Regulation of the growth hormone and luteinizing hormone response to endotoxin in sheep

Daniel, Joseph A; Whitlock, Brian K; Wagner, C G.; Sartin, James L.

doi:10.1016/s0739-7240(02)00171-6

Cited by 23 publications

(14 citation statements)

References 45 publications

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“…This change was faithfully reflected in the luteinizing hormone secretory pattern [22] . Furthermore, we demonstrated that AEA (50 ng/5 l) injected intracerebroventricularly reduced plasma luteinizing hormone levels in the rat [23] , similarly to the reduction of gonadotropin levels observed in sheep during endotoxemia induced by LPS [24] .…”

Section: Role Of the Endocannabinoid System In The Blockade Of The Resupporting

confidence: 68%

Endocannabinoids in TNF-α and Ethanol Actions

Rettori

Fernández‐Solari²,

Prestifilippo³

et al. 2007

Neuroimmunomodulation

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During marijuana and alcohol consumption as well as during inflammation the reproductive axis is inhibited, mainly through the inhibition of luteinizing hormone-releasing hormone release. In male rats, this inhibitory effect is mediated, at least in part, by the activation of hypothalamic cannabinoid type 1 receptors (CB1). During inflammation, this activation of the endocannabinoid system seems to be mediated by an increase in TNF-α production followed by anandamide augmentations, similarly the effect of intragastric administration of ethanol (3 g/kg) seems to be due to an increase in anandamide. On the other hand, a number of different actions mediated by the endocannabinoid system in various organs and tissues have been described. Both cannabinoid receptors, CB1 and CB2, are localized in the submandibular gland where they mediate the inhibitory effect of intrasubmandibular injections of the endocannabinoid anandamide (6 × 10^–5M) on salivary secretion. Lipopolysaccharide (5 mg/kg/3 h) injected intraperitoneally and ethanol (3 g/kg/1 h) injected intragastrically inhibited the salivary secretion induced by the sialogogue metacholine; this inhibitory effect was blocked by CB1 and/or CB2 receptor antagonists. Similar to the hypothalamus, these effects seem to be mediated by increased anandamide. In summary, similar mechanisms mediate the inhibitory actions of endocannabinoids and cannabinoids in both hypothalamus and submandibular gland during drug consumption and inflammation.

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Section: Role Of the Endocannabinoid System In The Blockade Of The Resupporting

confidence: 68%

Endocannabinoids in TNF-α and Ethanol Actions

Rettori

Fernández‐Solari²,

Prestifilippo³

et al. 2007

Neuroimmunomodulation

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“…The mRNA of several cytokines such as IL-1, IL-6, IL-11, LIF and MIF is expressed in the anterior pituitary gland and IL-6, LIF and MIF is produced by folliculo-stellate cells immunoreactive for S-100 protein (Arzt et al 1999;Inoue et al 1999). IL-1 induces increased release of GH in pituitary cell cultures (Arzt et al 1999) and stimulates GH release following intracerebroventricular (ICV) injection (Daniel et al 2002), while IL-1 inhibits GH surges by both intravenous and ICV injection (Wada et al 1995). On the other hand, GH enhances IL-1α, IL6 and TNFα production (Uronen-Hansson et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Localization of interleukin-18 and its receptor in somatotrophs of the bovine anterior pituitary gland

et al. 2005

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A pro-inflammatory cytokine, interleukin 18 (IL-18), induces intracellular expression of IL-1 and the release of IL-6. IL-1 and IL-6 has been detected in anterior pituitary cells, suggesting that IL-18 is produced in anterior pituitary cells and may serve to aid immuno-endocrine regulation. In the present study, we addressed this hypothesis by investigating the intracellular localization of IL-18 and its receptor in bovine anterior pituitary gland. IL-18 mRNA and its protein were detected in the anterior pituitary gland by RT-PCR and Western blotting. In situ hybridization showed that IL-18 mRNA was expressed in the anterior pituitary cells. Immunohistochemistry of IL-18 and specific hormones revealed the presence of IL-18 in somatotrophs. Furthermore, the expression of GH mRNA in IL-18 immunoreactive cells was confirmed by immuno-laser microdissection. These results first demonstrated that somatotrophs produced IL-18. Subsequently, the distribution of the IL-18 receptor alpha (IL-18Ralpha) was investigated in order to understand IL-18 signaling among the anterior pituitary cells. Bovine IL-18Ralpha cDNA was partially sequenced and detected in the anterior pituitary gland by RT-PCR. Immunohistochemistry of IL-18Ralpha, IL-18 and GH showed that IL-18Ralpha was co-localized in IL-18 immunoreactive cells or somatotrophs. These data suggest that IL-18 acts on somatotrophs as an immuno-endocrine mediator through the autocrine pathway.

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“…Recently, it has also been shown to affect the hormone secretion, acting at different levels of the hypothalamic-pituitary-adrenal axis [3, 14]. Some studies [3, 15] have revealed that IL-1 and its receptors are expressed in human and rodent pituitary glands; IL-1 induced the release of GH from pituitary cells [3, 7, 16, 17] and regulated growth and proliferation of pituitary cells [6, 18].…”

Section: Introductionmentioning

confidence: 99%

Stimulatory Effect of Interleukin-1β on Growth Hormone Gene Expression and Growth Hormone Release from Rat GH3 Cells

2005

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Our previous studies demonstrated that interferon gamma increases the human (h) growth hormone (GH) gene promoter activity in rat pituitary GH3 cells, and its regulatory mechanism may be different from the classical GH-releasing hormone-induced regulatory mechanism. Interleukin-1β (IL-1β) is thought to induce the release of GH by pituitary cells, but whether or not and by which mechanisms IL-1β regulates GH synthesis remains unclear. The purpose of our study was thus to investigate the effect of IL-1β on the hGH gene expression in GH3 rat pituitary tumor cells using stable transfection of the hGH promoter fused to a luciferase reporter gene. Our results showed that IL-1β (10–10⁴ U/ml) increased GH secretion and synthesis and that 10² to 10⁴ U/ml IL-1β promoted the luciferase expression in stable GH3 cells, with a maximal action of 1.61 times over that of controls. Among inhibitors of intracellular signaling transduction pathways, mitogen-activated protein kinase kinase (MAPKK/MEK) inhibitor PD98059 (40 µM) and p38 MAPK inhibitor SB203580 (5 µM)blocked completely the stimulatory effect of IL-1β, and the phosphoinositide 3-kinase inhibitor LY294002 (10 µM) blocked partially the induction of IL-1β. Western blot analysis demonstrated that IL-1β increased the activation of phosphorylated MEK and p38 MAPK in GH3 cells. Neither overexpression of Pit-1 nor inhibiting Pit-1 expression affected IL-1β induction of hGH promoter activity. To identify the DNA sequence that mediated the effect of IL-1β, six deletion constructs of hGH promoter were created. The stimulatory effect of IL-1β was abolished following deletion of the –196- to –132-bp fragment. In conclusion, our data show that IL-1β promotes GH secretion and synthesis by rat pituitary GH3 cells. The stimulatory effect of IL-1β on the hGH gene promoter appears to require the activation of MEK, p38 MAPK, and phosphoinositide 3-kinase and a fragment of promoter sequence that spans the –196- to –132-bp fragment of the gene, but is unrelated to the Pit-1 protein.

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Regulation of the growth hormone and luteinizing hormone response to endotoxin in sheep

Cited by 23 publications

References 45 publications

Endocannabinoids in TNF-α and Ethanol Actions

Endocannabinoids in TNF-α and Ethanol Actions

Localization of interleukin-18 and its receptor in somatotrophs of the bovine anterior pituitary gland

Stimulatory Effect of Interleukin-1β on Growth Hormone Gene Expression and Growth Hormone Release from Rat GH3 Cells

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