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These results provide direct evidence that endogenous apelin plays a crucial role in suppressing Ang II-induced cardiac dysfunction and pathological remodeling.
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this study provides the first evidence that SIRT1 mediates the anxiolytic effect of apelin-13 in chronic normobaric hypoxia -treated mice through the inhibition of NF-kappaB pathway
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Meanwhile ectopic expression of Apelin promoted cellular proliferation, migration and tube formation of EPCs in vitro. In summary, our results indicate that miR-503 regulates proliferation, migration and angiogenesis of EPCs by targeting Apelin.
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The study was conducted to determine the effect of DHA on the distribution of apelin and apelin receptor (APJ) in the central nervous system in 1-methyl-4-phenyl-1, 2, 3, 6 tetrahydropyridine (MPTP)-induced Parkinson's disease (PD) model.
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Activation of Aplnr signaling by Apelin peptide and small molecule ML-233 increased cell movement and expression of migration related gene and proteins including Actin and Vimentin. Similarly, reducing the expression of Aplnr and Apelin (Apln) by siRNA exposure inhibited cell migration of mouse fibroblast cells
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the expression of APLNR (APJ/AGTRL1), the only known receptor for apelin, is predominantly restricted to the endothelial cells.
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apelin effects on dynamic mechanical characteristics of single ventricular cardiomyocytes
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Study shows that apelin-13 ameliorates chronic normobaric hypoxia-induced anxiety-like behavior in mice. Anxiolytic effects of apelin-13 might be associated with an inhibition of NF-kappaB and microglial activation in the hippocampus.
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Results revealed that apelin-13 attenuated brain edema and reduced cellular death by suppressing apoptosis after intracerebral hemorrhage in mice.
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Apelin-36-[L28C(30kDa-PEG)] provides a starting point for the development of diabetes therapeutics that are devoid of the blood pressure effects associated with canonical APJ activation
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miR-503 promotes cardiac fibrosis via miR-503-Apelin-13-TGF-beta-CTGF-collagen production pathway.
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Apelin directly interferes with thrombin-mediated signaling pathways and platelet activation, secretion, and aggregation, but not with ADP and thromboxane A2-mediated pathways.
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Apelin regulates inflammatory response, diminishes inflammatory remote organ damage and improves survival in an experimental model of burn sepsis, which is at least partly mediated by a phosphatidylinositol 3-kinase/protein kinase B dependent pathway.
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apelin is a potential activator of inflammation factors through the PI3K/Akt and Erk signaling pathway and is potential therapeutically relevant to inflammatory responses of microglia cells
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we showed the effect of Apelin on RAW264.7 macrophage under normal and hypoxic condition, which could further influence the angiogenesis and inflammation process that promoted by macrophages.
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PDL- and Cer-induced CP resulted in increased production of the pancreatic BMP2, apelin, and PTHrP signaling systems and that significant cross talk occurred among pancreatic BMP2, apelin, and PTHrP
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Therapeutic potential of apelin to prevent myocardial metabolic abnormalities in heart failure paired with obesity.
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Data suggest that CTRP3 (cartducin) up-regulates expression and secretion of adipokines (adiponectin, leptin, visfatin, and apelin) in adipocytes; these responses to CTRP3 are down-regulated by insulin resistance or inhibition of AMPK signaling.
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apelin is produced by arterial endothelial cells (ECs) during embryogenesis, induces chemotaxis of venous ECs, and promotes the production of secreted Frizzled-related protein 1 by apelin receptor(+) ECs
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Findings demonstrate a stimulatory role for the islet cell apelin-APJ signaling axis in regulation of pancreatic islet homeostasis and in metabolic induced beta-cell hyperplasia.
