Anti-Apoptotic Effects of Arachidonic Acid and Prostaglandin E&lt;sub&gt;2&lt;/sub&gt; in Pancreatic β-Cells

Papadimitriou, Alexandros; King, Aileen; Jones, Peter M.; Persaud, Shanta J.

doi:10.1159/000107544

Cited by 47 publications

(48 citation statements)

References 50 publications

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“…These suppressions may reduce the biosynthesis of PGE2 from arachidonic acid via the cyclooxygenase and prostaglandin H synthase pathways [19]. It is evident that arachidonic acid and PGE2 are anti-apoptotic effects in various cancer cells and chemical-induced carcinogenesis in animal models [27], confirming our data obtained in the present study. In addition, cPLA2 is cleaved by caspase-3 and/or a related caspase in cells undergoing apoptosis [1,33].…”

Section: Expression or Activation Of Anti-apoptotic Proteins On A-549supporting

confidence: 90%

Anti-proliferative Effects of β-ionone on Human Lung Cancer A-549 Cells

Lee¹,

Kim²,

Jang³

et al. 2013

Journal of Life Science

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The anti-proliferative activity of β-ionone was investigated on human non-small lung cancer A-549 cells (designated A-549 cells). A-549 cells were treated with various concentrations of β-ionone (1, 5, 10, and 15 μM) for two, four, and six days. Biochemical markers related to the growth inhibition of A-549 cells by β-ionone were measured at the second day of incubation. β-Ionone inhibited the growth of A-549 cells by dose-and time-dependent manners, resulting in an IC50 of 5.0 μg/ml at the second day of incubation. β-Ionone induced apoptosis by a dose-dependent manner. β-Ionone increased levels of p53, p21, and Bax proteins, but suppressed expression of the Bcl-2 protein. Similarly, β-ionone enhanced cytochrome c release from the mitochondria to the cytosol, and induced activation of caspase-9 and -3. Additionally, β-ion-one reduced cPLA2 and COX-2 protein levels. These results suggest that the β-ionone inhibits the proliferation of A-549 cells through reciprocal regulation of Bax and Bcl-2 gene expression and suppression of cPLA2 and COX-2 protein expressions.

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Section: Expression or Activation Of Anti-apoptotic Proteins On A-549supporting

confidence: 90%

Anti-proliferative Effects of β-ionone on Human Lung Cancer A-549 Cells

Lee¹,

Kim²,

Jang³

et al. 2013

Journal of Life Science

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“…Islets were isolated from male ICR mice by collagenase digestion of the exocrine pancreas, essentially as described 49 and maintained in culture overnight in RPMI 1640 medium (11 mM glucose, 10% FBS) prior to use.…”

Section: Discussionmentioning

confidence: 99%

“…Changes in intracellular Ca 2+ were quantified as previously described. 49 All cannabinoid agonists were dissolved in DMSO and at the maximum concentration of vehicle used (0.1% v/v) there was no effect on Fura 2 fluorescence characteristics.…”

Section: Methodsmentioning

confidence: 99%

Expression and function of cannabinoid receptors in mouse islets

Bowe

Jones

et al. 2010

Islets

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“…Mouse islet isolation and maintenance Islets were isolated from 3-month-old Nupr1 −/− mice and their wild-type littermates by collagenase digestion as previously described [12] and maintained in culture for at least 24 h before use. Islet insulin and double-stranded (ds)DNA contents were quantified by RIA [13] and PicoGreen fluorescence, respectively, and the insulin per dsDNA ratios were calculated.…”

Section: Methodsmentioning

confidence: 99%

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass

et al. 2013

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Aims/hypothesis The stress-activated nuclear protein transcription regulator 1 (NUPR1) is induced in response to glucose and TNF-α, both of which are elevated in type 2 diabetes, and Nupr1 has been implicated in cell proliferation and apoptosis cascades. We used Nupr1 −/− mice to study the role of Nupr1 in glucose homeostasis under normal conditions and following maintenance on a high-fat diet (HFD). Methods Glucose homeostasis in vivo was determined by measuring glucose tolerance, insulin sensitivity and insulin secretion. Islet number, morphology and beta cell area were assessed by immunofluorescence and morphometric analysis, and islet cell proliferation was quantified by analysis of BrdU incorporation. Islet gene expression was measured by gene arrays and quantitative RT-PCR, and gene promoter activities were monitored by measuring luciferase activity. Results Nupr1 −/− mice had increased beta cell mass as a consequence of enhanced islet cell proliferation. Nupr1-dependent suppression of beta cell Ccna2 and Tcf19 promoter activities was identified as a mechanism through which Nupr1 may regulate beta cell cycle progression. Nupr1 −/− mice maintained on a normal diet were mildly insulin resistant, but were normoglycaemic with normal glucose tolerance because of compensatory increases in basal and glucose-induced insulin secretion. Nupr1 deletion was protective against HFD-induced obesity, insulin resistance and glucose intolerance. Conclusions/interpretation Inhibition of NUPR1 expression or activity has the potential to protect against the metabolic defects associated with obesity and type 2 diabetes.

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Anti-Apoptotic Effects of Arachidonic Acid and Prostaglandin E<sub>2</sub> in Pancreatic β-Cells

Cited by 47 publications

References 50 publications

Anti-proliferative Effects of β-ionone on Human Lung Cancer A-549 Cells

Anti-proliferative Effects of β-ionone on Human Lung Cancer A-549 Cells

Expression and function of cannabinoid receptors in mouse islets

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass

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