Apelin-13 protects neurovascular unit against ischemic injuries through the effects of vascular endothelial growth factor

Huang, Chuyi; Dai, Chuanfu; Gong, Kai; Zuo, Huancong; Chu, Hang

doi:10.1016/j.npep.2016.08.006

Cited by 26 publications

(15 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Accumulated evidence indicates that apelin/APLNR improves the recovery from ischemic stroke by inhibiting cell death and facilitating angiogenesis, which are mediated by the activation of PI3K/AKT and ERKs signaling pathways, respectively (Figure 3; Chuang et al, 2011; Tao et al, 2011; Gu et al, 2013; Wang et al, 2013; Zhu et al, 2013; Yang et al, 2014; Chen et al, 2015; Liu et al, 2015; Huang et al, 2016; Novakova et al, 2016; Zou et al, 2016). Oxidative stress is a major mechanism of ischemia/reperfusion injury, leading to cell death.…”

Section: Protective Effects Of Apelin/aplnr In Ischemic Stroke and Thmentioning

confidence: 99%

“…Apelin not only protects cells from death but also promotes angiogenesis against ischemic stroke and improves stroke recovery (Chen et al, 2015; Huang et al, 2016). Apelin facilitates angiogenesis and blood flow restoration, which is dependent on an increase in vascular endothelial growth factor- vascular endothelial growth factor receptor 2 (VEGF-VEGFR2) signaling .…”

Section: Protective Effects Of Apelin/aplnr In Ischemic Stroke and Thmentioning

confidence: 99%

See 1 more Smart Citation

Temporal Expression of Apelin/Apelin Receptor in Ischemic Stroke and its Therapeutic Potential

Wang

Zhou

et al. 2017

Front. Mol. Neurosci.

114

149

View full text Add to dashboard Cite

Stroke is one of the leading causes of death and disability worldwide, and ischemic stroke accounts for approximately 87% of cases. Improving post-stroke recovery is a major challenge in stroke treatment. Accumulated evidence indicates that the apelinergic system, consisting of apelin and apelin receptor (APLNR), is temporally dysregulated in ischemic stroke. Moreover, the apelinergic system plays a pivotal role in post-stroke recovery by inhibiting neuronal apoptosis and facilitating angiogenesis through various molecular pathways. In this review article, we summarize the temporal expression of apelin and APLNR in ischemic stroke and the mechanisms of their dysregulation. In addition, the protective role of the apelinergic system in ischemic stroke and the underlying mechanisms of its protective effects are discussed. Furthermore, critical issues in activating the apelinergic system as a potential therapy will also be discussed. The aim of this review article is to shed light on exploiting the activation of the apelinergic system to treat ischemic stroke.

show abstract

Section: Protective Effects Of Apelin/aplnr In Ischemic Stroke and Thmentioning

confidence: 99%

Section: Protective Effects Of Apelin/aplnr In Ischemic Stroke and Thmentioning

confidence: 99%

Temporal Expression of Apelin/Apelin Receptor in Ischemic Stroke and its Therapeutic Potential

Wang

Zhou

et al. 2017

Front. Mol. Neurosci.

114

149

View full text Add to dashboard Cite

show abstract

“…Moreover, apelin is able to induce the synthesis of VEGF and reinforce or replace the action of VEGF through VEGFR [22]. For instance, some authors have demonstrated that effects of apelin on ischemic neurovascular unit injuries are highly associated with the increase in VEGF binding to VEGFR-2, probably through the activation of the ERK and PI3K/ Akt pathways [23].…”

Section: Resultsmentioning

confidence: 99%

Vitamin D(3) regulates hepatic VEGF-A and apelin expression in experimental type 1 diabetes

Labudzynskyi¹,

Shymanskyi²,

Lisakovska³

et al. 2020

Ukr.Biochem.J

View full text Add to dashboard Cite

The deficiency of vitamin D is associated with the risk of various chronic diseases, including diabetes mellitus and its complications. Given the strong genomic action of vitamin D hormone-active form, its deficiency can lead to dysfunction of cytokine signaling pathways, including those dependent on vascular endothelial growth factors (VEGFs) and apelin. The present study was carried out to define the link between VEGF-A and apelin expression in liver, hepatocytes viability and vitamin D status at experimental type 1 diabetes in mice. We established that chronic hyperglycemia at streptozotocin-induced diabetes was accompanied by a 2.2-fold decrease in 25OHD content in the serum and increased hepatocytes apoptosis and necrosis. Vitamin D deficiency correlated with increased apelin and VEGF-A (8-and 1.6-fold respectively) expression. Almost complete restoration of circulatory 25OHD content in serum was achieved at vitamin D 3 treatment (800 IU/kg, per os, for 2 months) followed by reduced apelin and VEGF-A expression in liver and the decline of hepatocytes apoptosis. We conclude that vitamin D 3 can be involved in cell survival, angiogenesis and fibrogenesis by modulating VEGF-A and apelin dependent regulatory systems in diabetic liver.

show abstract

“…Middle cerebral artery occlusion model was prepared as previously reported (Huang et al, ). After anesthetized by chloral hydrate (350 mg/kg, intraperitoneally), the left common carotid artery, external carotid artery, and internal carotid artery of rats were exposed.…”

Section: Methodsmentioning

confidence: 99%

Reduction of Ischemic Brain Edema by Combined use of Paeoniflorin and Astragaloside IV via Down‐Regulating Connexin 43

Chu

Huang

Gao

et al. 2017

Phytotherapy Research

Self Cite

View full text Add to dashboard Cite

Paeoniflorin (PF) and astragaloside IV (AS-IV) have protective effects on cerebral ischemia. We aimed to test the effects of combined use of PF and AS-IV on ischemic brain edema and investigate whether the effects were dependent on connexin43 (Cx43). We detected the expression of Cx43 induced by PF and AS-IV after cerebral ischemia. We also examined the effects of combined use of PF and AS-IV on ischemic edema and further investigated the related pathways. We demonstrated PF and AS-IV decreased Cx43 and aquaporin4 (AQP4) associating with reduction of brain edema by dry-wet weight and brain-specific gravity methods after cerebral ischemia. Administration of PF and AS-IV displayed a further attenuation of brain edema with lower Cx43 levels. Meanwhile, Cx43 blockade inhibited AQP4 down-regulation by the two drugs. Moreover, phosphorylation of C-Jun amino-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) were increased by PF and AS-IV, respectively. The effects of PF and AS-IV to down-regulate Cx43 were suppressed by JNK and ERK inhibitors, respectively. Our data indicate that PF and AS-IV alleviate ischemic brain edema, which has close relation to Cx43 down-regulation causing decrease of AQP4 via JNK and ERK pathways activation, respectively. Combined administration elicits synergistic effects on brain edema reduction. Copyright © 2017 John Wiley & Sons, Ltd.

show abstract

Apelin-13 protects neurovascular unit against ischemic injuries through the effects of vascular endothelial growth factor

Cited by 26 publications

References 33 publications

Temporal Expression of Apelin/Apelin Receptor in Ischemic Stroke and its Therapeutic Potential

Temporal Expression of Apelin/Apelin Receptor in Ischemic Stroke and its Therapeutic Potential

Vitamin D(3) regulates hepatic VEGF-A and apelin expression in experimental type 1 diabetes

Reduction of Ischemic Brain Edema by Combined use of Paeoniflorin and Astragaloside IV via Down‐Regulating Connexin 43

Contact Info

Product

Resources

About