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Search Results: 1 - 10 of 241596 matches for " Bo R Rueda "
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Recent advancements in corpus luteum development, function, maintenance and regression: Forum introduction
John S Davis, Bo R Rueda
Reproductive Biology and Endocrinology , 2003, DOI: 10.1186/1477-7827-1-86
Abstract: The present series of reviews was designed to address some of these topics while focusing primarily on recent advances that have either not been covered or covered only superficially in recent reviews, and on areas of corpus luteum function that have changed considerably since they were originally addressed. In addition, the authors that contributed to this series of reviews were encouraged to identify areas that were controversial, to recognize differences among species, to convey a sense of direction that research efforts were taking, and finally to suggest areas for new research opportunities that will clarify or extend our knowledge of corpus luteum function.The corpus luteum forum is organized to sequentially convey recent developments in the development, function and regression of the corpus luteum. The initial review provides evidence gained from the phenotypic analysis of transgenic mice that has revealed unexpected and novel actions of particular molecules required for ovulation and corpus luteum function. The next set of reviews conveys the critical nature of angiogenesis for the overall development and function of the corpus luteum. The reviews also highlight the critical nature the endothelial cell as a pivotal element in the process of corpus luteum regression. Another series of reviews provides recent concepts on the control of the secretory nature of the corpus luteum. Highlighted are novel mechanisms for the control of luteal steroidogenesis, and recent developments in the regulation by prostaglandin F2α of prostaglandin and oxytocin secretion. The final series of reviews provide new directions for immune cell regulation of corpus luteum function via major histocompatibility complex molecules, chemokines and cytokines. The contributing authors have provided the state-of-the-art reviews that not only summarize our current knowledge of corpus luteum function but also to extend our insight into directions for further exploration.
Mutant mouse models and their contribution to our knowledge of corpus luteum development, function and regression
Luiz E Henkes, John S Davis, Bo R Rueda
Reproductive Biology and Endocrinology , 2003, DOI: 10.1186/1477-7827-1-87
Abstract: The corpus luteum is an important byproduct of the ovulating follicle. It is a transitory, hormonally regulated organ that consists of a heterogeneous cell population. Unlike the follicle, the different cell types are not segregated into distinct compartments, but are highly integrated. The steroidogenic cells synthesize progesterone for the establishment and maintenance of pregnancy. Other cell types include the endothelial cells and immune cells, typically thought to play supportive roles. There is evidence to suggest that the endothelial cells and the immune cells play an active role in luteal formation, maintenance and regression [1]. The vascular endothelial cells make up a large portion of the corpus luteum, whereas the immune cells vary in number dependent upon the stage of the luteal phase or pregnancy [1-3].Studies designed to elucidate the contributions of one or more of the luteal cell types are often difficult to interpret. More often than not these studies are based on in vitro cell culture models. Primary cultures of dispersed luteal tissue or enriched populations of specific cell types provide some opportunity for investigators to delineate potential signaling pathways, which may be engaged in response to a specific stimulus. Outcomes derived from in vitro studies are important but are often subject to criticism. For example, in vitro studies tend to favor one cell type or another. Moreover, the cell-cell interactions that are present in a multidimensional environment in vivo are removed when experiments are performed in a two dimensional field in vitro (eg, tissue culture dish). What effect this has on an outcome is not always fully appreciated and cannot be directly extrapolated to the in vivo model. For example prostaglandin F2α (PGF2α) is primarily considered a luteolytic agent in vivo, yet it has no direct lytic effect on endothelial cells or steroidogenic cells in vitro [1,4,5]. This raises a number of questions. Is the response observed in vitr
Microvascular endothelial cells of the corpus luteum
John S Davis, Bo R Rueda, Katherina Spanel-Borowski
Reproductive Biology and Endocrinology , 2003, DOI: 10.1186/1477-7827-1-89
Abstract: The vascular endothelium of the mature ovarian follicle maintains the capacity for rapid growth in response to angiogenic signals elaborated during the periovulatory process. New blood vessel growth is essential for the formation and function of the corpus luteum. Analogous to events occurring in the corpus luteum, the vascular endothelium of other tissues responds to extracellular signals during the physiologic processes of embryonic development and wound healing, and in the pathologic process of tumor angiogenesis. Although the corpus luteum is a transient tissue, it is one of the most highly vascularized tissues in the body [1] with endothelial cells representing greater than fifty percent of the total cells [2,3]. Endothelial cell proliferation and vascular changes have been examined throughout the luteal phase in rat [4,5], rabbit [6], pig [7], sheep [8,9], cow [10-13], horse [14], marmoset [15], macaque [16], and human [17] corpora lutea. The vascular elements in these studies were determined using markers of endothelial cells (von Willebrand factor VIII related antigen, FVIIIr antigen; angiotensin-converting enzyme, ACE; lectin binding, e.g., Griffonia Simplicifolia agglutinin and Ulex Europaeus agglutinin; and platelet/endothelial cell adhesion molecule-1, PECAM-1). Evidence of proliferating endothelial cells was determined by the presence of Ki-67 antigen-positive cells, bromodeoxyuridine-positive cells, or [3H] thymidine-positive cells. Collectively, these studies demonstrate that the rate of endothelial cell proliferation is highest during corpus luteum formation, then decreases and remains low during the mid-luteal phase and structural regression of the corpus luteum. The establishment of an extensive vascular network is an essential component of corpus luteum development, since the inhibition of angiogenesis during corpus luteum formation is associated with inadequate corpus luteum function [3,12,18-21].The regulation of endothelial cell proliferation i
Inhibition of AKT with the Orally Active Allosteric AKT Inhibitor, MK-2206, Sensitizes Endometrial Cancer Cells to Progestin
Alok Pant, Irene I. Lee, Zhenxiao Lu, Bo R. Rueda, Julian Schink, J. Julie Kim
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041593
Abstract: Progestin resistance is a major obstacle to treating early stage, well-differentiated endometrial cancer as well as recurrent endometrial cancer. The mechanism behind the suboptimal response to progestin is not well understood. The PTEN tumor suppressor gene is frequently mutated in type I endometrial cancers and this mutation results in hyperactivation of the PI3K/AKT pathway. We hypothesized that increased activation of AKT promotes an inadequate response to progestins in endometrial cancer cells. Ishikawa cells stably transfected with progesterone receptor B (PRB23 cells) were treated with the AKT inhibitor, MK-2206, which effectively decreased levels of p(Ser473)-AKT in a dose-dependent (10 nM to 1 uM) and time-dependent manner (0.5 h to 24 h). MK-2206 inhibited levels of p(Thr308)-AKT and a downstream target, p(Thr246)-PRAS40, but did not change levels of p(Thr202/Tyr204)ERK or p(Thr13/Tyr185)SAPK/JNK, demonstrating specificity of MK-2206 for AKT. Additionally, MK-2206 treatment of PRB23 cells resulted in a significant increase in levels of progesterone receptor B (PRB) protein. Microarray analysis of PRB23 cells identified PDK4 as the most highly upregulated gene among 70 upregulated genes in response to R5020. Inhibition of AKT further upregulated progestin-mediated expression of PDK4 but did not affect another progestin-responsive gene, SGK1. Treatment of PRB23 cells with R5020 and MK-2206 independently decreased viability of cells while the combination of R5020 and MK-2206 caused the greatest decrease in cell viability. Furthermore, mice with xenografted tumors treated with MK-2206 alone or with progesterone alone exhibited modest reductions in their tumor volume. The largest decrease in tumor size was observed in the mice treated with both MK-2206 and progesterone; these tumors exhibited the least proliferation (Ki67) and the most apoptosis (cleaved caspase-3) of all the treatment groups. In summary, inhibition of AKT stabilizes the Progesterone Receptor B and augments progesterone response in endometrial cancer cells that have hyperactivated AKT.
Signaling mechanisms in tumor necrosis factor alpha-induced death of microvascular endothelial cells of the corpus luteum
James K Pru, Maureen P Lynch, John S Davis, Bo R Rueda
Reproductive Biology and Endocrinology , 2003, DOI: 10.1186/1477-7827-1-17
Abstract: Progesterone derived from the corpus luteum (CL) is required for the establishment and maintenance of a suitable uterine environment during early pregnancy [1,2]. Inappropriate luteal function (i.e. luteal insufficiency) may contribute to the high incidence of spontaneous abortions that occur early in mammalian pregnancies [3]. In most species, the luteolytic cascade, starting with loss of progesterone production and followed by tissue regression (i.e. apoptosis), is initiated by prostaglandin F2α (PGF2α) in vivo [4]. However, this process can only be partially recapitulated in vitro using primary cultures of steroidogenic cells. Gonadotropin-induced progesterone production is attenuated by PGF2α treatment, but this prostanoid does not activate apoptosis of bovine steroidogenic cells in vitro [8]. These findings helped develop the concept that additional factors, such as immune cells [5-7] or cytokines [7,8], contribute to the luteolytic process. Indeed, tumor necrosis factor α (TNFα), interferon gamma (IFNγ) and/or interleukin-1 beta (IL-1β) have all been shown to reduce gonadotrophin-induced progesterone synthesis in a number of species [8-12], and TNFα and IFNγ are known to increase PGF2α production by steroidogenic cells [13-15]. Steroidogenic cell apoptotic paradigms are activated by cytokines generated by several cell types within the CL, including immune cells and endothelial cells [7,11,16]. The synergistic actions of IFNγ and TNFα, for example, induce steroidogenic cell apoptosis [13,17], as does soluble Fas ligand (FasL) [18-26]. Furthermore, several acute intracellular signaling events either required for, or associated with, the functional and structural aspects of luteal regression have been mapped using in vitro steroidogenic cell cultures [8,27,28].The microvasculature of the CL is thought to be the first structure to undergo degeneration via apoptosis during luteolysis [2,8]. In contrast to information available on steroidogenic cells of the CL, a ga
Leptin-signaling inhibition results in efficient anti-tumor activity in estrogen receptor positive or negative breast cancer
Ruben Rene Gonzalez, Amber Watters, Yanbo Xu, Udai P Singh, David R Mann, Bo R Rueda, Manuel L Penichet
Breast Cancer Research , 2009, DOI: 10.1186/bcr2321
Abstract: To test the contribution of leptin signaling to BC growth and expression of leptin-targeted molecules, PEG-LPrA2 treatment was applied to severe immunodeficient mice hosting established ER+ (MCF-7 cells; ovariectomized/supplemented with estradiol) and ER- (MDA-MB231 cells) BC xenografts. To further assess leptin and PEG-LPrA2 effects on ER+ and ER- BC, the expression of VEGF and VEGFR2 (protein and mRNA) was investigated in cell cultures.PEG-LPrA2 more effectively reduced the growth of ER+ (>40-fold) than ER- BC (twofold) and expression of pro-angiogenic (VEGF/VEGFR2, leptin/leptin receptor OB-R, and IL-1 receptor type I) and pro-proliferative molecules (proliferating cell nuclear antigen and cyclin D1) in ER+ than in ER- BC. Mouse tumor stroma in ER+ BC expressed high levels of VEGF and leptin that was induced by leptin signaling. Leptin upregulated the transcriptional expression of VEGF/VEGFR2 in MCF-7 and MDA-MB231 cells.These results suggest that leptin signaling plays an important role in the growth of both ER+ and ER- BC that is associated with the leptin regulation of pro-angiogenic and pro-proliferative molecules. These data provide support for the potential use of leptin-signaling inhibition as a novel treatment for ER+ and ER- BC.Leptin is a small nonglycosylated protein (16 kDa) product of the ob gene. White adipose tissue is the primary source of leptin in benign tissue, but leptin is also expressed and secreted by cancer cells [1]. Leptin exclusively binds to its receptor, OB-R. Several isoforms of OB-R are found in diverse tissues and in cancer cells including the long isoform, OB-Rb [2,3]. Upon leptin activation, the OB-R isoforms can utilize a number of diverse signaling pathways relevant to cancer growth [4,5]. The well-documented biological actions of leptin at the hypothalamic level occur through OB-Rb signals that are linked to the control of appetite and energy balance [4].Evidence is mounting to support the idea that leptin is the link between
Metformin therapy in a hyperandrogenic anovulatory mutant murine model with polycystic ovarian syndrome characteristics improves oocyte maturity during superovulation
Mary E Sabatini, Lankai Guo, Maureen P Lynch, Joseph O Doyle, HoJoon Lee, Bo R Rueda, Aaron K Styer
Journal of Ovarian Research , 2011, DOI: 10.1186/1757-2215-4-8
Abstract: We utilized metformin treatment in the transgenic ob/ob and db/db mutant murine models which demonstrate metabolic and reproductive characteristics similar to women with PCOS. Results: Metformin did not improve in vitro oocyte maturation nor did it have an appreciable effect on in vitro granulosa cell luteinization (progesterone production) in any genotype studied. Although both mutant strains have evidence of hyperandrogenemia, anovulation, and hyperinsulinemia, only db/db mice treated with metformin had a greater number of mature oocytes and total overall oocytes compared to control. There was no observed impact on body mass, or serum glucose and androgens in any genotype.Our data provide evidence to suggest that metformin may optimize ovulatory performance in mice with a specific reproductive and metabolic phenotype shared by women with PCOS. The only obvious difference between the mutant murine models is that the db/db mice have elevated leptin levels raising the questions of whether their response to metformin is related to elevated leptin levels and/or if a subset of PCOS women with hyperleptinemia may be responsive to metformin therapy. Further study is needed to better define a subset of women with PCOS that may be responsive to metformin.Polycystic ovarian syndrome (PCOS) is a complex, multifactorial endocrinopathy which affects approximately 4 to 10% of reproductive-aged women. Because it is a highly heterogeneous syndrome with a variable clinical presentation, criteria for diagnosis have been debated. Many authorities utilize the guidelines of Rotterdam/ASRM-sponsored PCOS Consensus Workshop Group [1] and require the presence of at least two of the following: oligoovulation and/or anovulation, evidence of clinical or biochemical hyperandrogenism, and the presence of polycystic ovarian morphology during ultrasound examination.PCOS is associated with several significant morbidities including infertility, obesity, insulin resistance, type 2 diabetes, dyslipi
Prostaglandin F2alpha- and FAS-activating antibody-induced regression of the corpus luteum involves caspase-8 and is defective in caspase-3 deficient mice
Silvia F Carambula, James K Pru, Maureen P Lynch, Tiina Matikainen, Paulo Bayard D Gon?alves, Richard A Flavell, Jonathan L Tilly, Bo R Rueda
Reproductive Biology and Endocrinology , 2003, DOI: 10.1186/1477-7827-1-15
Abstract: Prostaglandin F2α (PGF2α) has been implicated as a luteolysin in a number of mammalian species [1-3]. However, the exact mechanism(s) by which PGF2α elicits its response in the corpus luteum (CL) remains unclear. Results from previous studies have implicated so-called death receptor-activating cytokines, such as tumor necrosis factor α (TNFα) and Fas ligand (FasL), as being important mediators of PGF2α-initiated luteolysis [4-6]. Unfortunately, since the vast majority of evidence supporting a role for cytokines in luteal regression has been derived from in vitro studies of dispersed cells in culture [5,7-14], it is currently unknown if PGF2α modulates death receptor-coupled signaling pathways in the CL in vivo.At least 29 TNF receptor super family members have been identified in the human [15] some of which have been deemed death receptors either by their action or because they contain the highly homologous amino acid sequence corresponding to death domain (DD) [15,16]. The FAS/FasL system was chosen for study herein because FAS is recognized as a death receptor and indirect evidence suggests that it plays a significant role in luteal regression. For example, FAS immunostaining is observed in human granulosa-lutein cells during the early luteal phase, and progressively intensifies during the mid-luteal phase through the late luteal phase [17]. This expression pattern is also observed in the CL of mice [18] and rats [19,20]. In keeping with the proposal that FAS plays a role in luteolysis, in vitro studies have shown that FasL or FAS-activating antibodies induce luteal cell death in the human [10], mouse [5,18], rat [19,20] and cow [21]. Moreover, limited in vivo work has demonstrated that intravenous or intraperitoneal administration of FAS-activating antibody causes luteolysis in the mouse [18].Additional support for a functional role of FAS in luteal regression has been derived from experiments with homozygous lpr mice, which have non-functional or minimally-funct
On Two Complementary Types of Total Time Derivative in Classical Field Theories and Maxwell's Equations
R. Smirnov-Rueda
Physics , 2005, DOI: 10.1007/s10701-005-6515-8
Abstract: Close insight into mathematical and conceptual structure of classical field theories shows serious inconsistencies in their common basis. In other words, we claim in this work to have come across two severe mathematical blunders in the very foundations of theoretical hydrodynamics. One of the defects concerns the traditional treatment of time derivatives in Eulerian hydrodynamic description. The other one resides in the conventional demonstration of the so-called Convection Theorem. Both approaches are thought to be necessary for cross-verification of the standard differential form of continuity equation. Any revision of these fundamental results might have important implications for all classical field theories. Rigorous reconsideration of time derivatives in Eulerian description shows that it evokes Minkowski metric for any flow field domain without any previous postulation. Mathematical approach is developed within the framework of congruences for general 4-dimensional differentiable manifold and the final result is formulated in form of a theorem. A modified version of the Convection Theorem provides a necessary cross-verification for a reconsidered differential form of continuity equation. Although the approach is developed for one-component (scalar) flow field, it can be easily generalized to any tensor field. Some possible implications for classical electrodynamics are also explored.
On Mathematical Defect in Demonstration of Convection Theorem: Implications For Continuum Mechanics and Other Classical Field Theories
R. Smirnov-Rueda
Physics , 2005,
Abstract: Serious mathematical defect in the important kinematics theorem known in continuum mechanics as Convection (or Transport) Theorem is reported. We claim that the traditional demonstration does not take into account a special constraint on integrand functions given in Lagrangian representation. Thus, we put in doubt that the traditional procedure for the transition from integral formulations of physical laws of some classical field theories to their differential form is mathematically rigorous. Reconsidered formulation shows the way how the system of fundamental differential equations of continuum mechanics and some other field theories could be modified without any change of the original integral formulation. The continuity equation and the differential form of the equation of motion for continuous media are discussed as examples of modification.
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