The Experts below are selected from a list of 147 Experts worldwide ranked by ideXlab platform
Paul C Macdonald - One of the best experts on this subject based on the ideXlab platform.
-
transforming growth factor beta inhibits progesterone induced Enkephalinase expression in human endometrial stromal cells
The Journal of Clinical Endocrinology and Metabolism, 1996Co-Authors: M L Casey, Paul C MacdonaldAbstract:The specific activity of Enkephalinase in endometrial tissue of nonpregnant ovulatory women is correlated in a highly significant, positive manner with the plasma level of progesterone. The specific activity and levels of Enkephalinase messenger ribonucleic acid and immunoreactive protein also are increased in human endometrial stromal cells in culture by treatment with a synthetic progestin, medroxyprogesterone acetate (MPA), in a time- and dose-dependent manner. From an analysis of the temporal relationship between the specific activity and half-life of Enkephalinase in endometrial tissue and the level of progesterone in plasma, it appeared highly likely that some mechanism, in addition to progesterone withdrawal, was operative to reduce Enkephalinase activity in endometrium during the late luteal phase of the ovarian cycle before progesterone levels had declined below those known to be effective for progesterone action. In stromal cells previously (and concurrently) treated with MPA (10(-9) mol/L), the...
-
transforming growth factor beta 1 inhibits Enkephalinase ec 3 4 24 11 gene expression in human endometrial stromal cells and sex skin fibroblasts in culture
The Journal of Clinical Endocrinology and Metabolism, 1993Co-Authors: M L Casey, J W Smith, K Nagai, Paul C MacdonaldAbstract:This study was conducted to evaluate the negative regulation of Enkephalinase by an endogenously produced peptide, namely transforming growth factor-beta 1 (TGF beta 1). We found that TGF beta 1 acts in human endometrial stromal cells and sex skin fibroblasts in culture to cause a striking decrease (60% to > 90% in 3-7 days) in the specific activity of Enkephalinase (membrane metalloendopeptidase; EC 3.4.24.11) by reducing the levels of Enkephalinase mRNA and protein. Platelet-derived growth factor caused a slight reduction in Enkephalinase specific activity in endometrial stromal cells; epidermal growth factor caused a slight decrease in Enkephalinase specific activity in sex skin fibroblasts. In studies in which TGF beta 1 treatment and [35S]methionine labeling were conducted simultaneously, radiolabeling of Enkephalinase was decreased. When proteins were radiolabeled with [35S] methionine before treatment with TGF beta 1, the extent of Enkephalinase radiolabeling was similar to that in nontreated cells...
M L Casey - One of the best experts on this subject based on the ideXlab platform.
-
transforming growth factor beta inhibits progesterone induced Enkephalinase expression in human endometrial stromal cells
The Journal of Clinical Endocrinology and Metabolism, 1996Co-Authors: M L Casey, Paul C MacdonaldAbstract:The specific activity of Enkephalinase in endometrial tissue of nonpregnant ovulatory women is correlated in a highly significant, positive manner with the plasma level of progesterone. The specific activity and levels of Enkephalinase messenger ribonucleic acid and immunoreactive protein also are increased in human endometrial stromal cells in culture by treatment with a synthetic progestin, medroxyprogesterone acetate (MPA), in a time- and dose-dependent manner. From an analysis of the temporal relationship between the specific activity and half-life of Enkephalinase in endometrial tissue and the level of progesterone in plasma, it appeared highly likely that some mechanism, in addition to progesterone withdrawal, was operative to reduce Enkephalinase activity in endometrium during the late luteal phase of the ovarian cycle before progesterone levels had declined below those known to be effective for progesterone action. In stromal cells previously (and concurrently) treated with MPA (10(-9) mol/L), the...
-
transforming growth factor beta 1 inhibits Enkephalinase ec 3 4 24 11 gene expression in human endometrial stromal cells and sex skin fibroblasts in culture
The Journal of Clinical Endocrinology and Metabolism, 1993Co-Authors: M L Casey, J W Smith, K Nagai, Paul C MacdonaldAbstract:This study was conducted to evaluate the negative regulation of Enkephalinase by an endogenously produced peptide, namely transforming growth factor-beta 1 (TGF beta 1). We found that TGF beta 1 acts in human endometrial stromal cells and sex skin fibroblasts in culture to cause a striking decrease (60% to > 90% in 3-7 days) in the specific activity of Enkephalinase (membrane metalloendopeptidase; EC 3.4.24.11) by reducing the levels of Enkephalinase mRNA and protein. Platelet-derived growth factor caused a slight reduction in Enkephalinase specific activity in endometrial stromal cells; epidermal growth factor caused a slight decrease in Enkephalinase specific activity in sex skin fibroblasts. In studies in which TGF beta 1 treatment and [35S]methionine labeling were conducted simultaneously, radiolabeling of Enkephalinase was decreased. When proteins were radiolabeled with [35S] methionine before treatment with TGF beta 1, the extent of Enkephalinase radiolabeling was similar to that in nontreated cells...
Martin Kavaliers - One of the best experts on this subject based on the ideXlab platform.
-
Sex differences in the antinociceptive effects of the Enkephalinase inhibitor, SCH 34826.
Pharmacology Biochemistry and Behavior, 1993Co-Authors: Martin Kavaliers, Duncan G. L. InnesAbstract:Abstract The effects of endogenous opioid peptides are limited by proteolytic enzymes such as endopeptidase 24.11 (“Enkephalinase”), which cleaves the Gly-Phe bonds in Met- and Leu-enkephalin. SCH 34826 {(S)-N-[n-[1-[(2,2- dimethyl -1,3- dioxolan -4- yl ) methoxy ] carbonyl ]-2- phenylethyl ]- l - phenyl-alanine-B-alanine } is a potent, highly specific, Enkephalinase inhibitor that has marked analgesic effects in laboratory rodents. The present study compared the effects of SCH 34826 on nociception and restraint stress-induced opioid analgesia in reproductive adult male and female deer mice, Peromyscus maniculatus . SCH 34826 had significantly greater antinociceptive actions and facilitatory effects on stress-induced analgesia in male than female mice. These antinociceptive effects of SCH 34826 were reduced by the general opioid antagonist naloxone and completely blocked by the specific delta opioid receptor antagonist, ICI 174,864, and nonsignificantly affected by the mu and kappa opioid receptor antagonists, β-funaltrexamine and nor-binaltorphimine, respectively. These results show that there are sex differences in the effects of the Enkephalinase inhibitor, SCH 34826, on opioid-mediated antinociception and that these sex differences are associated with delta opioid mechanisms.
-
antinociceptive effects of the Enkephalinase inhibitor sch 34826 in the snail cepaea nemoralis
Peptides, 1993Co-Authors: Lisa M Saksida, Liisa A M Galea, Martin KavaliersAbstract:Abstract In vertebrates the effects of endogenous opioid peptides are limited by proteolytic enzymes such as endopeptidase 24.11 (Enkephalinase), which cleaves the Gly-Phe bonds in both methionine- and leucine-enkephalin. SCH 34826 { (S)-N-[n- [1-[(2,2-dimethyl-1,3-dioxolan-4yl) methoxy]carbonyl]-2-phenylethyl]- l -phenyl-alanine-B-alanine} is a potent, highly specific, Enkephalinase inhibitor that has marked analgesic effects in mammals. The present study examined the effects of SCH 34826 on opioid-mediated aversive thermal (nociceptive) responses of an invertebrate, the land snail, Cepaea nemoralis. SCH 34828 had significant, dose-related antinociceptive effects in Cepaea that were reduced by naloxone and completely blocked by the specific delta opiate antagonist, ICI-174,864, and only weakly affected by the specific kappa opiate antagonist nor-binaltrophimine. These findings with SCH 34826 suggest that an Enkephalinase similar to that in vertebrates is present and involved in the mediation of opioid (enkephalin) activity in the snail, Cepaea.
Bernard Malfroy - One of the best experts on this subject based on the ideXlab platform.
-
Substance P contracts the human iris sphincter: possible modulation by endogenous Enkephalinase.
Regulatory Peptides, 1990Co-Authors: Janet A. Anderson, Bernard Malfroy, Normand R. Richard, Laurie Kullerstrand, Catherine Lucas, Perry S. BinderAbstract:Abstract Substance P-immunoreactive neurons have been found in the irides of many species including humans. In several species, substance P has been shown to induce contraction of the sphincter muscle but this action of substance P has not been previously demonstrated in the human eye. Using an eye cup model in which the sensitivity of the iris muscle to substance P is increased compared to the isolated sphincter muscle, we have observed that nanomolar amounts of substance P induced contraction of the sphincter in the human iris. This contractile response was enhanced in eyes pretreated with thiorphan, an Enkephalinase inhibitor, suggesting that endogenous Enkephalinase (E.C. 3.4.24.11) may modulate the substance P contraction in the human iris. Further support for this hypothesis was the finding of Enkephalinase-like immunoreactivity and enzyme activity in the human iris sphincter muscle.
-
Recombinant Enkephalinase effectively inhibits substance P-induced miosis in the rabbit eye cup model
Current Eye Research, 1990Co-Authors: Janet A. Anderson, Edward Hernandez, Efraim Duzman, Bernard MalfroyAbstract:Enkephalinase (EC 3.4.24.11) is a naturally occurring, membrane-bound peptidase that degrades substance P in vivo and in vitro. Addition of this neutral endopeptidase to a rabbit eye cup model partially inhibits substance P-induced contraction of the iris sphincter muscle. Inactivation of substance P is reversed by thiorphan, a specific inhibitor of Enkephalinase. These results show that Enkephalinase degradation of substance P produces metabolites that are physiologically inactive in iris contraction. We also observed that atropine acts synergistically with Enkephalinase to completely abolish substance P-induced iris contraction suggesting that the action of substance P on the iris contains an acetylcholine-stimulatory effect which is not lost by Enkephalinase treatment.
-
Administration of recombinant Enkephalinase (neutral endopeptidase) prevents capsaicin-induced miosis in the rabbit eye in vivo.
Journal of Pharmacology and Experimental Therapeutics, 1990Co-Authors: Bernard Malfroy, R. Bridenbaugh, D Liggitt, J. F. Mccabe, R Baughman, H Kado-fong, K Mulholland, J AndersonAbstract:Substance P induced a dose-dependent contraction of iris sphincter muscles when applied in the presence of atropine to the isolated rabbit iris in vitro as evidenced by a decreased pupil diameter. Pretreatment of the iris with 20 micrograms of recombinant Enkephalinase (neutral endopeptidase; EC 3.4.24.11) totally abolished the contractile response to substance P. Injection of 10 micrograms of capsaicin into the anterior chamber of atropine-treated rabbit eyes in vivo induced an immediate and intense miosis. Injection of 100 micrograms of recombinant Enkephalinase, 1 or 5 min before capsaicin injection, significantly inhibited this miosis. This effect of Enkephalinase was totally abolished by preincubating the enzyme with thiorphan, a high-affinity Enkephalinase inhibitor. These results show that Enkephalinase, which is known to hydrolyze substance P in vitro with high efficiency, also hydrolyzes endogenously released substance P in vivo. Furthermore, our results suggest that Enkephalinase application may represent a novel therapeutic approach to treat substance P-mediated pathologies.
J W Smith - One of the best experts on this subject based on the ideXlab platform.
-
transforming growth factor beta 1 inhibits Enkephalinase ec 3 4 24 11 gene expression in human endometrial stromal cells and sex skin fibroblasts in culture
The Journal of Clinical Endocrinology and Metabolism, 1993Co-Authors: M L Casey, J W Smith, K Nagai, Paul C MacdonaldAbstract:This study was conducted to evaluate the negative regulation of Enkephalinase by an endogenously produced peptide, namely transforming growth factor-beta 1 (TGF beta 1). We found that TGF beta 1 acts in human endometrial stromal cells and sex skin fibroblasts in culture to cause a striking decrease (60% to > 90% in 3-7 days) in the specific activity of Enkephalinase (membrane metalloendopeptidase; EC 3.4.24.11) by reducing the levels of Enkephalinase mRNA and protein. Platelet-derived growth factor caused a slight reduction in Enkephalinase specific activity in endometrial stromal cells; epidermal growth factor caused a slight decrease in Enkephalinase specific activity in sex skin fibroblasts. In studies in which TGF beta 1 treatment and [35S]methionine labeling were conducted simultaneously, radiolabeling of Enkephalinase was decreased. When proteins were radiolabeled with [35S] methionine before treatment with TGF beta 1, the extent of Enkephalinase radiolabeling was similar to that in nontreated cells...