Arachidonic Acid-Induced Hormone Release in Somatotropes: Involvement of Calcium

Roudbaraki, Morad; Drouhault, R; Bacquart, Thierry; Vacher, Pierre

doi:10.1159/000126964

Cited by 15 publications

(9 citation statements)

References 13 publications

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“…Our observations that arachidonic acid (AA) induces calcium influx in Jurkat T-cells are in accordance with the reports of several investigators who have shown that this fatty acid induces calcium influx in different cell lines [17,[28][29][30][31]. To shed light on whether exogenous AA evoked capacitative calcium influx, we employed thapsigargin (TG) and conducted experiments in 0% Ca 2+ buffer.…”

Section: Discussionsupporting

confidence: 90%

Role of three isoforms of phospholipase A₂ in capacitative calcium influx in human T‐cells

Hichami¹,

Joshi²,

Simonin³

et al. 2002

European Journal of Biochemistry

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The present study was conducted on human Jurkat T-cell lines in order to elucidate the role of phospholipase A 2 in capacitative calcium entry. We have employed thapsigargin (TG) that induces increases in [Ca 2+ ] i by emptying the calcium pool of endoplasmic reticulum, followed by capacitative calcium entry. We designed a Ca 2+ free/Ca 2+ reintroduction (CFCR) protocol for the experiments, conducted in Ca 2+ -free medium. By employing CFCR protocol, we observed that addition of exogenous arachidonic acid (AA) stimulated TG-induced capacitative calcium influx. The liberation of endogenous AA and its autocrine action seems to be implicated during TGinduced capacitative calcium influx: TG potentiates the induction of constitutively expressed mRNA of four PLA 2 isoforms (type 1B, IV, V, VI), the inhibitors of the three PLA 2 isotypes (type 1B, V, VI) inhibit TG-induced release of [ 3 H]AA into the extracellular medium, and finally, these PLA 2 inhibitors do curtail TG-stimulated capacitative calcium entry in these cells. These results suggest that stimulation of three isoforms of PLA 2 by thapsigargin liberates free AA that, in turn, induces capacitative calcium influx in human T-cells.

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Section: Discussionsupporting

confidence: 90%

Role of three isoforms of phospholipase A₂ in capacitative calcium influx in human T‐cells

Hichami¹,

Joshi²,

Simonin³

et al. 2002

European Journal of Biochemistry

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“…Similarly, the inhibition of PLA 2 activation by chemical inhibitors and siRNA curtailed the TGinduced Ca 2+ influx in CD36-positive TBCs. These observations suggest that AA (exogenous or endogenous) evokes Ca 2+ influx in these cells as shown elsewhere (34,35), and its action on Ca 2+ influx is not influenced by its metabolites (36).…”

Section: Discussionsupporting

confidence: 72%

STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice

Dramane¹,

Abdoul-Azize²,

Hichami³

et al. 2012

J. Clin. Invest.

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Understanding the mechanisms underlying oro-gustatory detection of dietary fat is critical for the prevention and treatment of obesity. The lipid-binding glycoprotein CD36, which is expressed by circumvallate papillae (CVP) of the mouse tongue, has been implicated in oro-gustatory perception of dietary lipids. Here, we demonstrate that stromal interaction molecule 1 (STIM1), a sensor of Ca 2+ depletion in the endoplasmic reticulum, mediates fatty acid-induced Ca 2+ signaling in the mouse tongue and fat preference. We showed that linoleic acid (LA) induced the production of arachidonic acid (AA) and lysophosphatidylcholine (Lyso-PC) by activating multiple phospholipase A 2 isoforms via CD36. This activation triggered Ca 2+ influx in CD36-positive taste bud cells (TBCs) purified from mouse CVP. LA also induced the production of Ca 2+ influx factor (CIF). STIM1 was found to regulate LA-induced CIF production and the opening of multiple store-operated Ca 2+ (SOC) channels. Furthermore, CD36-positive TBCs from Stim1 -/-mice failed to release serotonin, and Stim1 -/-mice lost the spontaneous preference for fat that was observed in wild-type animals. Our results suggest that fatty acid-induced Ca 2+ signaling, regulated by STIM1 via CD36, might be implicated in oro-gustatory perception of dietary lipids and the spontaneous preference for fat. IntroductionThe sense of taste informs the organism about the quality of ingested food. Five basic taste modalities, e.g., sweet, sour, bitter, salty, and umami, have so far been identified (1). Recent compelling evidence from rodents raises the possibility of an additional sixth taste modality devoted to the perception of lipids (2-4) that are released by the action of lingual lipases, present in the salivary secretions (5). Fukuwatari et al. (6) and Laugerette et al. (2) have documented the expression of the receptor-like lipid-binding protein CD36 in rat and mouse circumvallate papillae (CVP), respectively. Laugerette et al. (2) have provided the first evidence for the involvement of lingual CD36 in dietary lipid perception in the mouse. Indeed, Cd36 gene inactivation completely abolished the spontaneous preference for long-chain fatty acids (LCFAs) observed in wild-type mice. This effect is lipid specific, since the preference for sweet and aversion to bitterness reported in controls were not altered in Cd36-null mice. These observations regarding the implication of CD36 in the perception of lipid taste have also been confirmed by other investigators (7).The coupling of CD36 cell signaling to a downstream second messenger cascade has been explored in mouse taste bud cells (TBCs) (3,8). The experiments conducted on CD36-positive TBCs purified from mouse CVP demonstrated that linoleic acid (LA), an LCFA, induced increases in free intracellular calcium concentrations, [Ca 2+ ] i by binding to CD36 (3). We have reported that LCFAs induced the production of inositol-1,4,5-trisphosphate (IP 3 ) and, consequently, recruited Ca 2+ from the endoplasmic reticulum, followed by Ca 2+ inf...

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“…The inhibitory effect of arthritis on GH does not seem to be mediated by the increased release of PGE 2 , since this prostanoid has been reported to be a GH secretagogue (12,43). A stimulatory effect of lipoxygenase products on pituitary GH synthesis and secretion has also been reported (12,53). Therefore, the inhibitory effect of arthritis on pituitary GH can be secondary to another inhibitory substance that is released after COX-2 activation.…”

Section: Discussionmentioning

confidence: 90%

Experimental arthritis inhibits the insulin-like growth factor-I axis and induces muscle wasting through cyclooxygenase-2 activation

Granado¹,

Martín²,

Villanúa³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Chronic arthritis induces cachexia associated with an inhibition of the growth hormone (GH)-insulin-like growth factor-I (IGF-I) system and an activation of the E3 ubiquitin-ligating enzymes muscle atrophy F-box (MAFbx) and muscle Ring finger 1 (MuRF1) in the skeletal muscle. The aim of this work was to study the role of cyclooxygenase (COX)-2 in chronic arthritis-induced cachexia. Arthritis was induced in rats by Freund's adjuvant injection, and the effects of two COX inhibitors (indomethacin, a nonspecific inhibitor, and meloxicam, a selective COX-2 inhibitor on pituitary GH and on liver and serum IGF-I levels) were tested. Arthritis decreased body weight gain and GH and liver IGF-I gene expression. In the arthritic rats, both inhibitors, indomethacin and meloxicam, prevented the inhibitory effect of arthritis on body weight gain. Indomethacin and meloxicam administration to arthritic rats increased pituitary GH and liver IGF-I mRNA as well as serum levels of IGF-I. These data suggest that induction of COX-2 during chronic inflammation is involved in the inhibition of the GH-IGF-I axis and in the body weight loss. In the gastrocnemius muscle, arthritis increased the gene expression of tumor necrosis factor (TNF)-α, the E3 ubiquitin-ligating enzymes MAFbx and MuRF1, as well as of IGF-I and IGF-binding protein-5 (IGFBP-5). Inhibition of COX-2 by meloxicam administration increased gastrocnemius weight and decreased MAFbx, MuRF1, TNF-α, and IGFBP-5 gene expression. In summary, our data indicate that chronic arthritis-induced cachexia and muscle wasting are mediated by the COX-2 pathway resulting in a decreased GH-IGF-I secretion and increased expression of MAFbx and MuRF1 mRNA.

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Arachidonic Acid-Induced Hormone Release in Somatotropes: Involvement of Calcium

Cited by 15 publications

References 13 publications

Role of three isoforms of phospholipase A₂ in capacitative calcium influx in human T‐cells

Role of three isoforms of phospholipase A₂ in capacitative calcium influx in human T‐cells

STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice

Experimental arthritis inhibits the insulin-like growth factor-I axis and induces muscle wasting through cyclooxygenase-2 activation

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Arachidonic Acid-Induced Hormone Release in Somatotropes: Involvement of Calcium

Cited by 15 publications

References 13 publications

Role of three isoforms of phospholipase A2 in capacitative calcium influx in human T‐cells

Role of three isoforms of phospholipase A2 in capacitative calcium influx in human T‐cells

STIM1 regulates calcium signaling in taste bud cells and preference for fat in mice

Experimental arthritis inhibits the insulin-like growth factor-I axis and induces muscle wasting through cyclooxygenase-2 activation

Contact Info

Product

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Role of three isoforms of phospholipase A₂ in capacitative calcium influx in human T‐cells

Role of three isoforms of phospholipase A₂ in capacitative calcium influx in human T‐cells