scholarly journals Induction of Cyclooxygenase-2 Gene in Pancreatic β-Cells by 12-Lipoxygenase Pathway Product 12-Hydroxyeicosatetraenoic Acid

2002 ◽  
Vol 16 (9) ◽  
pp. 2145-2154 ◽  
Author(s):  
Xiao Han ◽  
Songyuan Chen ◽  
Yujie Sun ◽  
Jerry L. Nadler ◽  
David Bleich
Keyword(s):  
Gene Expression ◽  
Prostaglandin E2 ◽  
Cyclooxygenase 2 ◽  
Pge2 Production ◽  
Hydroxyeicosatetraenoic Acid ◽  
Lipoxygenase Inhibitor ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Cox 2 ◽  
12 Lipoxygenase

Abstract Cyclooxygenase-2 (COX-2) gene and 12-lipoxygenase (12-LO) gene are preferentially expressed over other types of cyclooxygenase and lipoxygenase in pancreatic β-cells. Inhibition of either COX-2 or 12-LO can prevent cytokine-induced pancreatic β-cell dysfunction as defined by inhibition of glucose-stimulated insulin secretion. As cellular stress induces both genes and their respective end products in pancreatic β-cells, we evaluated the role of 12-hydroxyeicosatetraenoic acid (HETE) on COX-2 gene expression, protein expression, and prostaglandin E2 (PGE2) production. We demonstrate that 12-HETE significantly increases COX-2 gene expression and consequent product formation, whereas a closely related lipid, 15-HETE, does not. In addition, IL-1β-stimulated prostaglandin E2 production is completely inhibited by a preferential lipoxygenase inhibitor cinnaminyl-3,4-dihydroxy-α-cyanocinnamate. We then evaluated IL-1β-induced PGE2 production in islets purified from control C57BL/6 mice and 12-LO knockout mice lacking cytokine-inducible 12-HETE. IL-1β stimulated an 8-fold increase in PGE2 production in C57BL/6 islets but failed to stimulate PGE2 in 12-LO knockout islets. Addition of 12-HETE to 12-LO knockout islet cells produced a statistically significant rise in PGE2 production. Furthermore, 12-HETE, but not 15-HETE, stimulated COX-2 promoter and activator protein-1 binding activity. These data demonstrate that 12-HETE mediates cytokine-induced COX-2 gene transcription and resultant PGE2 production in pancreatic β-cells.

scholarly journals Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E2 Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 190 ◽  
Author(s):  
Jae Won Ha ◽  
Hyerim Song ◽  
Seong Su Hong ◽  
Yong Chool Boo
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Particulate Matter ◽  
Prostaglandin E2 ◽  
Pge2 Production ◽  
Ecklonia Cava ◽  
Epidermal Keratinocytes ◽  
Hacat Keratinocytes ◽  
Cox 2 ◽  
Cox 1

Atmospheric particulate matter (PM) is an important cause of skin damage, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of Ecklonia cava Kjellman, a perennial brown macroalga, can alleviate oxidative stress in epidermal keratinocytes exposed to PM less than 10 microns in diameter (PM10). The present study was undertaken to further examine the anti-inflammatory effects of E. cava extract and its major polyphenolic constituent, dieckol. HaCaT keratinocytes were exposed to PM10 in the presence or absence of E. cava extract or dieckol and analyzed for their viability, prostaglandin E2 (PGE2) release, and gene expression of cyclooxygenase (COX)-1, COX-2, microsomal prostaglandin E2 synthase (mPGES)-1, mPGES-2, and cytosolic prostaglandin E2 synthase (cPGES). PM10 treatment decreased cell viability and increased the production of PGE2, and these changes were partially abrogated by E. cava extract. E. cava extract also attenuated the expression of COX-1, COX-2, and mPGES-2 stimulated by PM10. Dieckol attenuated PGE2 production and the gene expression of COX-1, COX-2, and mPGES-1 stimulated by PM10. This study demonstrates that E. cava extract and dieckol alleviate airborne PM10-induced PGE2 production in keratinocytes through the inhibition of gene expression of COX-1, COX-2, mPGES-1, and/or mPGES-2. Thus, E. cava extract and dieckol are potentially useful natural cosmetic ingredients for counteracting the pro-inflammatory effects of airborne PM.

Several transcription factors regulate COX-2 gene expression in pancreatic β-cells

2007 ◽  
Vol 34 (3) ◽  
pp. 199-206 ◽  
Author(s):  
Xiongfei Zhang ◽  
Jingjing Zhang ◽  
Xiaomin Yang ◽  
Xiao Han
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Cox 2

scholarly journals Potential Role of NO in Modulation of COX-2 Expression and PGE2 Production in Pancreatic β-cells

2005 ◽  
Vol 37 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Jia-Jian Ling ◽  
Yu-Jie Sun ◽  
Dong-Ya Zhu ◽  
Qi Chen ◽  
Xiao Han
Keyword(s):  
Nitric Oxide ◽  
Protein Expression ◽  
Gene Transcription ◽  
Pge2 Production ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
No Formation ◽  
Cox 2

Abstract Cytokines have been implicated in pancreatic β-cell destruction leading to type 1 diabetes. Exposure to interleukin-1β (IL-1β) of pancreatic β-cells induces expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Subsequent formation of nitric oxide (NO) and prostaglandin E2 (PGE2) may impair β-cell function. Using NOS inhibitor NG-monomethyl-L-arginine (L-NMMA), we have further investigated the relation between NO formation and COX-2 expression. IL-1β stimulated the formation of NO and PGE2 by pancreatic β-cells. L-NMMA completely inhibited IL-1β-induced NO formation and attenuated PGE2 production. COX-2 gene transcription level and protein expression were determined by real-time PCR, Western blot and luciferase analysis. L-NMMA inhibited IL-1β-induced promoter activity, gene transcription and protein expression of COX-2 in pancreatic β-cells. Therefore, we concluded that NO-affected COX-2 activity is directly linked to COX-2 gene transcription and protein expression in pancreatic β-cells. The identification of a novel interaction of NO on the COX signaling pathway in β-cells provides a strategy of intervention for further evaluating the role of NO and PGE2 in autoimmune diabetes.

Mikroglia und immunologische Mechanismen in der neuropsychiatrischen Forschung

2014 ◽  
Vol 33 (11) ◽  
pp. 761-770
Author(s):  
M. J. Schwarz ◽  
B. Leitner ◽  
E. Weidinger ◽  
N. Müller
Keyword(s):  
Prostaglandin E2 ◽  
Cyclooxygenase 2 ◽  
Cox 2

ZusammenfassungDie Psychoneuroimmunologie beschäftigt sich mit den Wechselwirkungen zwischen der (gesunden) Psyche, psychischen Störungen und dem Immunsystem. Inzwischen hat sich gezeigt, dass zumindest bei Subgruppen psychischer Störungen wie Schizophrenie und Depression ein entzündlicher Prozess bei der Pathogenese eine Rolle spielt. Da für Schizophrenie und Depression auf diesem Gebiet die meisten Befunde vorliegen, konzentriert sich diese Übersicht auf diese beiden Störungsbilder. Die differenzielle Aktivierung von Mikrogliazellen und Astrozyten als funktionelle Träger des Immunsystems im ZNS, trägt zur Typ-1/Typ-2-Inbalance bei. Das entzündliche Geschehen ist verbunden mit höherer Prostaglandin-E2 (PGE-2)-Produktion und erhöhter Cyclooxygenase-2 (COX-2)-Expression. Zunehmende Evidenz aus klinischen Studien mit COX-2-Inhibitoren weisen auf einen günstigen Effekt antiinflammatorischer Therapie bei Schizophrenie hin, speziell in frühen Stadien der Krankheit. Sowohl bei Depression als auch bei Schizophrenie ist die Vulnerabilitäts- Stress-Hypothese weitgehend akzeptiert. So zeigte sich z. B. dass – bei entsprechender genetischer Disposition – Stress im frühen Lebensalter oder Separationsstress mit einem Anstieg proinflammatorischer Zytokine einhergehen und zu einer Immunaktivierung führen. Die Interaktionen zwischen dem Immunsystem, Neurotransmittern und dem Tryptophan- Kynurenin-System sind entscheidende Komponenten für die Pathogenese von Stress und Depression. Eine antientzündliche Behandlung, z. B. mit dem COX-2-Inhibitor Celecoxib, zeigt antidepressive Effekte.

scholarly journals Expression Profiles of the Progesterone Receptor, Cyclooxygenase-2, Growth Differentiation Factor 9, and Bone Morphogenetic Protein 15 Transcripts in the Canine Oviducts during the Oestrous Cycle

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 454
Author(s):  
Jaime Palomino ◽  
Javiera Flores ◽  
Georges Ramirez ◽  
Victor H. Parraguez ◽  
Monica De los Reyes
Keyword(s):  
Gene Expression ◽  
Bone Morphogenetic Protein ◽  
Cyclooxygenase 2 ◽  
Oestrous Cycle ◽  
Progesterone Concentration ◽  
Plasma Progesterone ◽  
Morphogenetic Protein ◽  
Growth Differentiation Factor 9 ◽  
Bone Morphogenetic Protein 15 ◽  
Cox 2

The gene expression in the canine oviduct, where oocyte maturation, fertilization, and early embryonic development occur, is still elusive. This study determined the oviductal expression of (PR), cyclooxygenase-2 (COX-2), growth differentiation factor 9 (GDF-9), and bone morphogenetic protein 15 (BMP-15) during the canine oestrous cycle. Samples were collected from bitches at anoestrus (9), proestrus (7), oestrus (8), and dioestrus (11), after routine ovariohysterectomy and the ovarian surface structures and plasma progesterone concentration evaluated the physiological status of each donor. The oviductal cells were isolated and pooled. Total RNA was isolated, and gene expression was assessed by qPCR followed by analysis using the t-test and ANOVA. The PR mRNA increased (P < 0.05) from the anoestrus to dioestrus with the plasma progesterone concentration (r = 0.8). COX-2 mRNA expression was low in the anoestrus and proestrus, and negligible in the oestrus, while it was around 10-fold higher (P < 0.05) in the dioestrus. The GDF-9 mRNA was expressed during all phases of the oestrous cycle and was most abundant (P < 0.05) during oestrus phase. The BMP-15 mRNA decreased (P < 0.05) in the anoestrus and proestrus phases. Thus, the transcripts were differentially expressed in a stage-dependent manner, suggesting the importance of oestrous cycle regulation for successful reproduction in dogs.

PPARγ is not required for the inhibitory actions of PGJ2 on cytokine signaling in pancreatic β-cells

2004 ◽  
Vol 286 (3) ◽  
pp. E329-E336 ◽  
Author(s):  
Sarah M. Weber ◽  
Anna L. Scarim ◽  
John A. Corbett
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Cytokine Signaling ◽  
Rinm5f Cells ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Inos Gene ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Inos Gene Expression

Peroxisome proliferator-activated receptor (PPAR)γ agonists, such as 15-deoxy-Δ12,14-prostaglandin J2 (PGJ2) and troglitazone, have been shown to elicit anti-inflammatory effects in pancreatic β-cells that include inhibition of cytokine-stimulated inducible nitric oxide synthase (iNOS) gene expression and production of nitric oxide. In addition, these ligands impair IL-1-induced NF-κB and MAPK as well as IFN-γ-stimulated signal transducer and activator of transcription (STAT)1 activation in β-cells. The purpose of this study was to determine if PPARγ activation participates in the anti-inflammatory actions of PGJ2 in β-cells. Pretreatment of RINm5F cells for 6 h with PGJ2 results in inhibition of IL-1-stimulated IκB degradation and IFN-γ-stimulated STAT1 phosphorylation. Overexpression of a dominant-negative (dn) PPARγ mutant or treatment with the PPARγ antagonist GW-9662 does not modulate the inhibitory actions of PGJ2 on cytokine signaling in RINm5F cells. Although these agents fail to attenuate the inhibitory actions of PGJ2 on cytokine signaling, they do inhibit PGJ2-stimulated PPARγ response element reporter activity. Consistent with the inability to attenuate the inhibitory actions of PGJ2 on cytokine signaling, neither dnPPARγ nor GW-9662 prevents the inhibitory actions of PGJ2 on IL-1-stimulated iNOS gene expression or nitric oxide production by RINm5F cells. These findings support a PPARγ-independent mechanism by which PPARγ ligands impair cytokine signaling and iNOS expression by islets.

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