Background: Constitutive cyclooxygenase-1 enzyme synthesizes prostaglandins which are thought to play an important role in the functional integrity of the stomach gastric mucosa. Recently, it was shown that cyclooxygenase-1 deficient mutant mice did not develop spontaneous gastric pathology and appear less sensitive to indomethacin-induced gastric damage.
Aim: To investigate gastric acid secretion in cyclooxygenase-1 deficient mutant mice.
Methods: The basal and histamine or isobutyl methylxanthine-stimulated acid secretion in stomachs of cyclooxygenase-1 deficient homozygous mice and the effect of indomethacin was compared with that of heterozygous and wild-type mice using isolated lumen perfused mouse stomachs, in organ baths, monitored by pH-electrodes.
Results: There was no significant difference in the basal or histamine stimulated gastric acid secretion between wild-type or heterozygous or homozygous mice. However, isobutyl methylxanthine was more potent in the cyclooxygenase-1 deficient and heterozygous mice than in wild-type mice. Indomethacin, at concentrations below 1 mM, had no effect on either basal or histamine stimulated acid secretion in any of the mice populations.
Conclusion: Gastric acid secretion is maintained without prostaglandin involvement in cyclooxygenase-1 deficient mice. The finding that basal and histamine-stimulated gastric acid secretion was similar in the cyclooxygenase-1 deficient, compared to wild-type mice is consistent with the lack of spontaneous gastric pathology in the cyclooxygenase-1 deficient mice.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1046/j.1365-2036.2000.00836.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Defective mitochondrial COX1 translation due to loss of COX14 function triggers ROS-induced inflammation in mouse liver.
Nat Commun
August 2024
Department of Cellular Biochemistry, University Medical Center Göttingen, 37073, Göttingen, Germany.
Mitochondrial oxidative phosphorylation (OXPHOS) fuels cellular ATP demands. OXPHOS defects lead to severe human disorders with unexplained tissue specific pathologies. Mitochondrial gene expression is essential for OXPHOS biogenesis since core subunits of the complexes are mitochondrial-encoded.
View Article and Find Full Text PDFProstacyclin Synthase Deficiency Leads to Exacerbation or Occurrence of Endothelium-Dependent Contraction and Causes Cardiovascular Disorders Mainly via the Non-TxA Prostanoids/TP Axis.
Circ Res
August 2024
Cardiovascular Research Center (J.G., Yingbi Zhou, K.X., J.L., X.C., G.Y., X.S., Y.X., D.H., B.L.), Shantou University Medical College, China.
Article Synopsis
- - Prostaglandin I, produced by COX in endothelial cells, can cause vasodilation in some blood vessels while paradoxically leading to endothelium-dependent constriction (EDC) in others, particularly in diseases like hypertension, though the effects of PGIS deficiency on EDC and related cardiovascular issues are not well understood.
- - The study utilized various mouse models, including wild-type and genetically modified knockouts, to measure the impact of PGIS deficiency and assess vasomotor responses, indicating alterations in nitric oxide production and signaling.
- - Results showed that PGIS deficiency worsened EDC and led to increases in blood pressure and cardiac issues over time, but additional removal of the thromboxane receptor improved vascular function and reduced
Effects of low-dose acetylsalicylic acid on the inflammatory response to experimental sleep restriction in healthy humans.
Brain Behav Immun
October 2024
Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, USA; Division of Sleep Medicine, Harvard Medical School, Boston, MA, USA. Electronic address:
Background: Sleep deficiencies, such as manifested in short sleep duration or insomnia symptoms, are known to increase the risk for multiple disease conditions involving immunopathology. Inflammation is hypothesized to be a mechanism through which deficient sleep acts as a risk factor for these conditions. Thus, one potential way to mitigate negative health consequences associated with deficient sleep is to target inflammation.
View Article and Find Full Text PDFThe human mitochondrial translation factor TACO1 alleviates mitoribosome stalling at polyproline stretches.
Nucleic Acids Res
September 2024
Department of Neurology, University of Miami Miller School of Medicine, 1600 NW 10th Ave., Miami, FL 33136, USA.
The prokaryotic translation elongation factor P (EF-P) and the eukaryotic/archaeal counterparts eIF5A/aIF5A are proteins that serve a crucial role in mitigating ribosomal stalling during the translation of specific sequences, notably those containing consecutive proline residues (1,2). Although mitochondrial DNA-encoded proteins synthesized by mitochondrial ribosomes also contain polyproline stretches, an EF-P/eIF5A mitochondrial counterpart remains unidentified. Here, we show that the missing factor is TACO1, a protein causative of a juvenile form of neurodegenerative Leigh's syndrome associated with cytochrome c oxidase deficiency, until now believed to be a translational activator of COX1 mRNA.
View Article and Find Full Text PDFDifferential Impact In Vivo of Pf4-ΔCre-Mediated and Gp1ba-ΔCre-Mediated Depletion of Cyclooxygenase-1 in Platelets in Mice.
Arterioscler Thromb Vasc Biol
June 2024
Institute for Translational Medicine and Therapeutics, Perelman School of Medicine (S.Y.T., R.L., H.M., B.J.A., E.J.H., A.S., U.S.D., R.J., R.M., G.R.G., E.R., T.G., A.M.W., G.A.F.), University of Pennsylvania, Philadelphia.
Background: Low-dose aspirin is widely used for the secondary prevention of cardiovascular disease. The beneficial effects of low-dose aspirin are attributable to its inhibition of platelet Cox (cyclooxygenase)-1-derived thromboxane A. Until recently, the use of the Pf4 (platelet factor 4) Cre has been the only genetic approach to generating megakaryocyte/platelet ablation of Cox-1 in mice.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!