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S Tabibzadeh

Publications and source records attributed to S Tabibzadeh.

At least 37 records · Page 2Linked to original sources
PubMed1997

Constitutive expression of the HTLV-I pX and env regions in Jurkat T-cells induces differential activation of SRE, CRE and NF kappa B pathways.

Human T-cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia/lymphoma (ATLL). HTLV Tax, the viral transcriptional activator, can activate a variety of cellular genes. HTLV-mediated T-cell transformation, however, may involve additional viral proteins expressed from singly- as well as doubly-spliced viral mRNA. To determine the combined effect of these viral proteins on cellular gene expression in Jurkat T-cells, we derived stable transfectants that constitutively express the HTLV-I pX and env regions (J3.9). J3.9 cells show substantially increased mRNA levels of egr-1 and c-jun but no induction of either CD25 or GM-CSF by Northern blotting. This pattern corresponded to the activation of an egr-1 but not a GM-CSF promoter-driven reporter construct in transient gene expression assays. In DNA electrophoretic mobility shift assays (EMSA), nuclear extract from J3.9 cells has significantly increased binding to CRE and SRE but not nuclear factor kappa B (NF kappa B) DNA oligos, as compared to J-Neo cell extract. These results suggest that low level expression of pX and env region gene products in Jurkat T-cells stimulates persistent activation of CRE- and SRE- but not NF kappa B-induced cellular genes.

Cyclic AMP Response Element-Binding Protein↗
PubMed1997

The progressive rise in the expression of alpha crystallin B chain in human endometrium is initiated during the implantation window: modulation of gene expression by steroid hormones.

Human endometrium undergoes sequential changes during the menstrual cycle and becomes receptive to implantation during a defined period in the secretory phase. We attempted to identify the genes expressed during this period by representational difference analysis (RDA). When the cDNAs of a proliferative endometrium were used as the driver and the cDNAs of a post-ovulatory day 5 endometrium were used as the tester, a number of bands were identified by RDA. DNA of the cloned RDA products revealed that the majority of the clones contained a fragment of a cDNA identical to that of a crystallin B chain. Northern blot analysis showed that the expression of the alpha crystallin B chain mRNA was absent during the proliferative phase. The expression of the mRNA of alpha crystallin B chain first appeared in the secretory phase, progressively increased during this phase and peaked in the late secretory endometria. The pattern of expression of alpha crystallin B chain mRNA in the endometrium of mature cycling baboons (Papio anubis) was similar to that seen in human endometrium. As revealed by Western blot analysis, the expression of the alpha crystallin B chain protein in human endometrium followed a pattern of expression similar to its mRNA. At the cellular level, the immunoreactive protein first appeared in the surface epithelial cells of human endometrium within the implantation window without significant immunoreactivity in the underlying glandular cells. During the mid- and late secretory phases, the intensity of staining in the epithelial cells was enhanced and an intense immunoreactivity was developed in the glandular epithelium, alpha crystallin B chain was virtually an epithelial product and no immunoreactivity for this protein was detectable in the stromal cells, endothelial cells or lymphoid cells. The expression of alpha crystallin B chain could be regulated, by medroxy progesterone acetate as well as by oestrogen withdrawal, in human endometrial carcinoma cells (EnCa-101), transplanted to nude mice. Based on the data presented here, the known function of alpha crystallin B chain and its distinct pattern of expression in human endometrium, we suggest that this protein is an important factor within the molecular repertoire that makes endometrium receptive to implantation.

Adult↗
PubMed1996

Heat shock proteins in human endometrium throughout the menstrual cycle.

Human endometrium is a steroid-sensitive tissue and there is evidence that supports the viewpoint that heat shock proteins (HSP) are implicated in the regulation of steroid function. Therefore, in this study we examined the expression of various members of the heat shock family of proteins in the steroid-responsive human endometrium. Western blot analysis revealed that the expression of HSP90 showed minimal changes throughout the menstrual cycle. When normalized to the amount of HSP90, the expression of HSP27, HSP60 and the constitutive form of heat shock protein 70 (HSC70) increased progressively during the late proliferative and early secretory phases, and diminished in the mid- to late secretory and menstrual phases. In contrast, the inducible form of heat shock protein 70 (HSP70) did not undergo these changes. The cellular and subcellular localizations of these proteins were examined in human endometria by immunohistochemical staining. With the exception of HSP70, which was found primarily in the epithelial cells, the immunoreactivity for other heat shock proteins was found in both the stroma and the epithelium. Immunoreactivity for HSP27 was found in the lymphoid aggregates within endometrial stroma, and both HSP27 and HSP90 were found in endothelial cells. The immunoreactive heat shock proteins were found in the nuclei and/or cytoplasm of cells. However, no consistent nuclear versus cytoplasmic staining emerged, and such localization was irrespective of the site, the cell type or the phase of the menstrual cycle. Our findings show that endometrium has a full complement of heat shock proteins. The menstrual cycle-dependent changes in the amounts of heat shock protein suggest regulation by steroid hormones.

Adult↗
PubMed1996

The signals and molecular pathways involved in human menstruation, a unique process of tissue destruction and remodelling.

Human endometrium is a specialized tissue that undergoes sequential phases of proliferation and secretory changes in order to support the implantation and growth of an embryo. If implantation does not occur, this tissue rapidly undergoes dissolution during the menstrual period. Tissue shedding during menstruation is associated with significant apoptosis, disordered expression of adhesion molecules, loss of filamentous (F) actin from cell borders and fragmentation of endometrial glands. On the other hand, compromise of integrity of vessels and dissolution of the extracellular matrix leads to bleeding and tissue dissolution. The processes of bleeding and tissue shedding during menstruation are precisely controlled by a number of systemic and local factors. The systemic signal that leads to menstruation is the withdrawal of the steroid hormones. The available evidence suggests but does not yet prove that tumour necrosis factor (TNF)-alpha may serve as the local signal contributing to the processes of menstrual shedding and bleeding. Secretion of metalloproteinases and their subsequent activation induced by plasmin facilitates degradation of extracellular matrices and bleeding. The menstrual process ceases by secretion of steroid hormones directly or through regulation of production or activation of signals that lead to tissue shedding and bleeding.

Actins↗
PubMed1996

Immunohistochemical analysis of the microanatomy of primate ovary.

The ovary is a complex organ composed of cells of diverse lineages. Therefore, in this study we examined whether immunolocalization of various cytoskeletal, epithelial, immune-cell, and neural-associated proteins can differentiate various cells in the baboon and human ovaries. Surface epithelial cells exhibited immunoreactivity for cytokeratin and desmin, however, they did not immunostain for other epithelial markers such as carcinoembryonic antigen or epithelial membrane antigen. Smooth muscle actin was distributed apically whereas vimentin was localized basally in these cells. Ova exhibited strong immunoreactivity for S-100, Leu-M1, and neurofilament and did not show immunoreactivity for epithelial and cytoskeletal proteins. In antral follicles and theca cells, and after formation of corpus luteum, both granulosa and theca cells expressed immunoreactivity for vimentin. Cytokeratins were absent in the preantral and antral follicles. However, atresia and development of apoptosis was associated with expression of immunoreactive cytokeratins in atretic follicles. Development of corpus luteum led to major changes in the immunophenotype of follicular cells. The mere presence of immunoreactivity for cytokeratin and a strong immunoreactivity for desmin in the luteinized granulosa and not in the theca cells allowed discrimination of these cells from each other and from their ancestral cells. Proliferating cell nuclear antigen was present in various ovarian cells except for ovum. The distinct patterns of expression of cytoskeletal, epithelial, and neural-associated proteins in various cells of the ovary facilitates their identification and discrimination.

Actins↗
PubMed1996

Murine IL-10 fails to reduce GVHD despite inhibition of alloreactivity in vitro.

Graft-versus-host disease (GVHD) is a serious complication following allogeneic bone marrow transplantation (BMT). Initial immunologic events that are thought to lead to clinical GVHD include allogeneic antigen presentation, CD4+ T cell proliferation and eventually generation of specific cytotoxic lymphocytes. Interleukin-10 (IL-10) has been shown to inhibit the function of antigen presenting cells (APC) and to reduce lymphocyte proliferation. In this study we investigated the possible role of recombinant murine IL-10 (rmIL-10) as prophylactic treatment of GVHD in a murine BMT model involving B10.BR donor mice (H-2k) and AKR recipients (H-2k). In particular, we wished to determine whether early post-BMT administration of IL-10 would suppress GVHD by interfering with macrophage function and inflammatory cytokine production during the proposed "afferent' phase of GVHD. In MLR assays, rmIL-10 significantly inhibited the proliferation of donor spleen cells when stimulated by irradiated recipient spleen cells in a dose-dependent manner. In murine BMT, rmIL-10 was administered exogenously by intraperitoneal injection of 100 U daily in two different dosage schedules, on days-1, 0, 1, 2, 3, 6 to target the early post-BMT phase, and days-1, 0, 3, 5, 7, 10 after BMT, to administer the same total dose throughout the engraftment period. IL-10 injected mice had lower plasma IL-1 alpha levels on day 3 (12 pg/ml vs 64 pg/ml in controls, P < 0.05), suggesting that both macrophage function and inflammatory cytokine production were inhibited. In contrast to the MLR data, no significant improvement in morbidity and mortality from GVHD was observed. Therefore, IL-10 does not appear to be useful in GVHD prophylaxis.

Animals↗
PubMed1995

The signals and molecular pathways involved in implantation, a symbiotic interaction between blastocyst and endometrium involving adhesion and tissue invasion.

Implantation is a complex process requiring the interaction of the blastocyst, and subsequently the developing embryo with the endometrium. Initially, the detailed cellular interactions implicated in this process were defined. More recently, many signals and molecular pathways are recognized that induce, or regulate the complex series of interactions required for implantation. In this review, the cellular and molecular interactions that take place during implantation are discussed.

Animals↗
PubMed1995

Signals and molecular pathways involved in apoptosis, with special emphasis on human endometrium.

Apoptosis is a selective process for deletion of cells in various biological systems. This event, similar to proliferation, is tightly regulated, with both processes playing essential roles in the homeostasis of renewable tissues. In human endometrium, proliferation and apoptosis occur at opposing poles of the menstrual cycle. The proliferative phase is marked by rapid growth of the endometrial epithelial lining, whereas progressive increase in apoptosis in this tissue is the hallmark of the secretory and menstrual phases. The purpose of this review is to highlight some of the signals and molecular events which are associated with and that may participate in apoptosis. This is followed by a review of the current literature regarding apoptosis in human endometrium.

Apoptosis↗
PubMed1995

Progressive rise in the expression of interleukin-6 in human endometrium during menstrual cycle is initiated during the implantation window.

In order to be prepared for implantation, human endometrium undergoes a predictable series of proliferative and secretory changes. Cytokines play an important role in regulation of these changes. Therefore, in this study, we immunolocalized the cytokine, interleukin-6 (IL-6), its receptor and the signal transducer gp130 in human endometrium throughout the menstrual cycle. During the entire menstrual cycle, the IL-6 receptor and gp130 were found primarily in the endometrial glands and to a lesser extent in the stroma. The immunoreactivity of these proteins did not change in endometrial cells during the entire menstrual cycle with an exception of reduced immunoreactivity of gp130 in endometrial glands during menstrual phase. Immunostaining showed that immunoreactive IL-6 was weakly expressed in human endometrium during the proliferative phase. Strong immunoreactivity for IL-6 appeared in endometrium during the putative 'implantation window'. Expression was by far most pronounced both in the glandular and surface epithelial cells. The amount of immunoreactive IL-6 in the epithelium progressively increased during the secretory/menstrual phases. During the late secretory phase, only stromal cells in the upper functionalis exhibited immunoreactivity for IL-6. Western blot analysis corroborated the immunohistochemical data. Human endometrial IL-6 consisted of a protein with an apparent mobility of 26 kDa. The immunoreactive band of IL-6 was weak in the proliferative phase. The expression of this protein increased progressively during the secretory/menstrual phases. The findings show a cell-specific pattern of distribution for immunoreactive IL-6 in human endometrium. The menstrual cycle-dependent expression of IL-6 suggests that this cytokine may play a role in changes in endometrium that prepare this tissue for implantation and menstrual shedding.

Adult↗
PubMed1995

Site and menstrual cycle-dependent expression of proteins of the tumour necrosis factor (TNF) receptor family, and BCL-2 oncoprotein and phase-specific production of TNF alpha in human endometrium.

Apoptosis in human endometrial epithelium progressively increases from early to late secretory/menstrual phases and remains consistently more prominent in the basalis. It has been suggested that tumour necrosis factor (TNF) alpha secreted during the secretory/menstrual phases plays a role in induction of programmed cell death in these cells. In the present study, we characterized expression of receptors of TNF alpha, Fas antigen and BCL-2 in endometrial cells to gain insight as to whether this type of cell death in endometrium may be related to differential or preferential expression of these proteins at specific phases of the menstrual cycle. In addition, to relate production of TNF alpha to the development of apoptosis, the amount of TNF alpha released by human endometrium was measured. Immunostaining demonstrated that the TNF receptor (TNFr; p55/60)-I, TNFr-II (p75/80) as well as Fas protein were expressed in endometrial epithelium throughout the entire menstrual cycle. This expression was progressively diminished from the basalis towards the upper functionalis. In the proliferative phase, the expression of BCL-2 was prominent in the endometrial glands particularly in those residing in the basalis. This expression became weak as early as the third post-ovulatory day and remained low during the remaining phases of the menstrual cycle. The amount of TNF alpha released by endometrial fragments obtained from various phases of the menstrual cycle was determined. The amount of TNF alpha released into the culture medium by the endometrium was low in the proliferative phase. However, the amount of released TNF alpha progressively increased in the secretory phase and peaked in the menstrual phase. TNFr-I, TNFr-II, Fas, BCL-2 and TNF alpha could be identified by Western blot analysis of proteins extracted from endometrium. Therefore, endometrial epithelium by virtue of expression of receptors of TNF alpha as well as Fas protein is properly poised to respond to ligand signals that regulate apoptosis. Induction of apoptosis in endometrial epithelium and menstrual shedding may be related to loss of the protective effect of BCL-2 as well as to the amount of TNF alpha.

Antigens, Surface↗
PubMed1995

Menstruation is associated with disordered expression of desmoplakin I/II and cadherin/catenins and conversion of F- to G-actin in endometrial epithelium.

Endometrium is unique since it is the only tissue that undergoes regular cyclic bleedings. Menstrual shedding is associated with the breakdown of endometrium, including the fragmentation of endometrial glands. To gain insight into the underlying basis of fragmentation of the endometrial epithelium during the menstrual phase, we examined the expression of proteins implicated in epithelial cell-cell binding in human endometria throughout the entire menstrual cycle. Western blotting failed to reveal differences in the relative amount of E-cadherin, alpha- or beta-catenin or actin in the menstrual endometria compared with those in the proliferative or secretory phases. However, specific changes in the expression pattern of these proteins as well as desmoplakin I/II were detected by immunohistochemical staining in epithelial cells of menstrual endometria. Desmoplakin I/II, E-cadherin, alpha- and beta-catenins and beta-actin were localized to intercellular borders as well as the luminal and basal regions of glandular epithelium during the proliferative and secretory phases. Immunoreactivity of E-cadherin and alpha-catenin was confined to epithelial cells, whereas beta-catenin and beta-actin were present in epithelial cells, as well as in stroma and endothelial cells. Binding of F-actin to fluorescein isothiocyanate-labelled phalloidin localized this form of actin to the intercellular borders, and the basal and luminal cytoplasm of epithelial cells in proliferative and secretory endometria. Menstrual shedding was associated with disorganization of the site-specific distribution of desmoplakin I/II, E-cadherin and alpha- and beta-catenins.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1995

Tumour necrosis factor-alpha-mediated dyscohesion of epithelial cells is associated with disordered expression of cadherin/beta-catenin and disassembly of actin filaments.

Tumour necrosis factor (TNF)-alpha induced, in a time- and dose-dependent fashion, dyscohesion (cell-cell dissociation) of the endometrial epithelial cells. TNF-alpha impaired the ability of cells to aggregate and to attain compaction. The cell-cell adherent junction is a specialized region of the plasma membrane where cadherin molecules act as adhesion molecules and actin filaments are densely associated with the plasma membrane through a well-developed plasmalemmal undercoat. Dyscohesion induced by TNF-alpha was associated with the disordered expression of cadherin/beta-catenin at the sites of cell-cell contact. In addition, within the time-frame that dyscohesion was induced, TNF-alpha down-regulated the expression of actin mRNA only at 100 ng/ml without modulating the overall amount of actin protein, its beta-isoform or the amount of ribosylated actin. However, TNF-alpha-mediated dyscohesion of epithelial cells was associated with loss of plasmalemmal undercoat as well as intracytoplasmic aggregates of F-actin and a simultaneous increase in G-actin. The effect of cytochalasin-B, which disrupts actin filaments on cell-cell binding, was less pronounced than the effect of TNF-alpha, suggesting that the effect of this cytokine on dyscohesion is not solely dependent on the disassembly of actin filaments. These findings show that the induction of disordered expression of adhesion molecules, as well as disassembly of actin filaments, are implicated in the dyscohesion induced by TNF-alpha.

Actins↗
PubMed1994

Regulatory roles of IFN-gamma in human endometrium.

Available data suggest that several microenvironments exist within the complex structure of human endometrium. Predecidual reaction which is associated with the expression of VLA-1 and alpha 1 PEG first appears in the stromal cells around the spiral arteries. Expression of Ber-EP4 is limited to a distinct group of stromal cells that reside around glands and underneath surface epithelium. A distinctly different group of stromal cells that surround lymphoid cells express HLA-DR molecules. The proliferative activity of endometrial epithelium is markedly higher in the upper functionalis and is gradually diminished towards the basalis. In addition, several proteins, including HLA-DR and some members of the integrin family of molecules are strongly expressed in the basalis epithelium. The expression of these proteins in endometrial epithelium is gradually diminished towards the surface. The gradual rather than abrupt changes in the expression of proteins and proliferative activity across the length of endometrial epithelium argues against separation of endometrium into the distinct regions of basalis and functionalis. Rather, such distribution is in favor of existence of a polarized microenvironment in human endometrium. Emerging evidence suggests that the development of this microenvironment is mediated by T cells activated within lymphoid aggregates with consequent secretion of IFN-gamma. IFN-gamma regulates HLA-DR expression and proliferation of endometrial epithelium. Maximal impact of the cytokine is exerted in regions close to the source of cytokine with a gradual dissipation of the effect distant from this source. Therefore, this cytokine may be the prototype of a group of paracrine factors that induce a polarized microenvironment in human endometrium.

Endometrium↗
PubMed1994

Cytokines and the hypothalamic-pituitary-ovarian-endometrial axis.

Recently, the demarcating boundaries that allowed separation of the fields of reproductive biology, endocrinology, immunology and neurobiology have faded. The missing link that now ties these disciplines together is the understanding that the language by which cells communicate within these diverse systems is unanimous. This language is the network of products collectively called cytokines. The effect of these factors spans from the hypothalamus to the endometrium and is undoubtedly involved in the maintenance of the delicate balance within the hypothalamic-pituitary-gonadal-endometrial axis. Orchestrated networks of these cytokines also seem to be linked to the steroid hormone signals, an essential feature for maintenance of normal menstrual cycles. Evidence in favour of these emerging concepts is discussed. Major emphasis is placed on interferons, interleukins, tumour necrosis factor, transforming growth factors and colony-stimulating factors.

Body Temperature Regulation↗
PubMed1994

Expression of adhesion molecules in human endometrial vasculature throughout the menstrual cycle.

In the present study, we examined the pattern of expression of human leukocyte antigen (HLA)-DR as well as several adhesion molecules implicated in leukocyte trafficking, including ICAM-1, E-selectin, and VCAM-1 in human endometrium. All of the vessels in endometrium exhibited HLA-DR and ICAM-1 throughout the menstrual cycle. In the proliferative phase, endothelial cells in the functionalis were weak to nonreactive for VCAM-1 and were E-selectin negative (E-selectin-). Endothelial cells of the vessels in the basalis and within myometrium were VCAM positive (VCAM-1+)/E-selectin-. In sharp contrast, in the secretory phase, endothelial cells in the basalis were VCAM-1+/E-selectin+. Surprisingly, endometrial glands, primarily those in the basalis, expressed E-selectin and VCAM-1 during the entire menstrual cycle. Stromal cells were ICAM-1+ and were focally HLA-DR+ around HLA-DR+ lymphoid cells during the entire menstrual cycle and were E-selectin-/VCAM-1- during the proliferative phase. Immunoreactivity for VCAM-1 and E-selectin, however, appeared in the stromal cells in the upper functionalis in the secretory phase. Immunoreactivity for VCAM-1 was the distinguishing feature that separated the lymphoid cells in the aggregates from other nonaggregated lymphoid cells. Recruitment of leukocytes to tissues is in part due to cytokine-regulated expression of specific molecules on endothelial cells. Therefore, we tested the effects of cytokines on the expression of these molecules in endothelial cells derived from microvasculature. ICAM-1 and VCAM-1 were inducible in a dose-dependent fashion in the endothelial cells by interleukin-1 alpha (IL-1 alpha), interferon-gamma (IFN gamma), and tumor necrosis factor-alpha (TNF alpha). Expression of HLA-DR in endothelial cells was inducible by IL-1 alpha and IFN gamma and not by TNF alpha. Expression of E-selectin on endothelial cells was induced only by IL-1 alpha, not by IFN gamma or TNF alpha. Cytokine treatment of endothelial cells significantly enhanced the binding of leukocytes to endothelial cells. The data show a heterogeneity in the vasculature of endometrium with respect to the expression of various adhesion molecules. This heterogeneity is potentially related to the type or amount of cytokine with which endothelial cells are activated. In addition, unique cell- and site-specific expression of adhesion molecules in human endometrium throughout the menstrual cycle may account for the distinct distribution pattern of leukocytes in this tissue.

Adult↗
PubMed1993

Induction of a polarized micro-environment by human T cells and interferon-gamma in three-dimensional spheroid cultures of human endometrial epithelial cells.

Expression of human leukocyte antigen (HLA)-DR molecules and proliferation of epithelium in human endometrium are polarized. We have suggested that the induction of such a polarized micro-environment is T cell and interferon (IFN)-gamma dependent. The present study was designed to demonstrate the induction of such a micro-environment around T cells and around the source of IFN-gamma. Spheroids reminiscent of endometrial glands were formed by allowing three-dimensional aggregation of endometrial epithelial cells of a cloned HLA-DR negative endometrial carcinoma cell line (ECC1) over agarose. Both HLA-DR expression and inhibition of proliferation were found to be directly dependent on the dose of IFN-gamma that was allowed to diffuse in the agarose beneath the spheroids. To show that the interaction of the epithelial cells with activated T cells also induces HLA-DR molecules in a paracrine fashion in the epithelial cells, ECC1 spheroids were co-cultured with increasing numbers of allogeneic peripheral blood T cells for various time-intervals. T cells bound to the ECC1 cells, and became activated as indicated by the expression of interleukin (IL)-2 receptor and HLA-DR molecules. A focal HLA-DR expression became apparent in the ECC1 cells adjacent to the T cells. As the number of T cells added to spheroid cultures was increased, a concomitant increase in the number of HLA-DR positive ECC1 cells occurred and HLA-DR immunoreactivity was enhanced in each cell. There was a corresponding decrease in the proliferation of the ECC1 cells in T cell-ECC1 spheroid co-cultures. Based on these data, we suggest that activation of T cells is associated with the induction of HLA-DR expression and inhibition of proliferation in a paracrine fashion in the epithelial cells and may be responsible for the creation of a polarized micro-environment in vivo.

Animals↗
PubMed1992

Patterns of expression of integrin molecules in human endometrium throughout the menstrual cycle.

A heterogeneous group of cells interact with each other and with the surrounding matrix to form the complex structure of human endometrium. Since the integrin superfamily of molecules is involved in the cell-cell and cell-matrix interactions, this study was designed to screen, in situ, the cellular distribution of CDW49a-f molecules in human endometrium throughout the menstrual cycle. The integrin molecules were localized by immunohistochemistry using monoclonal antibodies. Glandular epithelium expressed all integrin molecules. With the exception of CDW49d (alpha 4 beta 1), surface epithelium also expressed all these molecules. Endothelial cells were positive for all integrin molecules except CDW49a (alpha 1 beta 1). Endometrial lymphoid cells were positively immunostained for CDW49a, d and e (alpha 5 beta 1) and were negative for CDW49b (alpha 2 beta 1), CDW49c (alpha 3 beta 1) and CDW49f (alpha 6 beta 1). Regional differences in the expression of integrin molecules were observed. As compared to the functionalis epithelium, basalis epithelium characteristically exhibited higher expression of CDW49a, d and e. Two integrins in endometrium, CDW49a and d exhibited changes related to the menstrual cycle. CDW49a, which was not expressed in glandular epithelial cells in the proliferative phase, was strongly expressed in these cells after ovulation and its expression was diminished in the late secretory phase. This molecule was not expressed in the stromal cells, however, predecidual cells characteristically expressed this molecule in the late secretory phase. CDW49d was only expressed in the glandular epithelial cells in the mid-proliferative to mid-secretory phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Endometrium↗