were correlated with the clinical characteristics including pain intensity. TRPA1 and TRPV1 receptors were expressed in the healthy human endometrium at mRNA and protein levels. Sparse, scattered cytoplasmic TRPA1 and TRPV1 immunopositivities were found in the stroma and epithelial layers. We detected upregulated mRNA levels in deep infiltrating endometriosis lesions, and TRPV1 gene expression was also elevated in autocontrol endometrium of deep infiltrating endometriosis patients. Histological scoring revealed significant TRPA1 and TRPV1 difference between deep infiltrating endometriosis stroma and epithelium, and in deep infiltrating endometriosis epithelium compared to control samples. Besides, we measured elevated stromal TRPV1 immunopositivity in deep infiltrating endometriosis. Stromal TRPA1 and TRPV1 immunoreactivities strongly correlated with dysmenorrhoea severity, as well TRPV1 expression on ectopic epithelial cells and macrophages with dyspareunia. Epithelial TRPA1 and stromal TRPV1 immunopositivity also positively correlated with dyschezia severity. We provide the first evidence for the presence of non-neuronal TRPA1 receptor in the healthy human endometrium and confirm the expression of TRPV1 channels. Their upregulations in rectosigmoid deep infiltrating endometriosis lesions and correlations with pain intensity suggest potential roles in pathophysiological mechanisms of the disease.

TNFα-induced IKKβ complex activation influences epithelial, but not stromal cell survival in endometriosis.

Can the activity of the IκB kinase (IKKβ) complex in endometriotic cells contribute to endometriotic lesion survival? There is a constitutive activity of the IKKβ catalytic complex in peritoneal and deeply infiltrating lesions that can influence epithelial, but not stromal cell viability. Endometriotic lesions exist in an inflammatory microenvironment with higher local concentrations of cytokines, such as tumour necrosis factor α (TNFα). TNFα stimulates the activation of the IKKβ complex, an important nodal point in multiple signalling pathways that influence gene transcription, proliferation and apoptosis. However, few data on the regulation of IKKβ in endometriotic tissue are currently available. A retrospective analysis of endometriotic tissue from peritoneal, ovarian and deeply infiltrating lesions from 37 women. Basal and activated (phosphorylated) IKKβ concentrations were analysed by western blotting and immunohistochemistry. The relationship between the expression and activation of these proteins and peritoneal fluid (TNFα) concentrations, measured via ELISA, was examined. A subsequent in vitro analysis of TNFα treatment on the activation of IKKβ and the effect on epithelial and stromal cell viability by its inhibition with PS1145 was also performed. Levels of the phosphorylated IKKβ complex in endometriotic lesions had a significant positive correlation with peritoneal fluid TNFα concentrations. Phosphorylated IKKβ complex was more prevalent in peritoneal and deeply infiltrating endometriosis lesions compared with ovarian lesions. IKKβ was present in both epithelial and stromal cells in all lesions but active IKKβ was limited to epithelial cells. TNFα stimulated an increased expression of phosphorylated IKKβ and the inhibition of this kinase with PS1145 significantly influenced ectopic epithelial cells viability but not eutopic epithelial cells, or endometrial stromal cells. In vitro analysis on epithelial cells was performed with immortalized cell lines and not primary cell cultures and only low sample numbers were available for the study. The regulation of aberrant signalling pathways represents a promising yet relatively unexplored area of endometriosis progression. The IKKβ complex is activated by inflammation and is critical nodal point of numerous downstream kinase-signalling pathways, includingNFκB (nuclear factor κB), mTOR (mammalian target of rapamycin) and BAD (Bcl2-antagonist of cell death). This study shows a significant relationship between peritoneal fluid TNFα and IKKβ activation in epithelial cells that will have significant consequences for the continued survival of these cells at ectopic locations through the regulation of downstream pathways. None. The study was funded by the Swiss National Science Foundation (Grant Number 320030_140774). The authors have no conflict of interest to declare.

Endometriotic Epithelial Cell Response to Macrophage-Secreted Factors is Dependent on Extracellular Matrix Context.

Endometriosis is a chronic disease in which epithelial and stromal cells that resemble the eutopic endometrium are found in ectopic lesions. In order to examine how microenvironmental factors such as extracellular matrix and macrophages influence disease progression, 12Z (an immortalized ectopic epithelial cell line) were cultured on tissue culture plastic (TCP) or in gels of recombinant basement membrane (rBM) or collagen I. Unlike cells in other conditions, cells in rBM formed multi-cellular structures in a 67 kDa non-integrin laminin receptor (67LR)-dependent manner. To examine the impact of macrophage-secreted factors on cell behavior, 12Z cells on all three substrates were treated with conditioned media from differentiated THP-1 (an immortalized monocytic cell line). Significant proliferation and invasion was observed only with cells cultured in rBM, indicating that extracellular matrix cues help dictate cell response to soluble signals. Cells cultured on rBM were then treated with individual cytokines detected in the conditioned media, with increased proliferation observed following exposure to interleukin-8 (CXCL8/IL-8) and both increased proliferation and invasion following treatment with heparin-binding EGF-like growth factor (HB-EGF). This study suggests that rBM gels can be used to induce in vitro lesion formation in order to identify soluble factors that influence proliferation and invasion.

Ruptured intracranial dermoid cyst manifesting as new onset seizure: a case report

Intracranial dermoid cysts are rare tumors derived from ectopic epithelial cells. They are slow-growing benign entities, but can cause significant morbidity through compression of neurovascular structures and, rarely, rupture into the subarachnoid space. We present a rare case of a spontaneously ruptured intracranial dermoid cyst presenting as new onset seizures due to chemical meningitis caused by dissemination of fat droplets.

Expression of oct-4 and c-kit antigens in endometriosis

The objective of this study was to test the expression of the oct-4 and c-kit, both markers of stem cells, in the ectopic endometrial tissue of endometriotic lesions of women with severe endometriosis. Our findings show that ectopic epithelial cells express oct-4 and c-kit and this suggests that the ectopic endometrium in endometriosis has a stem cell origin and could explain the possible progression to ovarian cancer.

Studies on Function of P-Glycoprotein in Photodynamic Therapy of Endometriosis

The aim of the present study was to examine whether the effects of endometriosis-targeted photodynamic therapy (PDT), dependent on 5-aminolevulinic acid (ALA), rely on the presence of P-glycoprotein (P-gp), which is regarded as constituting one of the causes of multidrug resistance phenomenon. The significance of the undertaken studies reflects the complete absence of reports related to the modulation of P-gp activity and efficacy of PDT in patients with endometriosis. Tissue samples of normal endometria were obtained from eight women after hysterectomy who were diagnosed with cervical intra-epithelial neoplasia. Fragments of ovarian endometriosis were obtained from 15 women. Epithelial cells were isolated from the material and in in vitro conditions were preincubated with P-gp blocker-verapamil-before ALA-PDT. The cytotoxicity was evaluated using the XTT test, allowing us to estimate cell growth inhibition. Statistical analysis of the results involved the nonparametric Wilcoxon paired rank test and the Mann-Whitney U-test using the Statistica v5 software (p < 0.05). In parallel, P-gp presence in the analyzed material was evaluated using immunohistochemistry. In normal endometrial epithelium, verapamil was shown to intensify phototoxic effects at 2 and 4 mmol/L ALA (p < 0.05). In endometriotic epithelium, such intensification was noted in all examined concentrations of ALA (p < 0.001). Moreover, the ectopic epithelial cells were more sensitive than eutopic epithelial cells to PDT upon ALA alone, as well as after preincubation with verapamil. Immunohistohemical analysis allowed us to demonstrate the absence of glycoprotein P in normal endometrium. In endometriosis, P-gp was localised in both the epithelium and the stroma of the examined material. Phototoxic effects could be amplified in epithelial cells of endometriotic foci by appropriate action of verapamil and 5-aminolevulinic acid.

Endometriotic stromal cells lose the ability to regulate cell-survival signaling in endometrial epithelial cells in vitro

In normal endometrium, stromal factors regulate the growth of epithelial cells. However, epithelial cells in endometriotic lesions display increased proliferation and decreased apoptosis. This work tested the hypothesis that in endometriosis stromal cells lose the ability to regulate survival signaling and cell growth in epithelial cells. Primary normal, endometriotic eutopic and ectopic epithelial cells were cultured in the presence of medium conditioned by normal, eutopic and ectopic endometriotic endometrial stromal cells. Endometriotic epithelial cells showed higher Survivin expression than normal epithelial cells. Conditioned medium (CM) from normal or eutopic endometriotic stromal cells significantly inhibited the Survivin expression and AKt phosphorylation in normal or eutopic endometriotic epithelial cells. However, CM from ectopic endometriotic stromal cells did not have an inhibitory effect on normal or ectopic endometriotic epithelial cells. Inhibition of AKt phosphorylation and Survivin expression in normal or eutopic endometriotic epithelial cells in the presence of stromal factors from normal or eutopic endometriotic stromal cells was enhanced by progesterone, whereas progesterone had little effect in the presence of stromal factors from ectopic endometriotic stromal cells. The inability of ectopic endometriotic stromal cells to regulated PI3K/AKt/Survivin signaling and mediate the progesterone response in endometriotic epithelial cells may facilitate epithelial cell proliferation in endometriosis and promote the survival of endometriotic lesions.

Stem cell antigens in ectopic epithelial cells of endometriotic lesions: is endometriosis a disease originated from stem cells?

Oct-4 is a transcription factor, molecular marker for pluripotent cells and plays an essential role in maintaining the undifferentiated state necessary for cell pluripotency. It is well known that this protein is expressed in embryonic stem cells, germ cells and in embryo at various stages of development. Furthermore, it has been recently found in the epithelial cells of normal endometrium. We tested the expression of the Oct-4 and c-kit, both marker of stem cells, in the ectopic endometrial tissue of endometriotic lesions.

Wound healing by the rat lens after neodymium-YAG laser injury

Wound healing of the ocular lens after exposure to neodymium-YAG laser energy (3·9 − 4·2 mJ) was studied. Male Sprague-Dawley rats were killed 5 min and 5, 9 and 15 days after the anterior lens epithelium was injured by a laser pulse. Gross and biomicroscopic examination revealed that a white, opaque mass formed on the lens surface after about 30 min. Five days later, the opacified mass present on the lens surface was found to be composed of ectopic epithelial cells, protruding lens fibers and a variety of other cell types. Epithelial cells were also present in abundance on the capsule surface in the immediate vicinity of the wound. Deep to the capsule, the lens fibers were greatly swollen. Half of the epithelial mounts obtained 5 days after surgery showed disorganization of the epithelium at points distant from the eosinophilic scar. The opacified external mass had disappeared from all of the lenses obtained at the 15-day period. However, the scar was readily identifiable in epithelial whole mounts, methacrylate sections and SEM specimens obtained from lenses at this time period. At every time period, many cortical fibers were swollen although the amount of swelling was less at 15 days than at earlier periods. The changes observed are similar to the lenticular alterations that occur after experimentally induced, transcorneal mechanical injury of the lens.