Prostaglandin synthesis by microsomes of circular and longitudinal gastrointestinal muscles

Sanders, Katherine; Northrup, Thomas E.

doi:10.1152/ajpgi.1983.244.4.g442

Cited by 23 publications

(17 citation statements)

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“…The supporting effect of reduced glutathione on prostanoid formation has been described by Blackwell et al [14] and Sanders et al [16] . Hemoglobin has been shown to be also necessary for the hydroperoxidase part of the synthase reaction 191 ; Roth et al' 111 investigated the integration of heme into the enzyme by spectroscopy.…”

Section: Discussionmentioning

confidence: 58%

Prostaglandin D₂and E₂Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester

Grewe¹,

Duyster²,

Dieter³

et al. 1992

Biological Chemistry Hoppe-Seyler

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Prostaglandin-synthesizing activities were demonstrated in cell-free extracts of rat Kupffer cells and characterized.The enzymatic properties of PGH 2 synthase were found to be similar to those of synthases present in other organs or cell types. The specific activity of the enzyme was not changed by substances that stimulate prostanoid release by intact Kupffer cells; however, it was reduced by pretreatment of the cells with glucocorticoid hormones. On the other hand, the activities of PGD 2 and PGE 2 synthase were influenced differently by the kind of cell stimulation. While pretreatment of the intact cells with endotoxin and/or inhibition of protein kinase C led to an enhanced PGE 2 formation in cell-free extracts, exposure to agents that enhance protein kinase C-dependent signalling pathways, e.g. phagocytotic stimuli or phorbol ester, suppressed PGE 2 synthase activity and, therefore, led to enhanced PGD 2 synthesis. It is in line with this observation that in vitro activation of protein kinase C of Kupffer cells resulted in a reduced PGE 2 and an enhanced PGD 2 synthase activity. Die Prostaglandin D 2 -und E 2 -Synthesen in Kupffer-Zellen der Ratte werden durch Lipopolysaccharid und Phorbolester antagonistisch reguliertZusammenfassung: In zellfreien Extrakten von Kupffer-Zellen der Ratte wurden prostaglandinsynthetisierende Enzymaktivitäten nachgewiesen und charakterisiert. Die enzymatischen Eigenschaften der PGH 2 -Synthase erwiesen sich als vergleichbar mit den entsprechenden Enzymen, die für andere Zellen oder Organe beschrieben wurden. Die spezifische Aktivität dieses Enzyms änderte sich nicht nach Behandlung der Kupffer-Zellen mit Stimulatoren der Prostanoidfreisetzung; allerdings ist die spezifische Enzymaktivität durch Vorbehandlung der intakten Zellen mit Glucocortikoiden signifikant reduziert. Andererseits wurden die enzymatischen Aktivitäten für die PGD 2 -und PGE 2 -Synthese, in Abhängigkeit von der Art der Zellstimulation, unterschiedlich beeinflußt. Während eine Vorbehandlung der Zellen mit

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Section: Discussionmentioning

confidence: 58%

Prostaglandin D₂and E₂Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester

Grewe¹,

Duyster²,

Dieter³

et al. 1992

Biological Chemistry Hoppe-Seyler

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“…PGs are known to be potent regulators of the electrical and mechanical activities of GI smooth muscle. 35,36) The activity of bifunctional COX-1 and COX-2 enzymes generated PGs. COX-1 is constitutively expressed in various tissue but, COX-2 may be highly induced by cytokines and other participants in inflammatory processes.…”

Section: Discussionmentioning

confidence: 99%

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Kim

Chae

Kwon

et al. 2010

Biological & Pharmaceutical Bulletin

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The interstitial cells of Cajal (ICCs) are pacemakers in the gastrointestinal tract. The possibility of whether imatinib mesylate, a Kit receptor tyrosine kinase inhibitor, modulates pacemaker activities in the ICC was examined using the whole cell patch clamp technique. Imatinib decreased the amplitude of pacemaker potentials in a dose-dependent manner in current-clamp mode. Because the effects of imatinib on pacemaker potentials were the same as those of pinacidil, we examined the effect of glibenclamide on ICC exposed to imatinib. The effects of imatinib on pacemaker potentials were blocked by glibenclamide. To see whether the production of prostaglandins (PGs) is involved in the inhibitory effect of imatinib on pacemaker potentials, we tested the effects of naproxen (a non-selective cyclooxygenase inhibitor) and AH6809 (a prostaglandin EP1 and EP2 receptor antagonist). Naproxen and AH6809 blocked the inhibitory effects of imatinib on ICC. Butaprost (an EP2 receptor agonist) showed the actions on pacemaker potentials in the same manner as imatinib. However, SC 19220 (an EP1 receptor antagonist) has no effects. To investigate the involvement of cAMP and protein kinase A (PKA) in the effects of imatinib on ICC, SQ 22536 (an inhibitor of adenylate cyclase) and mPKAI (an inhibitor of myristoylated PKA) were used. Both SQ-22536 and mPKAI blocked the imatinib-mediated inhibition of pacemaker potentials. However, the protein kinase C (PKC) inhibitors did not block the imatinib-mediated inhibition of pacemaker potentials. These results indicate that imatinib inhibits the pacemaker potentials of ICC by activating ATP-sensitive K ؉ ؉ channels and PKA-dependent, PKC-independent manner.

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“…Many prostaglandins (e.g., PGE 2 , PGD 2 , PGF 2␣ , PGI 2 , PGA 2 ) are synthesized in mammalian GI tunica muscularis, and PGE 2 was found to be a prominent species produced in gastric muscles (28). Both cyclooxygenase (COX) 1 and 2 are constitutively expressed in murine gastric muscles, and COX-2 was specifically localized in neurons containing nitric oxide synthase and intramuscular ICC (24).…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, little is known about the pathophysiological mechanism(s) leading to the development of gastric arrhythmias, or the consequences of altering gastric pacemaker frequency on functional coupling. Several naturally occurring compounds have chronotropic effects on antral muscles, including prostaglandins (28) and cholinergic agonists (8). Chronotropic effects of these agonists appear to be mediated by EP 3 receptors (17) and M 3 muscarinic (18) receptors, respectively, which might couple to generation of inositol 1,4,5-trisphosphate (IP 3 ) and acceleration of the pacemaker clock mechanism (27).…”

mentioning

confidence: 99%

Prostaglandin regulation of gastric slow waves and peristalsis

Forrest

Hennig²,

Jokela-Willis³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Gastric emptying depends on functional coupling of slow waves between the corpus and antrum, to allow slow waves initiated in the gastric corpus to propagate to the pyloric sphincter and generate gastric peristalsis. Functional coupling depends on a frequency gradient where slow waves are generated at higher frequency in the corpus and drive the activity of distal pacemakers. Simultaneous intracellular recording from corpus and antrum was used to characterize the effects of PGE(2) on slow waves in the murine stomach. PGE(2) increased slow-wave frequency, and this effect was mimicked by EP(3), but not by EP(2), receptor agonists. Chronotropic effects were due to EP(3) receptors expressed by intramuscular interstitial cells of Cajal because these effects were not observed in W/W(V) mice. Although the integrated chronotropic effects of EP(3) receptor agonists were deduced from electrophysiological experiments, no clear evidence of functional uncoupling was observed with two-point electrical recording. Gastric peristalsis was also monitored by video imaging and spatiotemporal maps to study the impact of chronotropic agonists on propagating contractions. EP(3) receptor agonists increased the frequency of peristaltic contractions and caused ectopic sites of origin and collisions of peristaltic waves. The impact of selective regional application of chronotropic agonists was investigated by use of a partitioned bath. Antral slow waves followed enhanced frequencies induced by stimulation of the corpus, and corpus slow waves followed when slow-wave frequency was elevated in the antrum. This demonstrated reversal of slow-wave propagation with selective antral chronotropic stimulation. These studies demonstrate the impact of chronotropic agonists on regional intrinsic pacemaker frequency and integrated gastric peristalsis.

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Prostaglandin synthesis by microsomes of circular and longitudinal gastrointestinal muscles

Cited by 23 publications

References 0 publications

Prostaglandin D₂and E₂Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester

Prostaglandin D₂and E₂Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Prostaglandin regulation of gastric slow waves and peristalsis

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Prostaglandin synthesis by microsomes of circular and longitudinal gastrointestinal muscles

Cited by 23 publications

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Prostaglandin D2and E2Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester

Prostaglandin D2and E2Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester

Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine

Prostaglandin regulation of gastric slow waves and peristalsis

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Prostaglandin D₂and E₂Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester

Prostaglandin D₂and E₂Syntheses in Rat Kupffer Cells are Antagonistically Regulated by Lipopolysaccharide and Phorbol Ester