Behavioral, neuroendocrine and thermoregulatory actions of apelin-13

Jászberényi, Miklós; Bujdosó, E.; Telegdy, Gyula

doi:10.1016/j.neuroscience.2004.08.007

Cited by 79 publications

(51 citation statements)

References 32 publications

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“…Altogether, these data suggest that apelin is involved in not only the regulation of posterior but also anterior pituitary hormone release. In agreement with this hypothesis, intracerebroventricular administration of pE13F to adult rats significantly increases plasma ACTH and corticosterone release (15,39). Moreover, in vitro pE13F stimulates corticotropin-releasing hormone (CRH) release from hypothalamic explants (39).…”

supporting

confidence: 52%

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Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

Goazigo¹,

Alvear-Perez²,

Zizzari³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Reaux-Le Goazigo A, Alvear-Perez R, Zizzari P, Epelbaum J, Bluet-Pajot MT, Llorens-Cortes C. Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release. Am J Physiol Endocrinol Metab 292: E7-E15, 2007. First published August 8, 2006; doi:10.1152/ajpendo.00521.2005.-Apelin is a bioactive peptide recently identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ. The presence of apelin-immunoreactive nerve fibers, together with the detection of apelin receptor mRNA in the parvocellular part of the paraventricular nucleus and the stimulatory action of apelin on corticotropin-releasing hormone release, indicate that apelin modulates adrenocorticotropin (ACTH) release via an indirect action on the hypothalamus. However, a direct action of apelin in the anterior pituitary cannot be excluded. Here, we provided evidence for the existence of an apelinergic system within the adult male rat pituitary gland. Double immunofluorescence staining indicated that apelin is highly coexpressed in the anterior pituitary, mainly in corticotrophs (96.5 Ϯ 0.3%) and to a much lower extent in somatotropes (3.2 Ϯ 0.2%). Using in situ hybridization combined with immunohistochemistry, a high expression of apelin receptor mRNA was also found in corticotrophs, suggesting a local interaction between apelin and ACTH. In an ex vivo perifusion system of anterior pituitaries, apelin 17 (K17F, 10 Ϫ6 M) significantly increased basal ACTH release by 41%, whereas apelin 10 (R10F, 10 Ϫ6 M), an inactive apelin fragment, was ineffective. In addition, K17F but not R10F induced a dose-dependent increase in K ϩ -evoked ACTH release, with maximal increase being observed for a 10 Ϫ6 M concentration. Taken together, these data outline the potential role of apelin as an autocrine/paracrine-acting peptide on ACTH release and provide morphological and neuroendocrine basis for further studies that explore the physiological role of apelin in the regulation of anterior pituitary functions.hypothalamo-pituitary-adrenal axis; apelin; apelin receptor; adrenocorticotropin APELIN IS A BIOACTIVE PEPTIDE recently isolated from bovine stomach extracts and identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ (26,40). Apelin is a 36-amino acid peptide derived from 77-amino acid precursor proapelin, for which cDNAs have been cloned from humans, cattle, rats, and mice (12,18,40). This precursor exhibits a fully conserved COOH-terminal sequence between Trp-55 and Phe-77, including the COOH-terminal 17 (LysPhe-Arg-Arg-Gln-Arg-Pro-Arg-Leu-Ser-His-Lys-Gly-ProMet-Pro-Phe, apelin 17, or K17F) and 13 (Gln-Arg-Pro-ArgLeu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe, apelin 13, or Q13F) amino acid sequences. In vivo, in the rat hypothalamus and plasma, we have characterized the predominant molecular forms of endogenous apelin as corresponding to the pyroglutamyl form of Q13F (pE13F) and, to a lesser extent, to K17F (8). These apelin fragments display the...

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confidence: 52%

“…Administration of apelin by the intracerebroventricular route was shown to significantly increase plasma ACTH (39) and corticosterone (15,39) release at least in part via a stimulatory action on CRH release (39). In a latter study (40), pE13F (100 nM) significantly stimulated the release of CRF and AVP from hypothalamic explants in vitro.…”

Section: Discussionmentioning

confidence: 77%

Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

Goazigo¹,

Alvear-Perez²,

Zizzari³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…However, increases in plasma ACTH and CORT levels observed after i.c.v. administration of (Pyr 1 )apelin-13 in mice are reduced to control levels by pre-treatment with the CRH receptor antagonist a-helical CRH 9-41 (Jaszberenyi et al 2004), while (Pyr 1 )apelin-13-mediated increases in plasma ACTH levels are abolished in VP V1b receptor KO mice ), indicating that apelin also modulates the release of ACTH via an indirect action on the hypothalamus involving both CRH-and VP-dependent mechanisms. Recently, using APJ KO mice, APJ has been shown to play a regulatory role in the modulation of the HPA axis responses to some acute stressors including LPS challenge (an immune stressor), insulin-induced hypoglycaemia (a metabolic stressor) and forced swim (a physical/psychological stressor) (Newson et al 2013).…”

Section: Apelin/apj and The Neuroendocrine Response To Stressmentioning

confidence: 99%

The apelin receptor APJ: journey from an orphan to a multifaceted regulator of homeostasis

O’Carroll

Lolait

Harris

et al. 2013

Journal of Endocrinology

282

216

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The apelin receptor (APJ; gene symbol APLNR) is a member of the G protein-coupled receptor gene family. Neural gene expression patterns of APJ, and its cognate ligand apelin, in the brain implicate the apelinergic system in the regulation of a number of physiological processes. APJ and apelin are highly expressed in the hypothalamo-neurohypophysial system, which regulates fluid homeostasis, in the hypothalamic-pituitary-adrenal axis, which controls the neuroendocrine response to stress, and in the forebrain and lower brainstem regions, which are involved in cardiovascular function. Recently, apelin, synthesised and secreted by adipocytes, has been described as a beneficial adipokine related to obesity, and there is growing awareness of a potential role for apelin and APJ in glucose and energy metabolism. In this review we provide a comprehensive overview of the structure, expression pattern and regulation of apelin and its receptor, as well as the main second messengers and signalling proteins activated by apelin. We also highlight the physiological and pathological roles that support this system as a novel therapeutic target for pharmacological intervention in treating conditions related to altered water balance, stress-induced disorders such as anxiety and depression, and cardiovascular and metabolic disorders.

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“…К ним могут быть отнесены p38 и JNK киназы и JAK-STAT сигнальный путь, которые также вовлечены в снижение необратимого повреждения кардиомиоцитов [7,28]. Имеются экспериментальные подтверждения того факта, что инотропные и эндотелий-зависимые вазодилатационные свойства [Pyr 1 ]апелина-13, апелина-13 и -36, опосредованы активацией циклооксигеназы и образованием простациклина и не зависят от ингибирования NOS [29,30].…”

Section: таблицаunclassified

The influence of inhibiting no formation on metabolic recovery of ischemic rat heart by apelin-12

IuA

et al. 2012

BIOMED KHIM

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Apelin 12 (A-12) was synthesized by the automatic solid phase method with use of Fmoc 1H-NMR spectroscopy and mass spectrometry. Effects of apelin-12 (a peptide comprised of 12 aminoacids, A-12) on recovery of energy metabolism and cardiac function were studied in isolated working rat hearts perfused with Krebs buffer (KB) containing 11 mM glucose that were subjected to global ischemia and reperfusion. A short-term infusion of μM 140 A-12 in KB prior to ischemia enhanced myocardial ATP, the total adenine nucleotide pool (ΣAN=ATP+ADP+AMP) and the energy charge of cardiomyocites ((ATP+0.5ADP)/ΣAN) at the end of reperfusion compared with control (KB infusion) and reduced lactate content and lactate/pyruvate ratio in reperfused myocardium to the initial values. This effect was accompanied by improved recovery of coronary flow and cardiac function. Coadministration of 140 μM A-12 and 100 μM L-NAME (the nonspecific NOS inhibitor) profoundly attenuated the peptide influence on metabolic and functional recovery of reperfused hearts. The results indicate involvement of NO, formed under the peptide action, in mechanisms of cardioprotection that are tightly associated with recovery of energy metabolism in postischemic heart.

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Behavioral, neuroendocrine and thermoregulatory actions of apelin-13

Cited by 79 publications

References 32 publications

Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

The apelin receptor APJ: journey from an orphan to a multifaceted regulator of homeostasis

The influence of inhibiting no formation on metabolic recovery of ischemic rat heart by apelin-12

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