Interleukin-1-β Modulation of Prolactin Secretion from Rat Anterior Pituitary Cells: Involvement of Adenylate Cyclase Activity and Calcium Mobilization*

Schettini, Gennaro; Florio, Tullio; Meucci, Olimpia; Landolfi, E.; Grimaldi, M.; Lombardi, Gaetano; Scala, Giuseppe; Leong, Denis A.

doi:10.1210/endo-126-3-1435

Cited by 31 publications

(16 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is supported by a study in rats which showed that IL1b was able to inhibit prolactin release. 32 However, inhibitory as well as stimulatory effects of cytokines on prolactin release have been described, and future research will be needed to clarify this issue.…”

Section: Discussionmentioning

confidence: 99%

Decreased prolactin response to hypoglycaemia in patients with rheumatoid arthritis: correlation with disease activity

Eijsbouts

Hoogen²,

Laan³

et al. 2004

Annals of the Rheumatic Diseases

View full text Add to dashboard Cite

Objective: To compare basal and stimulated prolactin levels between patients with rheumatoid arthritis and healthy controls, and to assess the effects of antirheumatic treatment on prolactin concentrations. Methods: Serum prolactin was assessed under basal conditions and during an insulin tolerance test (ITT) in 20 patients with recently diagnosed active rheumatoid arthritis and 20 age and sex matched controls. The patients were reassessed after two weeks' treatment with naproxen and after six months' additional treatment with either sulfasalazine or methotrexate. Disease activity was assessed by the disease activity score (DAS). Results: Basal levels of prolactin were not significantly different between patients with rheumatoid arthritis and controls. Prolactin responses to hypoglycaemia were less in untreated rheumatoid patients than in controls. DAS scores correlated negatively with the area under the curve (AUC) for prolactin concentrations during the ITT. Treatment with naproxen for two weeks did not influence either basal or stimulated prolactin levels. After six months of antirheumatic treatment, prolactin responses to hypoglycaemia increased significantly to levels observed in controls. At the same time point, DAS had improved considerably. The improvement correlated with the increase in AUC of prolactin during the ITT (r = 0.48; p = 0.05). Conclusions: Patients with active rheumatoid arthritis have a decreased prolactin response to hypoglycaemia induced stress. The response recovers following treatment with antirheumatic drugs.

show abstract

Section: Discussionmentioning

confidence: 99%

Decreased prolactin response to hypoglycaemia in patients with rheumatoid arthritis: correlation with disease activity

Eijsbouts

Hoogen²,

Laan³

et al. 2004

Annals of the Rheumatic Diseases

View full text Add to dashboard Cite

show abstract

“…IL-1 whose receptor was detected within mouse adenohypophysis [104], inhibits prolactin (PRL) secretion from dispersed rat pituitary cells through the regulation of both cAMP production and agonist-induced Ca ++ fluxes [105][106][107]. IL-1 mRNA was identified in rat anterior pituitary cells supporting an autocrine/paracrine regulation of pituitary function in situations in which stimulation of IL-1 secretion is induced, such as during infectious processes [108].…”

Section: Autocrine/paracrine Functions Of Chemokine In Normal Pituitarymentioning

confidence: 98%

The Chemokine SDF1/CXCL12: A Novel Autocrine/Paracrine Factor Involved In Pituitary Adenoma Development

Barbieri¹

2011

TONEUROEJ

View full text Add to dashboard Cite

Abstract:The relevance of the chemokine/chemokine receptor system has broaden to several tissues. Besides their physiologic role as chemotactic cytokines in immune surveillance, it is now clear that chemokines are key players in several pathological processes such as inflammation, infection, and cancer. In particular the altered expression of SDF1/CXCL12 and its receptor CXCR4 strongly affects cancer cell proliferation, recruitment of immunosuppressive cells, neovascularization and metastasization. CXCL12 and CXCR4 are widely expressed in central nervous system cells including hypotalamus and pituitary gland. Increasing evidence supports now the hypothesis that CXCL12 acts as a neuromodulatory activity on the hypothalamus/pituitary axis and is a regulatory molecule of pituitary function. Moreover, the differential expression of CXCL12 and CXCR4 in normal and tumor pituitary adenoma cells suggests their involvement in pituitary tumor development through autocrine/paracrine mechanisms leading to adenoma cell proliferation and hormone hypersecretion. Future studies focusing the pathways sustained by chemokines may help identify the tumor-initiating events and accordingly possible strategies may be developed targeting these pathways in human pituitary tumors.

show abstract

“…In particular, it was reported that interleukin 1 b (IL-1b), that is produced by hypothalamic neurons (Johnson et al 2004) inhibit prolactin secretion from dispersed rat pituitary cells through the regulation of both cAMP production and agonist-induced Ca CC fluxes (Schettini et al 1990). Indeed, the expression of its receptors was detected within the mouse adenohypophysis (Cunningham et al 1992).…”

Section: Chemokine Modulation Of Normal Pituitary Functionmentioning

confidence: 99%

Role of stromal cell-derived factor 1 (SDF1/CXCL12) in regulating anterior pituitary function

Barbieri¹,

Bajetto²,

Porcile³

et al. 2007

Journal of Molecular Endocrinology

Self Cite

View full text Add to dashboard Cite

Chemokines are key factors involved in the regulation of immune response, through the activation and control of leukocyte traffic, lymphopoiesis and immune surveillance. However, a large number of chemokines and their receptors are expressed in central nervous system (CNS) cells, either constitutively or induced by inflammatory stimuli, playing a role in many neuropathological processes. Stromal cell-derived factor 1 (SDF1) is a chemokine whose extra-immunological localization and functions have been extensively studied. SDF1 and its receptor CXCR4 were identified in both neurons and glia of many brain areas, including the hypothalamus, as well as at the pituitary level. Importantly, SDF1 and CXCR4 expression is increased in brain tumors in which their activity induced tumor cell proliferation and brain parenchyma invasion. Despite their localization, to date very few reports addressed the role of CXCR4 and SDF1 in the modulation of the hypothalamus/pituitary axis and their possible involvement in the development of pituitary adenomas. In this review, we discuss previous literature data on the role of chemokines in normal and adenomatous pituitary cells, focusing on recent data from our group showing that CXCR4 activation controls proliferation and both prolactin and GH release in the pituitary adenoma cell line GH4C1 through a complex network of intracellular signals. Thus, the SDF1/CXCR4 system together with other chemokinergic ligand-receptor pairs, may represent a novel regulatory pathway for pituitary function and, possibly, be involved in pituitary adenoma development. These lines of evidence suggest that the inhibition of chemokine receptors may represent a novel pharmacological target for the treatment of pituitary adenomas.

show abstract

Interleukin-1-β Modulation of Prolactin Secretion from Rat Anterior Pituitary Cells: Involvement of Adenylate Cyclase Activity and Calcium Mobilization*

Cited by 31 publications

References 36 publications

Decreased prolactin response to hypoglycaemia in patients with rheumatoid arthritis: correlation with disease activity

Decreased prolactin response to hypoglycaemia in patients with rheumatoid arthritis: correlation with disease activity

The Chemokine SDF1/CXCL12: A Novel Autocrine/Paracrine Factor Involved In Pituitary Adenoma Development

Role of stromal cell-derived factor 1 (SDF1/CXCL12) in regulating anterior pituitary function

Contact Info

Product

Resources

About