The Experts below are selected from a list of 150 Experts worldwide ranked by ideXlab platform
Ayman Al-hendy - One of the best experts on this subject based on the ideXlab platform.
-
Towards non-surgical therapy for uterine fibroids: catechol-O-Methyl Transferase inhibitor shrinks uterine fibroid lesions in the Eker rat model
Human reproduction (Oxford England), 2011Co-Authors: Memy H. Hassan, Hala Fouad, S. Bahashwan, Ayman Al-hendyAbstract:BACKGROUND Uterine leiomyomas (fibroids) are the most common pelvic tumors in women. We assessed the potential therapeutic utility of Ro 41-0960, a synthetic catechol-O-Methyl Transferase inhibitor (COMTI), in the Eker rat.
-
Progesterone-Mediated Regulation of Catechol-O-Methyl Transferase Expression in Endometrial Cancer Cells
Reproductive sciences (Thousand Oaks Calif.), 2007Co-Authors: Sana M. Salih, Salama A. Salama, Amin A. Fadl, Manubai Nagamani, Mohammad Jamaluddin, Leen J. Blok, Curt W. Burger, Ayman Al-hendyAbstract:The effects of estrogen and progesterone on the expression of estrogen-metabolizing enzymes such as catechol-O-Methyl Transferase (COMT) are not known. COMT converts genotoxic catecholestrogens to anticarcinogenic methoxyestrogens in the endometrium. The aim of this study is to investigate the effect of progesterone on COMT expression in well-differentiated endometrial cancer cells. The wild-type Ishikawa cell line as well as progesterone receptor A- or progesterone receptor B-transfected Ishikawa cells were used for in vitro studies. The regulation of COMT expression by progesterone was studied using Western blots, Hoechst dye DNA proliferation studies, and wild-type and/or site-directed mutagenesis of COMT promoter 1-luciferase reporter gene. Progesterone upregulated COMT protein expression in Ishikawa cells through progesterone receptor A isoform. COMT promoter activity was differentially regulated by the 3 half-site progesterone response elements in the COMT promoter. High doses of 2-ME2 inhibited Ishikawa cell proliferation. These data suggest that COMT expression is hormonally regulated in well-differentiated human endometrial cancer cells. COMT regulation and 2-ME2 production in the endometrium may affect endometrial carcinogenesis.
-
Expression and cyclic variations of catechol-O-Methyl Transferase in human endometrial stroma.
Fertility and sterility, 2007Co-Authors: Sana M. Salih, Salama A. Salama, Amin A. Fadl, Manubai Nagamani, Ayman Al-hendyAbstract:Objective To investigate the role of catechol-O-Methyl Transferase (COMT) in the regulation of estrogen metabolism in human endometrium. Design Laboratory study. Setting Academic research laboratory. Intervention(s) Immunohistochemistry was used to localize COMT protein in human endometrial tissues. Catechol-O-Methyl Transferase promoter–luciferace reporter gene transactivation assay was used to assess COMT promoter activity in response to estrogen and progesterone treatment in primary human endometrial stroma (pHES) cells. Catechol-O-Methyl Transferase protein and mRNA expression were determined by Western blot and/or real-time polymerase chain reaction. The effect of 2-methoxy estrogen treatment on DNA proliferation, B-cell lymphoma 2, and vascular epithelial growth factor protein expression were assessed by Hoechst and Western blot analyses, respectively. Main Outcome Measure(s) Catechol-O-Methyl Transferase protein and mRNA subcellular localization and expression in human endometrial tissues and pHES cells. Result(s) Catechol-O-Methyl Transferase protein expression in human endometrial tissues was up-regulated in the proliferative phase and down-regulated in the midsecretory phase of the menstrual cycle. Estrogen induced a dose-dependent increase in COMT proximal promotor–luciferace transactivation in pHES cells whereas progesterone inhibited it. Estrogen up-regulated soluble COMT protein isoform expression whereas the addition of progesterone down-regulated it in pHES cells. High doses of 2-methoxy estrogen inhibited endometrial stroma cell proliferation, and down-regulated B-cell lymphoma 2 and vascular epithelial growth factor protein expression. Conclusion(s) Catechol-O-Methyl Transferase expression is hormonally regulated in human endometrial stroma. Catechol-O-Methyl Transferase product, 2-methoxy estrogen, inhibited endometrial stroma cell proliferation and decreased vascular epithelial growth factor and B-cell lymphoma 2 protein expression.
-
Hormonal regulation of catechol-O-Methyl Transferase activity in women with uterine leiomyomas
Fertility and sterility, 2006Co-Authors: Salama A. Salama, Hui Qun Wang, Jukka Tenhunen, Carola Tilgmann, Ayman Al-hendyAbstract:Catechol-O-Methyl Transferase (COMT) expression is higher in leiomyomas compared with paired normal myometrium. The expression of COMT in leiomyoma cells is hormonally regulated-estrogen down-regulates, whereas P and dexamethasone up-regulate, COMT expression.
Salama A. Salama - One of the best experts on this subject based on the ideXlab platform.
-
Progesterone-Mediated Regulation of Catechol-O-Methyl Transferase Expression in Endometrial Cancer Cells
Reproductive sciences (Thousand Oaks Calif.), 2007Co-Authors: Sana M. Salih, Salama A. Salama, Amin A. Fadl, Manubai Nagamani, Mohammad Jamaluddin, Leen J. Blok, Curt W. Burger, Ayman Al-hendyAbstract:The effects of estrogen and progesterone on the expression of estrogen-metabolizing enzymes such as catechol-O-Methyl Transferase (COMT) are not known. COMT converts genotoxic catecholestrogens to anticarcinogenic methoxyestrogens in the endometrium. The aim of this study is to investigate the effect of progesterone on COMT expression in well-differentiated endometrial cancer cells. The wild-type Ishikawa cell line as well as progesterone receptor A- or progesterone receptor B-transfected Ishikawa cells were used for in vitro studies. The regulation of COMT expression by progesterone was studied using Western blots, Hoechst dye DNA proliferation studies, and wild-type and/or site-directed mutagenesis of COMT promoter 1-luciferase reporter gene. Progesterone upregulated COMT protein expression in Ishikawa cells through progesterone receptor A isoform. COMT promoter activity was differentially regulated by the 3 half-site progesterone response elements in the COMT promoter. High doses of 2-ME2 inhibited Ishikawa cell proliferation. These data suggest that COMT expression is hormonally regulated in well-differentiated human endometrial cancer cells. COMT regulation and 2-ME2 production in the endometrium may affect endometrial carcinogenesis.
-
Expression and cyclic variations of catechol-O-Methyl Transferase in human endometrial stroma.
Fertility and sterility, 2007Co-Authors: Sana M. Salih, Salama A. Salama, Amin A. Fadl, Manubai Nagamani, Ayman Al-hendyAbstract:Objective To investigate the role of catechol-O-Methyl Transferase (COMT) in the regulation of estrogen metabolism in human endometrium. Design Laboratory study. Setting Academic research laboratory. Intervention(s) Immunohistochemistry was used to localize COMT protein in human endometrial tissues. Catechol-O-Methyl Transferase promoter–luciferace reporter gene transactivation assay was used to assess COMT promoter activity in response to estrogen and progesterone treatment in primary human endometrial stroma (pHES) cells. Catechol-O-Methyl Transferase protein and mRNA expression were determined by Western blot and/or real-time polymerase chain reaction. The effect of 2-methoxy estrogen treatment on DNA proliferation, B-cell lymphoma 2, and vascular epithelial growth factor protein expression were assessed by Hoechst and Western blot analyses, respectively. Main Outcome Measure(s) Catechol-O-Methyl Transferase protein and mRNA subcellular localization and expression in human endometrial tissues and pHES cells. Result(s) Catechol-O-Methyl Transferase protein expression in human endometrial tissues was up-regulated in the proliferative phase and down-regulated in the midsecretory phase of the menstrual cycle. Estrogen induced a dose-dependent increase in COMT proximal promotor–luciferace transactivation in pHES cells whereas progesterone inhibited it. Estrogen up-regulated soluble COMT protein isoform expression whereas the addition of progesterone down-regulated it in pHES cells. High doses of 2-methoxy estrogen inhibited endometrial stroma cell proliferation, and down-regulated B-cell lymphoma 2 and vascular epithelial growth factor protein expression. Conclusion(s) Catechol-O-Methyl Transferase expression is hormonally regulated in human endometrial stroma. Catechol-O-Methyl Transferase product, 2-methoxy estrogen, inhibited endometrial stroma cell proliferation and decreased vascular epithelial growth factor and B-cell lymphoma 2 protein expression.
-
Hormonal regulation of catechol-O-Methyl Transferase activity in women with uterine leiomyomas
Fertility and sterility, 2006Co-Authors: Salama A. Salama, Hui Qun Wang, Jukka Tenhunen, Carola Tilgmann, Ayman Al-hendyAbstract:Catechol-O-Methyl Transferase (COMT) expression is higher in leiomyomas compared with paired normal myometrium. The expression of COMT in leiomyoma cells is hormonally regulated-estrogen down-regulates, whereas P and dexamethasone up-regulate, COMT expression.
Eva W.c. Chow - One of the best experts on this subject based on the ideXlab platform.
-
Catechol-O-Methyl Transferase and Expression of Schizophrenia in 73 Adults with 22q11 Deletion Syndrome
Biological Psychiatry, 2007Co-Authors: Anne S. Bassett, Oana Caluseriu, Donald A. Young, Rosanna Weksberg, Eva W.c. ChowAbstract:Background Catechol-O-Methyl Transferase (COMT) is a candidate gene for schizophrenia with a role in dopamine metabolism, particularly in frontal cortex. COMT is within the region commonly deleted in 22q11 deletion syndrome (22q11DS), a syndrome with high prevalence of schizophrenia. We examined the role of COMT in schizophrenia-related expression in 22q11DS. Methods We genotyped the COMT functional Val 158/108 Met allele in 73 Caucasian adults with 22q11DS (36 men, 37 women; aged 33.8, SD 10.1 years; 37 Met, 36 Val hemizygosity) blind to clinical data and assessed effects on symptoms and frontal functioning. Results The lower activity Met allele was not significantly more prevalent than the Val allele in 33 subjects with schizophrenia. Excitement symptoms were more severe, however, and three frontal cognitive tests (theory of mind, Trails B, and olfactory identification), communication, and social functioning measures showed significantly worse performance with Met allele hemizygosity, even after accounting for effects of schizophrenia. Conclusions The results suggest that hemizygosity of the COMT functional allele exerts an effect on some measures of frontal functioning in 22q11DS. Elevated levels of tonic dopamine activation associated with the COMT Met allele may underlie these aspects of expression. We must look elsewhere for causes of the high prevalence of schizophrenia in 22q11DS, however.
Christine Cedraschi - One of the best experts on this subject based on the ideXlab platform.
-
Psychological distress in fibromyalgia patients: a role for catechol-O-Methyl-Transferase Val158met polymorphism
Health Psychology Review, 2012Co-Authors: Jules Alexandre Desmeules, Valérie Piguet, Marie Besson, Jocelyne Chabert, Elisabetta Rapiti Aylward, Michela Rebsamen, Michel F. Rossier, François Curtin, Pierre Dayer, Christine CedraschiAbstract:Fibromyalgia (FM) has been related to biochemical alterations, central pain sensitization and psychological distress. Among genetic and environmental hypotheses, a role was suggested for catechol-O-Methyl-Transferase (COMT), a modulator in the metabolism of monoaminergic neurotransmitters.
Pramod K. Dash - One of the best experts on this subject based on the ideXlab platform.
-
TRAUMATIC BRAIN INJURY STIMULATES HIPPOCAMPAL CATECHOL-O-Methyl Transferase EXPRESSION IN MICROGLIA
Neuroscience letters, 2006Co-Authors: John B. Redell, Pramod K. DashAbstract:Outcome following traumatic brain injury (TBI) is in large part determined by the combined action of multiple processes. In order to better understand the response of the central nervous system to injury, we utilized an antibody array to simultaneously screen 507 proteins for altered expression in the injured hippocampus, a structure critical for memory formation. Array analysis indicated 41 candidate proteins have altered expression levels 24 hours after TBI. Of particular interest was catechol-O-Methyl Transferase (COMT), an enzyme involved in metabolizing catecholamines released following neuronal activity. Altered catecholamine signaling has been observed after brain injury, and may contribute to the cognitive dysfunctions and behavioral deficits often experienced after TBI. Our data shows that COMT expression in the injured ipsilateral hippocampus was elevated for at least 14 days after controlled cortical impact injury. We found strong co-localization of COMT immunoreactivity with the microglia marker Iba1 near the injury site. Since dopamine transporter expression has been reported to be down-regulated after brain injury, COMT-mediated catecholamine metabolism may play a more prominent role in terminating catecholamine signaling in injured areas.
