The Experts below are selected from a list of 921 Experts worldwide ranked by ideXlab platform
Jose Behar - One of the best experts on this subject based on the ideXlab platform.
-
Mechanism of Gallbladder Relaxation in the Cat: Role of Norepinephrine1,2
2016Co-Authors: Qian Chen, Piero Biancani, Zuoliang Xiao, Kwang Lee, Jose BeharAbstract:We investigated the mechanisms of neurally mediated relaxation of cat Gallbladder Muscle. Muscle strips from the Gallbladder corpus placed in the Muscle bath with oxygenated Krebs ’ solution developed spontaneous active tension. Tension was measured with isometric force transducers, and Muscle relaxation was ex-pressed as percent decrease of active basal tension. Electrical field stimulation (EFS) evoked a tetrodotoxin-sensitive and hexa-methonium-insensitive frequency-dependent relaxation with a maximal relaxation at 20 Hz. Gallbladder Muscle strips also re-laxed in response to increasing concentrations of vasoactive in-testinal peptide (VIP), isoproterenol and, after pretreatment with phentolamine, norepinephrine. Nitric oxide synthase inhibitors Nv-nitro-L-arginine and Nv-nitro-L-arginine methyl ester at a concen-tration of 100 mM, which blocked EFS-induced relaxation in th
-
effects of cholesterol on cck 1 receptors and caveolin 3 proteins recycling in human Gallbladder Muscle
American Journal of Physiology-gastrointestinal and Liver Physiology, 2010Co-Authors: Ping Cong, Piero Biancani, Victor E Pricolo, Jose BeharAbstract:The contraction of Gallbladders (GBs) with cholesterol stones is impaired due to high cholesterol concentrations in caveolae compared with GBs with pigment stones. The reduced contraction is caused by a lower cholecystokinin (CCK)-8 binding to CCK-1 receptors (CCK-1R) due to caveolar sequestration of receptors. We aimed to examine the mechanism of cholesterol-induced sequestration of receptors. Muscle cells from human and guinea pig GBs were studied. Antibodies were used to examine CCK-1R, antigens of early and recycling endosomes, and total (CAV-3) and phosphorylated caveolar-3 protein (pCAV-3) by Western blots. Contraction was measured in Muscle cells transfected with CAV3 mRNA or clathrin heavy-chain small-interfering RNA (siRNA). CCK-1R returned back to the bulk plasma membrane (PM) 30 min after CCK-8 recycled by endosomes, peaking at 5 min in early endosomes and at 20 min in recycling endosomes. Pretreatment with cholesterol-rich liposomes inhibited the transfer of CCK-1R and of CAV-3 in the endosomes by blocking CAV-3 phosphorylation. 4-Amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (inhibitor of tyrosine kinase) reproduced these effects by blocking pCAV-3 formation, increasing CAV-3 and CCK-1R sequestration in the caveolae and impairing CCK-8-induced contraction. CAV-3 siRNA reduced CAV-3 protein expression, decreased CCK-8-induced contraction, and accumulated CCK-1R in the caveolae. Abnormal concentrations of caveolar cholesterol had no effect on met-enkephalin that stimulates a delta-opioid receptor that internalizes through clathrin. We found that impaired Muscle contraction in GBs with cholesterol stones is due to high caveolar levels of cholesterol that inhibits pCAV-3 generation. Caveolar cholesterol increases the caveolar sequestration of CAV-3 and CCK-1R caused by their reduced recycling to the PM.
-
high levels of caveolar cholesterol inhibit progesterone induced genomic actions in human and guinea pig Gallbladder Muscle
American Journal of Physiology-gastrointestinal and Liver Physiology, 2009Co-Authors: Ping Cong, Piero Biancani, Victor E Pricolo, Jose BeharAbstract:Gallbladder disease is prevalent during pregnancy. It has been suggested that this complication of pregnancy is attributable to increased bile cholesterol (Ch) induced by estrogens and to gallbladd...
-
decreased number of activated macrophages in Gallbladder Muscle layer of cholesterol gallstone patients following ursodeoxycholic acid
Gut, 2008Co-Authors: Michele Pier Luca Guarino, Jose Behar, Simone Carotti, Giuseppe Perrone, Rossana Alloni, Sergio Morini, Annamaria Altomare, R Caviglia, Sara Emerenziani, Carla RabittiAbstract:We recently reported that, in symptomatic cholesterol gallstone patients, ursodeoxycholic acid (UDCA) improves Gallbladder (GB) Muscle contractility and decreases the biochemical parameters of oxidative stress and inflammation.1 UDCA also antagonises the hydrophobic bile acid damage to the liver by preventing hydrophobic bile acid-induced stimulation of macrophage oxidative processes.2 3 Macrophages also play a dominant role in the inflammatory and oxidative response in other conditions associated with impairment of intestinal motility, such as post-operative ileus.4–6 Following these findings, we carried out additional studies aimed at examining: the presence of macrophage infiltration and cyclooxygenase-2 (COX-2) expression in the GB Muscle layer and the effect of short-term UDCA administration. From February 2004 to August 2007, …
-
role of caveolae in the pathogenesis of cholesterol induced Gallbladder Muscle hypomotility
American Journal of Physiology-gastrointestinal and Liver Physiology, 2007Co-Authors: Zuoliang Xiao, Piero Biancani, Frank Schmitz, Victor E Pricolo, Jose BeharAbstract:Muscle cells from human Gallbladders (GB) with cholesterol stones (ChS) exhibit a defective contraction, excess cholesterol (Ch) in the plasma membrane, and lower binding of CCK-1 receptors. These abnormalities improved after Muscle cells were incubated with Ch-free liposomes that remove the excess Ch from the plasma membrane. The present studies were designed to investigate the role of caveolin-3 proteins (Cav-3) in the pathogenesis of these abnormalities. Muscle cells from GB with ChS exhibit higher Ch levels in the plasma membrane that were mostly localized in caveolae and associated with parallel increases in the expression of Cav-3 in the caveolae compared with that in GB with pigment stones (PS). The overall number of CCK-1 receptors in the plasma membrane was not different between Muscle cells from GB with ChS and PS, but they were increased in the caveolae in Muscle cells from GB with ChS. Treatment of Muscle cells from GB with ChS with a Galpha(i3) protein fragment increased the total binding of CCK-1 receptors (from 8.3 to 11.2%) and Muscle contraction induced by CCK-8 (from 11.2 to 17.3% shortening). However, Galpha(q/11) protein fragment had no such effect. Moreover, neither fragment had any effect on Muscle cells from GB with PS. We conclude that the defective contraction of Muscle cells with excessive Ch levels in the plasma membrane is due to an increased expression of Cav-3 that results in the sequestration of CCK-1 receptors in the caveolae, probably by inhibiting the functions of Galpha(i3) proteins.
Piero Biancani - One of the best experts on this subject based on the ideXlab platform.
-
Mechanism of Gallbladder Relaxation in the Cat: Role of Norepinephrine1,2
2016Co-Authors: Qian Chen, Piero Biancani, Zuoliang Xiao, Kwang Lee, Jose BeharAbstract:We investigated the mechanisms of neurally mediated relaxation of cat Gallbladder Muscle. Muscle strips from the Gallbladder corpus placed in the Muscle bath with oxygenated Krebs ’ solution developed spontaneous active tension. Tension was measured with isometric force transducers, and Muscle relaxation was ex-pressed as percent decrease of active basal tension. Electrical field stimulation (EFS) evoked a tetrodotoxin-sensitive and hexa-methonium-insensitive frequency-dependent relaxation with a maximal relaxation at 20 Hz. Gallbladder Muscle strips also re-laxed in response to increasing concentrations of vasoactive in-testinal peptide (VIP), isoproterenol and, after pretreatment with phentolamine, norepinephrine. Nitric oxide synthase inhibitors Nv-nitro-L-arginine and Nv-nitro-L-arginine methyl ester at a concen-tration of 100 mM, which blocked EFS-induced relaxation in th
-
effects of cholesterol on cck 1 receptors and caveolin 3 proteins recycling in human Gallbladder Muscle
American Journal of Physiology-gastrointestinal and Liver Physiology, 2010Co-Authors: Ping Cong, Piero Biancani, Victor E Pricolo, Jose BeharAbstract:The contraction of Gallbladders (GBs) with cholesterol stones is impaired due to high cholesterol concentrations in caveolae compared with GBs with pigment stones. The reduced contraction is caused by a lower cholecystokinin (CCK)-8 binding to CCK-1 receptors (CCK-1R) due to caveolar sequestration of receptors. We aimed to examine the mechanism of cholesterol-induced sequestration of receptors. Muscle cells from human and guinea pig GBs were studied. Antibodies were used to examine CCK-1R, antigens of early and recycling endosomes, and total (CAV-3) and phosphorylated caveolar-3 protein (pCAV-3) by Western blots. Contraction was measured in Muscle cells transfected with CAV3 mRNA or clathrin heavy-chain small-interfering RNA (siRNA). CCK-1R returned back to the bulk plasma membrane (PM) 30 min after CCK-8 recycled by endosomes, peaking at 5 min in early endosomes and at 20 min in recycling endosomes. Pretreatment with cholesterol-rich liposomes inhibited the transfer of CCK-1R and of CAV-3 in the endosomes by blocking CAV-3 phosphorylation. 4-Amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (inhibitor of tyrosine kinase) reproduced these effects by blocking pCAV-3 formation, increasing CAV-3 and CCK-1R sequestration in the caveolae and impairing CCK-8-induced contraction. CAV-3 siRNA reduced CAV-3 protein expression, decreased CCK-8-induced contraction, and accumulated CCK-1R in the caveolae. Abnormal concentrations of caveolar cholesterol had no effect on met-enkephalin that stimulates a delta-opioid receptor that internalizes through clathrin. We found that impaired Muscle contraction in GBs with cholesterol stones is due to high caveolar levels of cholesterol that inhibits pCAV-3 generation. Caveolar cholesterol increases the caveolar sequestration of CAV-3 and CCK-1R caused by their reduced recycling to the PM.
-
high levels of caveolar cholesterol inhibit progesterone induced genomic actions in human and guinea pig Gallbladder Muscle
American Journal of Physiology-gastrointestinal and Liver Physiology, 2009Co-Authors: Ping Cong, Piero Biancani, Victor E Pricolo, Jose BeharAbstract:Gallbladder disease is prevalent during pregnancy. It has been suggested that this complication of pregnancy is attributable to increased bile cholesterol (Ch) induced by estrogens and to gallbladd...
-
role of caveolae in the pathogenesis of cholesterol induced Gallbladder Muscle hypomotility
American Journal of Physiology-gastrointestinal and Liver Physiology, 2007Co-Authors: Zuoliang Xiao, Piero Biancani, Frank Schmitz, Victor E Pricolo, Jose BeharAbstract:Muscle cells from human Gallbladders (GB) with cholesterol stones (ChS) exhibit a defective contraction, excess cholesterol (Ch) in the plasma membrane, and lower binding of CCK-1 receptors. These abnormalities improved after Muscle cells were incubated with Ch-free liposomes that remove the excess Ch from the plasma membrane. The present studies were designed to investigate the role of caveolin-3 proteins (Cav-3) in the pathogenesis of these abnormalities. Muscle cells from GB with ChS exhibit higher Ch levels in the plasma membrane that were mostly localized in caveolae and associated with parallel increases in the expression of Cav-3 in the caveolae compared with that in GB with pigment stones (PS). The overall number of CCK-1 receptors in the plasma membrane was not different between Muscle cells from GB with ChS and PS, but they were increased in the caveolae in Muscle cells from GB with ChS. Treatment of Muscle cells from GB with ChS with a Galpha(i3) protein fragment increased the total binding of CCK-1 receptors (from 8.3 to 11.2%) and Muscle contraction induced by CCK-8 (from 11.2 to 17.3% shortening). However, Galpha(q/11) protein fragment had no such effect. Moreover, neither fragment had any effect on Muscle cells from GB with PS. We conclude that the defective contraction of Muscle cells with excessive Ch levels in the plasma membrane is due to an increased expression of Cav-3 that results in the sequestration of CCK-1 receptors in the caveolae, probably by inhibiting the functions of Galpha(i3) proteins.
-
role of pge2 on Gallbladder Muscle cytoprotection of guinea pigs
American Journal of Physiology-gastrointestinal and Liver Physiology, 2004Co-Authors: Zuoliang Xiao, Piero Biancani, Jose BeharAbstract:H2O2 and taurochenodeoxycholic acid (TCDC) impair the contraction induced by CCK-8, ACh, and KCl without affecting the actions of PGE2 and damage functions of membrane proteins except for PGE2 receptors. The aim of this study was to examine whether the preserved PGE2 actions contribute to cytoprotective mechanisms against reactive oxygen species. Muscle cells from guinea pig Gallbladder were obtained by enzymatic digestion. Levels of lipid peroxidation and activities of SOD and catalase were determined by spectrophotometry. Pretreatment with PGE2 prevented the inhibition of H2O2 or TCDC on agonist (CCK-8, ACh, and KCl)-induced contraction and reduced the expected increase in lipid peroxidation and activities of catalase and SOD caused by H2O2 and TCDC. Incubation with CCK-8 for 60 min desensitized CCK-1 receptors up to 30 min, whereas no receptor desensitization was observed after PGE2 pretreatment. Cholesterol-rich liposome treatment enhanced the inhibition of H2O2 and TCDC on agonists-induced contraction, including that of PGE2. Pretreatment with PGE2 before H2O2 and TCDC did not completely block their inhibition on agonist-induced contraction. Cholesterol-rich liposome treatment impaired the expected increase in catalase activities in response to PGE2. We conclude that pretreatment with PGE2 prevents the Muscle cell damage caused by H2O2 and TCDC due to the resistance of PGE2 receptors to agonist-induced desensitization. The preservation of PGE2 receptors may be designed to conserve these cytoprotective functions that are, however, impaired by the presence of excess cholesterol in the plasma membrane.
Zuoliang Xiao - One of the best experts on this subject based on the ideXlab platform.
-
Mechanism of Gallbladder Relaxation in the Cat: Role of Norepinephrine1,2
2016Co-Authors: Qian Chen, Piero Biancani, Zuoliang Xiao, Kwang Lee, Jose BeharAbstract:We investigated the mechanisms of neurally mediated relaxation of cat Gallbladder Muscle. Muscle strips from the Gallbladder corpus placed in the Muscle bath with oxygenated Krebs ’ solution developed spontaneous active tension. Tension was measured with isometric force transducers, and Muscle relaxation was ex-pressed as percent decrease of active basal tension. Electrical field stimulation (EFS) evoked a tetrodotoxin-sensitive and hexa-methonium-insensitive frequency-dependent relaxation with a maximal relaxation at 20 Hz. Gallbladder Muscle strips also re-laxed in response to increasing concentrations of vasoactive in-testinal peptide (VIP), isoproterenol and, after pretreatment with phentolamine, norepinephrine. Nitric oxide synthase inhibitors Nv-nitro-L-arginine and Nv-nitro-L-arginine methyl ester at a concen-tration of 100 mM, which blocked EFS-induced relaxation in th
-
role of caveolae in the pathogenesis of cholesterol induced Gallbladder Muscle hypomotility
American Journal of Physiology-gastrointestinal and Liver Physiology, 2007Co-Authors: Zuoliang Xiao, Piero Biancani, Frank Schmitz, Victor E Pricolo, Jose BeharAbstract:Muscle cells from human Gallbladders (GB) with cholesterol stones (ChS) exhibit a defective contraction, excess cholesterol (Ch) in the plasma membrane, and lower binding of CCK-1 receptors. These abnormalities improved after Muscle cells were incubated with Ch-free liposomes that remove the excess Ch from the plasma membrane. The present studies were designed to investigate the role of caveolin-3 proteins (Cav-3) in the pathogenesis of these abnormalities. Muscle cells from GB with ChS exhibit higher Ch levels in the plasma membrane that were mostly localized in caveolae and associated with parallel increases in the expression of Cav-3 in the caveolae compared with that in GB with pigment stones (PS). The overall number of CCK-1 receptors in the plasma membrane was not different between Muscle cells from GB with ChS and PS, but they were increased in the caveolae in Muscle cells from GB with ChS. Treatment of Muscle cells from GB with ChS with a Galpha(i3) protein fragment increased the total binding of CCK-1 receptors (from 8.3 to 11.2%) and Muscle contraction induced by CCK-8 (from 11.2 to 17.3% shortening). However, Galpha(q/11) protein fragment had no such effect. Moreover, neither fragment had any effect on Muscle cells from GB with PS. We conclude that the defective contraction of Muscle cells with excessive Ch levels in the plasma membrane is due to an increased expression of Cav-3 that results in the sequestration of CCK-1 receptors in the caveolae, probably by inhibiting the functions of Galpha(i3) proteins.
-
role of pge2 on Gallbladder Muscle cytoprotection of guinea pigs
American Journal of Physiology-gastrointestinal and Liver Physiology, 2004Co-Authors: Zuoliang Xiao, Piero Biancani, Jose BeharAbstract:H2O2 and taurochenodeoxycholic acid (TCDC) impair the contraction induced by CCK-8, ACh, and KCl without affecting the actions of PGE2 and damage functions of membrane proteins except for PGE2 receptors. The aim of this study was to examine whether the preserved PGE2 actions contribute to cytoprotective mechanisms against reactive oxygen species. Muscle cells from guinea pig Gallbladder were obtained by enzymatic digestion. Levels of lipid peroxidation and activities of SOD and catalase were determined by spectrophotometry. Pretreatment with PGE2 prevented the inhibition of H2O2 or TCDC on agonist (CCK-8, ACh, and KCl)-induced contraction and reduced the expected increase in lipid peroxidation and activities of catalase and SOD caused by H2O2 and TCDC. Incubation with CCK-8 for 60 min desensitized CCK-1 receptors up to 30 min, whereas no receptor desensitization was observed after PGE2 pretreatment. Cholesterol-rich liposome treatment enhanced the inhibition of H2O2 and TCDC on agonists-induced contraction, including that of PGE2. Pretreatment with PGE2 before H2O2 and TCDC did not completely block their inhibition on agonist-induced contraction. Cholesterol-rich liposome treatment impaired the expected increase in catalase activities in response to PGE2. We conclude that pretreatment with PGE2 prevents the Muscle cell damage caused by H2O2 and TCDC due to the resistance of PGE2 receptors to agonist-induced desensitization. The preservation of PGE2 receptors may be designed to conserve these cytoprotective functions that are, however, impaired by the presence of excess cholesterol in the plasma membrane.
-
paf like lipids and paf induced Gallbladder Muscle contraction is mediated by different pathways in guinea pigs
American Journal of Physiology-gastrointestinal and Liver Physiology, 2003Co-Authors: Michele P L Guarino, Piero Biancani, Zuoliang Xiao, Jose BeharAbstract:H2O2 stimulates Gallbladder Muscle contraction and scavengers of free radicals through the generation of PGE2. Oxidative stress causes lipid peroxidation and generation of platelet-activating facto...
-
hydrophilic but not hydrophobic bile acids prevent Gallbladder Muscle dysfunction in acute cholecystitis
Hepatology, 2003Co-Authors: Zuoliang Xiao, Martin C. Carey, Piero Biancani, M Jose D BeharAbstract:The pathogenesis of acute cholecystitis (AC) is controversial. Bile acids may be involved in the pathogenesis of AC because the hydrophobic chenodeoxycholic acid (CDCA) reproduced in vitro the Muscle dysfunction observed in AC and was prevented by the hydrophilic ursodeoxycholic acid (UDCA). The present study examined the in vivo effects of UDCA or CDCA on Gallbladder Muscle dysfunction caused by AC. Guinea pigs were treated with placebo, UDCA, or CDCA for 2 weeks before sham operation or induction of AC by bile duct ligation (BDL) for 3 days. Pretreatment with oral UDCA prevented the defective contraction in response to agonists (acetylcholine [ACh], cholecystokinin 8 [CCK-8], and KCl) that occurs after BDL. Prostaglandin (PG) E(2)-induced contraction remained normal in the placebo and UDCA-treated groups but was impaired in the CDCA-treated group. Treatment with UDCA also prevented the expected increase in the levels of H(2)O(2), lipid peroxidation, and PGE(2) content in the placebo-treated AC group, whereas CDCA caused further increases in these oxidative stress markers. The binding capacity of PGE(2) to its receptors and the activity of catalase were reduced after treatment with CDCA. Treatment with UDCA enriched Gallbladder bile acids with its conjugates and reduced the percentage of CDCA conjugates. In contrast, treatment with CDCA significantly decreased the percentage of UDCA in bile. In conclusion, oral treatment with UDCA prevents Gallbladder Muscle damage caused by BDL, whereas oral treatment with CDCA worsens the defective Muscle contractility and the oxidative stress.
Qian Chen - One of the best experts on this subject based on the ideXlab platform.
-
Mechanism of Gallbladder Relaxation in the Cat: Role of Norepinephrine1,2
2016Co-Authors: Qian Chen, Piero Biancani, Zuoliang Xiao, Kwang Lee, Jose BeharAbstract:We investigated the mechanisms of neurally mediated relaxation of cat Gallbladder Muscle. Muscle strips from the Gallbladder corpus placed in the Muscle bath with oxygenated Krebs ’ solution developed spontaneous active tension. Tension was measured with isometric force transducers, and Muscle relaxation was ex-pressed as percent decrease of active basal tension. Electrical field stimulation (EFS) evoked a tetrodotoxin-sensitive and hexa-methonium-insensitive frequency-dependent relaxation with a maximal relaxation at 20 Hz. Gallbladder Muscle strips also re-laxed in response to increasing concentrations of vasoactive in-testinal peptide (VIP), isoproterenol and, after pretreatment with phentolamine, norepinephrine. Nitric oxide synthase inhibitors Nv-nitro-L-arginine and Nv-nitro-L-arginine methyl ester at a concen-tration of 100 mM, which blocked EFS-induced relaxation in th
-
abnormalities of Gallbladder Muscle associated with acute inflammation in guinea pigs
American Journal of Physiology-gastrointestinal and Liver Physiology, 2001Co-Authors: Zuoliang Xiao, Qian Chen, Piero Biancani, Jose BeharAbstract:Muscle strips from experimental acute cholecystitis (AC) exhibit a defective contraction. The mechanisms responsible for this impaired contraction are not known. The present studies investigated th...
-
Gallbladder Muscle dysfunction in patients with chronic acalculous disease
Gastroenterology, 2001Co-Authors: Joseph Amaral, Qian Chen, Piero Biancani, Zuoliang Xiao, Jose BeharAbstract:Abstract Background & Aims: The mechanisms responsible for the abnormalities of Gallbladder emptying in patients with chronic acalculous Gallbladder disease (AGD) have not been elucidated. This study was designed to determine whether a Muscle defect could explain this Gallbladder dysfunction. Methods: Gallbladder contraction induced by a continuous intravenous cholecystokinin octapeptide (CCK-8) infusion was determined by ultrasonography in control subjects, patients with AGD, pigment stones, and cholesterol stones. Muscle cells were obtained by enzymatic digestion. 125 I–CCK-8 binding and [ 35 S]guanosine triphosphate γS (GTPγS) binding studies were performed. Results: In vivo Gallbladder contraction induced by CCK-8 was significantly lower in AGD (29.4%) and cholesterol stones (28.8%) than in pigment stones (59.8%) and normal controls (57.8%; P 4 and with the second messenger 1,2-dioctanoyl-sn-glycerol. However, GTPγS binding induced by CCK-8 and vasoactive intestinal polypeptide and the binding capacity of CCK receptors were not different between AGD and pigment stones. Conclusions: These findings suggest that there is a good correlation between in vivo and in vitro Gallbladder response to CCK-8 in patients with AGD. Unlike those found in cholesterol stones, the Muscle defects in AGD appear to reside in the contractile apparatus. GASTROENTEROLOGY 2001;120:506-511
-
Excess membrane cholesterol alters human Gallbladder Muscle contractility and membrane fluidity.
Gastroenterology, 1999Co-Authors: Qian Chen, Piero Biancani, Joseph Amaral, Jose BeharAbstract:Abstract Background & Aims: The relationship between Muscle contractility, plasma membrane cholesterol, and fluidity was investigated in human Gallbladders with gallstones. Methods: Isolated Gallbladder Muscle cells were used to measure contraction. Plasma membranes of Gallbladder Muscle were purified in a sucrose gradient and measured for cholesterol content and cholesterol/phospholipid mole ratio. Membrane fluidity was determined by using fluorescence polarization and was expressed as the reciprocal of anisotropy. Results: The maximal contraction induced by cholecystokinin octapeptide was significantly less in Gallbladders with cholesterol stones than in those with pigment stones. The membrane cholesterol content and cholesterol/phospholipid mole ratio were significantly higher in Gallbladders with cholesterol stones than in those with pigment stones. Membrane anisotropy was also higher than in Gallbladders with pigment stones, reflecting lower membrane fluidity in Gallbladders with cholesterol stones. After Muscle cells from cholesterol stone Gallbladders were incubated with cholesterol-free liposomes for 4 hours, cholecystokinin octapeptide–induced contraction, membrane cholesterol content and cholesterol/phospholipid ratio, and membrane fluidity returned to normal levels. Conclusions: Gallbladder Muscle from patients with cholesterol stones has increased membrane cholesterol/phospholipid mole ratio and decreased membrane fluidity resulting in impaired Muscle contractility. These abnormalities are corrected by removing the excess cholesterol from the plasma membranes. GASTROENTEROLOGY 1999;116:678-685
-
signal transduction pathways mediating cck induced Gallbladder Muscle contraction
American Journal of Physiology-gastrointestinal and Liver Physiology, 1998Co-Authors: Qian Chen, Piero Biancani, Zuoliang Xiao, Karen M Harnett, Jose BeharAbstract:The signal transduction that mediates CCK-induced contraction of Gallbladder Muscle was investigated in the cat. Contraction was measured by scanning micrometry in single Muscle cells isolated enzy...
James P Ryan - One of the best experts on this subject based on the ideXlab platform.
-
myosin light chain phosphorylation correlates with contractile force in guinea pig Gallbladder Muscle
Digestive Diseases and Sciences, 2001Co-Authors: Henry P Parkman, Rita Garbarino, James P RyanAbstract:Acetylcholine (ACh) -induced Gallbladder smooth Muscle contraction involves myosin light chain phosphorylation (MLCP). ACh-induced contraction is dose dependent. Whether MLCP by ACh is also dose dependent and how it correlates with contractile force have not been carefully evaluated. This study investigated the correlation between Gallbladder Muscle contraction and MLCP. Guinea pig Gallbladder Muscle strips were studied isometrically and frozen after different doses of ACh (0, 0.1, 5, 100 μM) for different periods of incubation (0.5, 1, 2, 3, 4 min). MLCP was determined using gel electrophoresis. Both contraction and MLCP in response to ACh were concentration dependent. Peak MLCP to ACh 100 μM occurred at 30 sec. There was a high correlation between active force and MLCP (r = 0.991; P = 0.009 at 30 sec stimulation). Nifedipine 1 μM reduced ACh-induced contraction and MLCP by a similar degree (31% and 33%, respectively). In conclusion, Gallbladder contractile force significantly correlates with MLCP. This is consistent with the hypothesis that initiation of Gallbladder cholinergic contraction is dependent on phosphorylation of myosin light chains.
-
the contractile action of platelet activating factor on Gallbladder smooth Muscle
American Journal of Physiology-gastrointestinal and Liver Physiology, 2000Co-Authors: Henry P Parkman, Arlene N James, James P RyanAbstract:Platelet-activating factor (PAF) may be a mediator of some sequelae of cholecystitis, a disorder with Gallbladder motor dysfunction. The aims of this study were to determine the effect and mechanism of PAF on Gallbladder Muscle. Exogenous administration of PAF-16 or PAF-18 caused dose-dependent contractions of Gallbladder Muscle strips in vitro with threshold doses of 1 ng/ml and 10 ng/ml, respectively. The PAF-induced contractions were not significantly reduced by TTX, atropine, or hexamethonium but were significantly inhibited with the PAF receptor antagonists ginkolide B and CV-3988. The PAF-induced contraction was reduced by indomethacin. Preventing influx of extracellular calcium with a calcium-free solution nearly abolished the PAF contractile response. Nifedipine inhibited the PAF contractile response, whereas ryanodine had no effect. Pertussis toxin reduced the PAF contractile response. In conclusion, PAF causes Gallbladder contraction through specific PAF receptors on Gallbladder Muscle. These PAF receptors appear to be linked to a prostaglandin-mediated mechanism and to pertussis toxin-sensitive G proteins. The contractile response is largely mediated through the utilization of extracellular calcium influx through voltage-dependent calcium channels.
-
dual effects of pacap on guinea pig Gallbladder Muscle via pacap preferring and vip pacap preferring receptors
American Journal of Physiology-gastrointestinal and Liver Physiology, 1997Co-Authors: Henry P Parkman, Anthony P Pagano, James P RyanAbstract:The aims of this study were to determine the effect and mechanism of action of pituitary adenylate cyclase-activating peptide (PACAP) on Gallbladder Muscle. Guinea pig Gallbladder Muscle strips were studied isometrically. In noncontracted Muscle strips, PACAP-27 and PACAP-38 caused dose-dependent contractions, whereas vasoactive intestinal peptide (VIP) caused dose-dependent relaxation. PACAP-27 contractions were resistant to tetrodotoxin, atropine, and the substance P receptor antagonist [D-Arg1,D-Trp7,9,Leu11]substance P (Spantide) but were inhibited by the selective PACAP receptor antagonist PACAP-(6-38) and slightly increased with the VIP receptor antagonist [4-chloro-D-Phe6,Leu17]VIP. In cholecystokinin-precontracted Muscle strips, both VIP and PACAP caused relaxations. This relaxant effect of PACAP-27 was inhibited by PACAP-(6-38) and [4-chloro-D-Phe6,Leu17]VIP, but not by tetrodotoxin. These studies suggest that PACAP has dual excitatory and inhibitory effects on guinea pig Gallbladder Muscle. The contractile effect of PACAP is a direct action on Muscle through PACAP-preferring receptors. The relaxant effect of PACAP is seen in precontracted Muscle strips and mediated through VIP/ PACAP-preferring receptors.
