Adropin reduces paracellular permeability of rat brain endothelial cells exposed to ischemia-like conditions

Yang, Changjun; DeMars, Kelly M.; Hawkins, Kimberly E.; Candelario‐Jalil, Eduardo

doi:10.1016/j.peptides.2016.03.009

Cited by 46 publications

(63 citation statements)

References 48 publications

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“…This implied that adropin may be a signaling peptide that participated in liver-brain crosstalk. Hypoxia stress may magnify these effects because adropin is up-regulated and cerebrovascular endothelial permeability is increased (Yang C. et al, 2016). In fact, adropin was significantly increased in the first day of hypoxia, and was maintained at a high level until the third day.…”

Section: Discussionmentioning

confidence: 99%

“…Enzyme-linked immunosorbent assays (ELISA) were performed as previously reported (Yang C. et al, 2016). After centrifugation at 3000 g for 20 min, serum adropin was quantified in the supernatant by ELISA according to the manufacturer’s instructions (Cloud-Clone Corp, Carlsbad, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Hypoxia enhances catabolism, which may elevate serum adropin. For instance, increased serum adropin is often regarded as a candidate diagnostic marker for myocardial hypoxic-ischemic injury (Aydin et al, 2014; Yang C. et al, 2016). Our previous studies revealed that hypoxia activated TRPV calcium channel in CVOs, which was related to anti-dipsogenic effects.…”

Section: Introductionmentioning

confidence: 99%

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Adropin Is a Key Mediator of Hypoxia Induced Anti-Dipsogenic Effects via TRPV4-CamKK-AMPK Signaling in the Circumventricular Organs of Rats

Yang

Zhou

et al. 2017

Front. Mol. Neurosci.

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Water intake reduction (anti-dipsogenic effects) under hypoxia has been well established, but the underlying reason remains unknown. Our previous report indicated that activated TRPV4 neurons in SFO are associated with anti-dipsogenic effects under hypoxia. Although low partial pressure of blood oxygen directly activates TRPV4, humoral factors could also be involved. In the present study, we hypothesize that adropin, a new endogenous peptide hormone, was rapidly increased (serum and brain) concomitant with reduced water intake in early hypoxia. Also, the nuclear expression of c-Fos, a marker for neuronal activation, related to water-consumption (SFO and MnPO) was inhibited. These effects were mitigated by a scavenger, rat adropin neutralizing antibody, which effectively neutralized adropin under hypoxia. Interestingly, injection of recombinant adropin in the third ventricle of the rats also triggered anti-dipsogenic effects and reduced c-Fos positive cells in SFO, but these effects were absent when TRPV4 was knocked down by shRNA. Moreover, adropin-activated CamKK-AMPK signaling related to TRPV4 calcium channel in SFO in normoxia. These results revealed that dissociative adropin was elevated in acute hypoxia, which was responsible for anti-dipsogenic effects by altering TRPV4-CamKK-AMPK signaling in SFO.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adropin Is a Key Mediator of Hypoxia Induced Anti-Dipsogenic Effects via TRPV4-CamKK-AMPK Signaling in the Circumventricular Organs of Rats

Yang

Zhou

et al. 2017

Front. Mol. Neurosci.

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“…Moreover, in apolipoprotein E (Apoe) deficient mice (animal model of atherosclerosis [48]) synthetic adropin led to attenuation of atherosclerotic lesions and monocyte/macrophage infiltration in the aorta [47]. In the context of the cardiovascular system, adropin may modulate the patency of the blood-brain barrier [49]. Yang et al showed that exogenous adropin causes attenuation of endothelial cell permeability during ischemia, an effect mediated via the ROCK-MLC2 signaling pathway [49].…”

Section: Adropin In the Cardiovascular Systemmentioning

confidence: 99%

Adropin as A Fat-Burning Hormone with Multiple Functions—Review of a Decade of Research

et al. 2020

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Adropin is a unique hormone encoded by the energy homeostasis-associated (Enho) gene. Adropin is produced in the liver and brain, and also in peripheral tissues such as in the heart and gastrointestinal tract. Furthermore, adropin is present in the circulatory system. A decade after its discovery, there is evidence that adropin may contribute to body weight regulation, glucose and lipid homeostasis, and cardiovascular system functions. In this review, we summarize and discuss the physiological, metabolic, and pathophysiological factors regulating Enho as well as adropin. Furthermore, we review the literature addressing the role of adropin in adiposity and type 2 diabetes. Finally, we elaborate on the role of adropin in the context of the cardiovascular system, liver diseases, and cancer.

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“…These results indicated that adropin may influence the anti-inflammatory response and reduce atherosclerosis (9). Yang et al (10) demonstrated that adropin reduces endothelial cell permeability and modulates ischemia-induced blood-brain barrier injury. However, to the best of our knowledge, the role of adropin in myocardial reperfusion injury has not yet been assessed.…”

Section: Introductionmentioning

confidence: 99%

Adropin reduces hypoxia/reoxygenation‑induced myocardial injury via the reperfusion injury salvage kinase pathway

Fang

Yuan

et al. 2019

Exp Ther Med

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Adropin is a secreted polypeptide that has been demonstrated to serve an important role in protecting the vascular endothelium. Pharmacological activation of pro-survival kinases, such as PI3K-Akt and ERK1/2, are involved in the reperfusion injury salvage kinase (RISK) pathway. In the present study, the effects of adropin in cardiomyocyte injury induced by simulated ischemia/reperfusion (SI/R) were assessed. Additionally, the current study also assessed the mechanisms that govern SI/R in a H9c2 cardiomyoblast cell model. Cell viability was measured using an MTT assay. Cell injury was assessed using creatine kinase MB measurements. Apoptosis was assessed using flow cytometry and caspase-3 activity. The inflammatory response was measured using tumor necrosis factor α and interleukin-10 expression. Oxidative stress was assessed using malondialdehyde and superoxide dismutase. The expression levels of Akt, ERK1/2, glycogen synthase kinase 3β (GSK3β), Bcl-2 and Bax were determined using western blot analysis. The results of the current study revealed that moderate-dose adropin increased cell viability, reduced early apoptosis and caspase-3 activity, promoted Bcl-2 expression, inhibited Bax and increased the Bcl-2/Bax ratio. Adropin significantly increased the phosphorylation of Akt, ERK1/2 and GSK3β, whereas inhibitors of PI3K and ERK1/2, respectively, LY294002 and PD98059, abolished the cardioprotective role of adropin. Furthermore, no significant difference was observed in phosphorylated-STAT3/total-STAT3 expression between the adropin and SI/R groups and Janus kinase 2 inhibitor AG490 did not significantly inhibit the protective role of adropin. These results indicate that adropin exerts a protective effect against SI/R injury through the RISK pathway instead of the survivor activating factor enhancement pathway.

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Adropin reduces paracellular permeability of rat brain endothelial cells exposed to ischemia-like conditions

Cited by 46 publications

References 48 publications

Adropin Is a Key Mediator of Hypoxia Induced Anti-Dipsogenic Effects via TRPV4-CamKK-AMPK Signaling in the Circumventricular Organs of Rats

Adropin Is a Key Mediator of Hypoxia Induced Anti-Dipsogenic Effects via TRPV4-CamKK-AMPK Signaling in the Circumventricular Organs of Rats

Adropin as A Fat-Burning Hormone with Multiple Functions—Review of a Decade of Research

Adropin reduces hypoxia/reoxygenation‑induced myocardial injury via the reperfusion injury salvage kinase pathway

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