Apelin receptor

2006 ◽  
Author(s):  
Yves Audigier
Keyword(s):  
Apelin Receptor

Metabolically stable apelin-analogues, incorporating cyclohexylalanine and homoarginine, as potent apelin receptor activators

2021 ◽  
Author(s):  
Kleinberg X. Fernandez ◽  
Conrad Fischer ◽  
Jennie Vu ◽  
Mahmoud Gheblawi ◽  
Wang Wang ◽  
...  
Keyword(s):  
Hypotensive Effect ◽  
Apelin Receptor

Cyclohexylalanine- and homoarginine-substituted apelin analogues are demonstrated to be metabolically stable APJR agonistic peptides with hypotensive effect.

scholarly journals The apelin receptor: physiology, pathology, cell signalling, and ligand modulation of a peptide-activated class A GPCR

2014 ◽  
Vol 92 (6) ◽  
pp. 431-440 ◽  
Author(s):  
Nigel A. Chapman ◽  
Denis J. Dupré ◽  
Jan K. Rainey
Keyword(s):  
G Protein ◽  
Cell Signalling ◽  
Wide Distribution ◽  
Peptide Ligand ◽  
Cellular Effects ◽  
Class A ◽  
Promising Therapeutic Target ◽  
Apelin Receptor ◽  
Obesity And Cancer ◽  
G Protein Coupled

The apelin receptor (AR or APJ) is a class A (rhodopsin-like) G-protein-coupled receptor with wide distribution throughout the human body. Activation of the AR by its cognate peptide ligand, apelin, induces diverse physiological effects including vasoconstriction and dilation, strengthening of heart muscle contractility, angiogenesis, and regulation of energy metabolism and fluid homeostasis. Recently, another endogenous peptidic activator of the AR, Toddler/ELABELA, was identified as having a crucial role in zebrafish (Danio rerio) embryonic development. The AR is also implicated in pathologies including cardiovascular disease, diabetes, obesity, and cancer, making it a promising therapeutic target. Despite its established importance, the precise roles of AR signalling remain poorly understood. Moreover, little is known about the mechanisms of peptide–AR activation. Additional complexity arises from modulation of the AR by 2 endogenous peptide ligands, both with multiple bioactive isoforms of variable length and distribution. The various apelin and Toddler/ELABELA isoforms may also produce distinct cellular effects. Further complexity arises through formation of functionally distinct heterodimers between the AR and other G-protein-coupled receptors. This minireview outlines key (patho)physiological actions of the AR, addresses what is known about signal transduction downstream of AR activation, and concludes by discussing unique properties of the endogenous peptidic ligands of the AR.

scholarly journals Preclinical study of a new Apelin receptor antagonist against glioblastoma

2017 ◽  
Vol 9 (2) ◽  
pp. 194
Author(s):  
G. Andre-Gregoire ◽  
E. Harford-Wright ◽  
A. Davenport ◽  
R. Glen ◽  
J. Gavard
Keyword(s):  
Receptor Antagonist ◽  
Preclinical Study ◽  
Apelin Receptor

Apelin and the proopiomelanocortin system: a new regulatory pathway of hypothalamic α-MSH release

2011 ◽  
Vol 301 (5) ◽  
pp. E955-E966 ◽  
Author(s):  
Annabelle Reaux-Le Goazigo ◽  
Laurence Bodineau ◽  
Nadia De Mota ◽  
Lydie Jeandel ◽  
Nicolas Chartrel ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuronal Cell ◽  
Nerve Fibers ◽  
Zucker Rats ◽  
Direct Stimulation ◽  
Melanocyte Stimulating Hormone ◽  
System A ◽  
Neuronal Cell Bodies ◽  
Hypothalamic Arcuate Nucleus ◽  
Apelin Receptor

Neuronal networks originating in the hypothalamic arcuate nucleus (Arc) play a fundamental role in controlling energy balance. In the Arc, neuropeptide Y (NPY)-producing neurons stimulate food intake, whereas neurons releasing the proopiomelanocortin (POMC)-derived peptide α-melanocyte-stimulating hormone (α-MSH) strongly decrease food intake. There is growing evidence to suggest that apelin and its receptor may play a role in the central control of food intake, and both are concentrated in the Arc. We investigated the presence of apelin and its receptor in Arc NPY- and POMC-containing neurons and the effects of apelin on α-MSH release in the hypothalamus. We showed, by immunofluorescence and confocal microscopy, that apelin-immunoreactive (IR) neuronal cell bodies were distributed throughout the rostrocaudal extent of the Arc and that apelin was strongly colocalized with POMC, but weakly colocalized with NPY. However, there were numerous NPY-IR nerve fibers close to the apelin-IR neuronal cell bodies. By combining in situ hybridization with immunohistochemistry, we demonstrated the presence of apelin receptor mRNA in Arc POMC neurons. Moreover, using a perifusion technique for hypothalamic explants, we demonstrated that apelin-17 (K17F) increased α-MSH release, suggesting that apelin released somato-dendritically or axonally from POMC neurons may stimulate α-MSH release in an autocrine manner. Consistent with these data, hypothalamic apelin levels were found to be higher in obese db/db mice and fa/fa Zucker rats than in wild-type animals. These findings support the hypothesis that central apelin is involved in regulating body weight and feeding behavior through the direct stimulation of α-MSH release.

Systemic Administration of an Apelin Receptor Agonist Prevents NMDA-Induced Loss of Retinal Neuronal Cells in Mice

2020 ◽  
Vol 45 (4) ◽  
pp. 752-759 ◽  
Author(s):  
Fumiya Shibagaki ◽  
Yuki Ishimaru ◽  
Akihide Sumino ◽  
Akiko Yamamuro ◽  
Yasuhiro Yoshioka ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Neuronal Cells ◽  
Systemic Administration ◽  
Apelin Receptor

scholarly journals APELA Expression in Glioma, and Its Association with Patient Survival and Tumor Grade

2019 ◽  
Vol 12 (1) ◽  
pp. 45 ◽  
Author(s):  
Debolina Ganguly ◽  
Chun Cai ◽  
Michelle Sims ◽  
Chuan Yang ◽  
Matthew Thomas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Tumor ◽  
Patient Survival ◽  
Receptor Gene ◽  
Embryonic Stem ◽  
Tumor Grade ◽  
Adult Brain ◽  
Tumor Initiating Cells ◽  
Apelin Receptor ◽  
Cell Niche

Glioblastoma (GBM) is the most common and deadliest primary adult brain tumor. Invasion, resistance to therapy, and tumor recurrence in GBM can be attributed in part to brain tumor-initiating cells (BTICs). BTICs isolated from various patient-derived xenografts showed high expression of the poorly characterized Apelin early ligand A (APELA) gene. Although originally considered to be a non-coding gene, the APELA gene encodes a protein that binds to the Apelin receptor and promotes the growth of human embryonic stem cells and the formation of the embryonic vasculature. We found that both APELA mRNA and protein are expressed at high levels in a subset of brain tumor patients, and that APELA is also expressed in putative stem cell niche in GBM tumor tissue. Analysis of APELA and the Apelin receptor gene expression in brain tumor datasets showed that high APELA expression was associated with poor patient survival in both glioma and glioblastoma, and APELA expression correlated with glioma grade. In contrast, gene expression of the Apelin receptor or Apelin was not found to be associated with patient survival, or glioma grade. Consequently, APELA may play an important role in glioblastoma tumorigenesis and may be a future therapeutic target.

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