Regulation of Pituitary Function by Cytokines

Haedo, Mariana; Gerez, Juan; Fuertes, Mariana; Giacomini, Damiana; Páez-Pereda, Marcelo; Labeur, Marta; Renner, Ulrich; Stalla, Günter; Arzt, Eduardo

doi:10.1159/000245928

Cited by 43 publications

(42 citation statements)

References 147 publications

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“…The strong association between the SASP pattern and the other senescence biomarkers (p21, pATM, and Sa-b-gal) led us to connect these increased cytokine expressions with emerging pituitary senescence within estrogen-induced pituitary tumors. A putative role for IL6 in pituitary senescence induction has been previously suggested (Fuertes et al 2010), with TGFb1 and IL1b also having a known impact on pituitary tissue homeostasis (Haedo et al 2009). We have recently demonstrated somatolactotroph GH3B6 tumoral cells exhibiting a refractory behavior to the TGFb1 inhibitory effects on cell cycle progression, as a consequence of the crosstalk with proliferative pathways that counterbalances the TGFb1 signal (Petiti et al 2015).…”

Section: Discussionmentioning

confidence: 93%

Evidence of cellular senescence during the development of estrogen-induced pituitary tumors

Sabatino

Petiti

Sosa

et al. 2015

Endocrine-Related Cancer

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Although pituitary adenomas represent 25% of intracranial tumors, they are usually benign, with the mechanisms by which these tumors usually avoid an invasive profile and metastatic growth development still remaining unclear. In this context, cellular senescence might constitute a plausible explanation for the benign nature of pituitary adenomas. In this study, we investigated the emergence of cellular senescence as a growth control mechanism during the progression of estrogen-induced pituitary tumors. The quantification of Ki67-immunopositive cells in the pituitaries of estrogenized male rats after 10, 20, 40, and 60 days revealed that the mitogenic potential rate was not sustained for the whole period analyzed and successively decreased after 10 days of estrogen exposure. In addition, the expression of cellular senescence features, such as the progressive rise in the enzymatic senescenceassociated b-galactosidase (SA-b-gal) activity, IL6, IL1b, and TGFb expression, was observed throughout pituitary tumor development. Furthermore, tumoral pituitary cells also displayed nuclear pATM expression, indicating activated DNA damage signaling, with a significant increase in p21 expression also being detected. The associations among DNA damage signaling activation, SA-b-gal expression, and p21 may provide a reliable combination of senescence-associated markers for in vivo pituitary senescence detection. These results suggest a role for this cellular process in the regulation of pituitary cell growth. Thus, cellular senescence should be conceived as a contributing component to the benign nature of pituitary adenomas, thereby influencing the capability of the pituitary gland to avoid unregulated cell proliferation.

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Section: Discussionmentioning

confidence: 93%

Evidence of cellular senescence during the development of estrogen-induced pituitary tumors

Sabatino

Petiti

Sosa

et al. 2015

Endocrine-Related Cancer

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“…Cytokines, such as IL-1, IL-2, TNF and TGF , act in an autocrine/paracrine manner in the pituitary, affecting hormone secretion and pituitary growth [103].…”

Section: Autocrine/paracrine Functions Of Chemokine In Normal Pituitarymentioning

confidence: 99%

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

Barbieri¹

2011

TONEUROEJ

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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.

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“…Furthermore, IL-6 is a pro-inflammatory cytokine that affects the secretion of several neuroendocrine hormones [23,24]. Here, we show that non-selective β-adrenoreceptor antagonist propranolol treatment induced the production of IL-6 and TNF-α in rat alveolar macrophages exposure to LPS.…”

Section: Discussionmentioning

confidence: 59%

Chronic β-adrenoceptor Antagonists Upregulate the Rat Alveolar Macrophage Adrenergic System Through the β<sub>1</sub>-Subtype

Yue-ping

Liu²,

Li³

et al. 2011

Cell Physiol Biochem

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Background: Previous studies demonstrate that macrophages synthesis and release catecholamines, which regulate the immune responses in an autocrine manner. These responses are mediated in part by β-adrenoceptors expressed on macrophages. Some β-adrenoceptor antagonists are commonly used in clinical conditions. Here we investigated whether the chronic administration of β-adrenoceptor antagonists upregulate adrenergic system of alveolar macrophage and the potential mechanims. Methods: Propranolol (30 mg/kg·d) or atenolol (5 mg/kg·d) was administered by gavage to rats for 4 weeks. Then alveolar macrophages were isolated and the expression of β 1 or β 2 -adrenoceptor was detected by flow cytometric analysis. Dopamine β-hydroxylase expression was assessed by Western blot assay and the concentrations of noradrenaline, IL-6, and TNF-α in cell supernatants were measured using ELISA after 2 h or 24 h exposure of alveolar macrophages to 100 ng/ml lipopolysaccharide (LPS). Results: Propranolol increased the mean fluorescence intensity (MFI) of β 1 , β 2 -adrenoceptor and the frequency of β 1 -,β 2 -adrenoceptor positive macrophages. However, only the MFI of β 1 -adrenoceptor and the frequency of β 1 -adrenoceptor positive macrophages were increased by atenolol. Furthermore, both propranolol and atenolol promoted LPS-mediated dopamine β-hydroxylase protein expression and increased noradrenaline production in rat alveolar macrophages. This was accompanied by increased LPS-mediated IL-6 and TNF-α production in cell supernatants of alveolar macrophages. Conclusion: These findings demonstrate that propranolol or atenolol upregulates alveolar macrophage adrenergic system, and the response may be β 1 -adrenergic receptor subtype dependent.

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Regulation of Pituitary Function by Cytokines

Cited by 43 publications

References 147 publications

Evidence of cellular senescence during the development of estrogen-induced pituitary tumors

Evidence of cellular senescence during the development of estrogen-induced pituitary tumors

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

Chronic β-adrenoceptor Antagonists Upregulate the Rat Alveolar Macrophage Adrenergic System Through the β<sub>1</sub>-Subtype

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