Phoenixin-14 protects human brain vascular endothelial cells against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced inflammation and permeability

Zhang, Benping; Li, Jiebing

doi:10.1016/j.abb.2020.108275

Cited by 29 publications

(27 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NO is key factor that is released from vascular endothelial cells to promote vasodilation to allow blood flow to the brain. 5 Meanwhile, NO also restrained the inflammation and thrombosis upon ischemic injury. 5 Therefore, restoring the levels of eNOs and NO is considered as a potential therapeutic strategy.…”

Section: Discussionmentioning

confidence: 99%

“… 5 Meanwhile, NO also restrained the inflammation and thrombosis upon ischemic injury. 5 Therefore, restoring the levels of eNOs and NO is considered as a potential therapeutic strategy. 6 ET-1 played an opposite role with NO to constrict the vessel.…”

Section: Discussionmentioning

confidence: 99%

“…NO is an important protective molecular that protects endothelial cells against ischemia-induced injury through accelerating vasodilation to allow the blood flow to brain. 5 The levels of eNOs and NO are reduced during OGD. Restoring the levels of eNOs and NO is a promising method for attenuating ischemia-mediated injury.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

Shen¹,

Wang²,

Xu³

et al. 2021

NDT

View full text Add to dashboard Cite

Background:The aim of our study was to explore the role of long non-coding RNA (lncRNA) growth arrest-specific 5 (GAS5) in ischemic stroke using oxygen-glucose deprivation/reperfusion (OGD/R)-induced bEnd.3 cells as in vitro cell model. Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were adopted to analyze RNA and protein expression. Cell viability and apoptosis were analyzed by Cell Counting Kit-8 (CCK8) assay and flow cytometry. The levels of nitric oxide (NO) and endothelin-1 (ET-1) in culture supernatant were examined by their matching commercial kits. The intermolecular target interaction was predicted by starBase software and tested by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results: OGD/R-induced apoptosis and dysregulation in vascular endocrine system were largely alleviated by the knockdown of GAS5. GAS5 interacted with microRNA-34b-3p (miR-34b-3p), and GAS5 silencing protected bEnd.3 cells from OGD/R-induced injury partly through up-regulating miR-34b-3p. EPH receptor A4 (EPHA4) was a target of miR-34b-3p. GAS5 acted as the molecular sponge of miR-34b-3p to up-regulate EPHA4 in bEnd.3 cells. GAS5 interference protected against OGD/R-induced damage in bEnd.3 cells partly through down-regulating EPHA4. Conclusion: LncRNA GAS5 knockdown protected brain microvascular endothelial cells bEnd.3 from OGD/R-induced injury depending on the regulation of miR-34b-3p/EPHA4 axis.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

Shen¹,

Wang²,

Xu³

et al. 2021

NDT

View full text Add to dashboard Cite

show abstract

“…In addition, phoenixin-14 attenuated the LPS-induced increase in high mobility group box one (HMGB1) protein [69], which also induces the expression of NLRP3 [70]. This reduction in HMBG1 due to phoenixin-14 was also found in an oxygen-glucose-deprivation-reperfusion stress (OGD/R) cell culture model (Figure 1) [71].…”

Section: Potential Involvement In Stress Responsementioning

confidence: 71%

“…During reperfusion stress in a cell culture stroke model, phoenixin-14 was shown to reduce the production of reactive oxygen species (ROS) after OGD/R [71], thereby reducing neuronal cell damage and inflammation caused by ROS [73]. This was attributed to a decrease in NADPH-Oxidase-1 (NOX-1) expression, which is a ROS producer, due to phoenixin-14 [71]. As previously mentioned, another effect was a reduction in HMBG1 expression, which induces the inflammatory response after cell injury [71].…”

Section: Potential Involvement In Stress Responsementioning

confidence: 99%

Role of the Novel Peptide Phoenixin in Stress Response and Possible Interactions with Nesfatin-1

Friedrich

Stengel

2021

IJMS

View full text Add to dashboard Cite

The novel peptide phoenixin was shown to be involved in several physiological processes ranging from reproduction to food intake. Interest in this protein has steadily increased over the last few years and its known implications have become much broader, playing a role in glucose homeostasis, anxiety, nociception, and pruritus. Phoenixin is expressed in a multitude of organs such as the small intestine, pancreas, and in the hypothalamus, as well as several other brain nuclei influencing numerous physiological functions. Its highly conserved amino-acid sequence amongst species leads to the assumption, that phoenixin might be involved in essential physiological functions. Its co-expression and opposing functionality to the extensively studied peptide nesfatin-1 has given rise to the idea of a possible counterbalancing role. Several recent publications focused on phoenixin’s role in stress reactions, namely restraint stress and lipopolysaccharide-induced inflammation response, in which also nesfatin-1 is known to be altered. This review provides an overview on the phoenixins and nesfatin-1 properties and putative effects, and especially highlights the recent developments on their role and interaction in the response to response.

show abstract

Phoenixin‐14 maintains the contractile type of vascular smooth muscle cells in cerebral aneurysms rats

Ling,

Yang,

Zhang

et al. 2024

J Biochem & Molecular Tox

View full text Add to dashboard Cite

The rupture of intracranial aneurysm (IA) is the primary reason contributing to the occurrence of life‐threatening subarachnoid hemorrhages. The oxidative stress‐induced phenotypic transformation from the contractile phenotype to the synthetic phenotype of vascular smooth muscle cells (VSMCs) plays a pivotal role in IA formation and rupture. Our study aimed to figure out the role of phoenixin‐14 in VSMC phenotypic switching during the pathogenesis of IA by using both cellular and animal models. Primary rat VSMCs were isolated from the Willis circle of male Sprague‐Dawley rats. VSMCs were stimulated by hydrogen peroxide (H2O2) to establish a cell oxidative damage model. After pretreatment with phoenixin‐14 and exposure to H2O2, VSMC viability, migration, and invasion were examined through cell counting kit‐8 (CCK‐8), wound healing, and Transwell assays. Intracellular reactive oxygen species (ROS) production in VSMCs was evaluated by using 2′,7′‐Dichlorofluorescin diacetate (DCFH‐DA) fluorescence probes and flow cytometry. Rat IA models were established by ligation of the left common carotid arteries and posterior branches of both renal arteries. The histopathological changes of rat intracranial blood vessels were observed through hematoxylin and eosin staining. The levels of contractile phenotype markers (alpha‐smooth muscle actin [α‐SMA] and smooth muscle 22 alpha [SM22α]) in VSMCs and rat arterial rings were determined through real‐time quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis. Our results showed that H2O2 stimulated the production of intracellular ROS and induced oxidative stress in VSMCs, while phoenixin‐14 pretreatment attenuated intracellular ROS levels in H2O2‐exposed VSMCs. H2O2 exposure promoted VSMC migration and invasion, which, however, was reversed by phoenixin‐14 pretreatment. Besides, phoenixin‐14 administration inhibited IA formation and rupture in rat models. The decrease in α‐SMA and SM22α levels in H2O2‐exposed VSMCs and IA rat models was antagonized by phoenixin‐14. Collectively, phoenixin‐14 ameliorates the progression of IA through preventing the loss of the contractile phenotype of VSMCs.

show abstract

Phoenixin-14 protects human brain vascular endothelial cells against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced inflammation and permeability

Cited by 29 publications

References 31 publications

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4

Role of the Novel Peptide Phoenixin in Stress Response and Possible Interactions with Nesfatin-1

Phoenixin‐14 maintains the contractile type of vascular smooth muscle cells in cerebral aneurysms rats

Contact Info

Product

Resources

About