The Apelin/APJ System in Psychosis and Neuropathy

Lv, Shuangyu; Chen, Weidong; Wang, Yandong

doi:10.3389/fphar.2020.00320

Cited by 42 publications

(30 citation statements)

References 68 publications

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“…There was a significant decrease in the proportion of cells expressing both aplnr and apln in the AP of SHRs in comparison to WKY rats (24 % vs 41 [32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47]% respectively, p<0.05). No change in the percentage co-localization of aplnr with apln was seen in the OVLT or SFO of SHRs in comparison to WKY rats (36 [29][30][31][32][33][34][35][36][37][38][39][40]% vs 31 % and 15 [12][13][14][15][16][17][18][19][20]% vs 20 [17][18][19][20][21][22][23][24][25][26]% respectively, p>0.05).…”

Section: Co-localization Of Aplnr and Apln In Normotensive And Shr Cvosmentioning

confidence: 78%

“…hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei) and lower brainstem structures (e.g. nucleus of the solitary tract (NTS), area postrema (AP)) [7], thus allowing for multiple roles in the central regulation of physiological systems such as cardiovascular control [8,9], angiogenesis [10], autonomic signalling [11][12][13], neuroprotection [14], fluid homeostasis [15], and modulation of hypothalamic-pituitary-adrenal axis activity [16,17]. In some brain structures, e.g.…”

Section: Introductionmentioning

confidence: 99%

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Increased apelin receptor gene expression in the subfornical organ of spontaneously hypertensive rats

et al. 2020

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The vascular organ of the lamina terminalis, subfornical organ (SFO), and area postrema comprise the sensory circumventricular organs (CVO) which are central structures that lie outside the blood brain barrier and are thought to provide an interface between peripherally circulating signals and the brain through their projections to central autonomic structures. The SFO expresses mRNA for the G protein-coupled apelin receptor (APJ, gene name aplnr) and exogenous microinjection of the neuropeptide apelin (apln) to the SFO elicits a depressor effect. Here we investigated the expression and cellular distribution of aplnr, apln and the recently described ligand apela (apela) in the CVOs and investigated whether differences in the levels of expression of apelinergic gene transcripts in these regions might underlie the chronic elevated blood pressure seen in hypertension. We carried out multiplex in situ hybridization histochemistry on CVO tissue sections from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) controls. Confocal immunofluorescent images indicated strong aplnr expression, with lower levels of apln and modest apela expression, in the CVOs of both WKY rats and SHRs, in both neurons and glia. The expression level of aplnr transcripts was increased in the SFO of SHRs compared to WKY rats. Our data may highlight a potential dysfunction in the communication between CVOs and downstream signalling pathways in SHRs, which may contribute to its different phenotype/s.

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Section: Co-localization Of Aplnr and Apln In Normotensive And Shr Cvosmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Increased apelin receptor gene expression in the subfornical organ of spontaneously hypertensive rats

et al. 2020

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“…The APLN/APLNR pathway may also serve as a promising therapeutic target for the treatment of psychosis and neuropathy (Lv et al, 2020). We further investigated the influence of APLN/APLNR pathway polymorphisms on the risks of depression and anxiety in patients with CHD.…”

Section: Discussionmentioning

confidence: 99%

“…The APLN/APLNR signaling pathway is involved in various pathological processes and physiological functions, including cardiovascular disease, angiogenesis, energy metabolism, and central nervous system disease (Lv et al, 2020). A previous meta-analysis has shown that the circulating apelin level is a prominent athero-protective marker against the development of CAD, while the APLNR rs9943582 polymorphism in the APLNR promoter, is associated with an increased risk of CAD (Chen et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Association of Apelin and Apelin Receptor Polymorphisms With the Risk of Comorbid Depression and Anxiety in Coronary Heart Disease Patients

Wang

Liu

et al. 2020

Front. Genet.

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The Apelin (APLN)/apelin receptor (APLNR) signaling pathway is a newly identified regulator in various cardiovascular diseases, which is considered as a candidate pathway for the occurrence of coronary heart disease (CHD), depression, and anxiety. The goal of this study was to investigate the association between APLN/APLNR gene polymorphisms and the risk of depression and anxiety in CHD patients. To this end, a case-control study involving 269 CHD patients and 184 healthy control individuals was conducted. The 269 patients with CHD including 122 patients with and 147 patients without depression, and 56 patients with and 213 patients without anxiety Four single nucleotide polymorphisms were selected and successfully genotyped using Sanger sequencing. The APLN rs2235310T allele and APLNR rs9943582C allele were found to be associated with an increased risk of CHD after multiple test correction (Padjust < 0.05). The patients with CHD who carried the rs9943582C allele had a higher risk of depression, after adjusting for alcohol drinking habits, insomnia, hypertension, and stroke history, with the Bonferroni correction (P-adjust = 0.018). The APLNR rs2282623 T allele was associated with an increased risk of anxiety in CHD patients after adjusting for related disease complications, with the Bonferroni correction (Padjust = 0.022). We reported for the first time that the APLN rs2235310 and APLNR rs2282623 polymorphisms are associated with the risks of psychiatric disorders in CHD patients and may serve as novel biomarkers for therapy.

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“…The apelin/APJ system is involved in a broad range of physiological functions and pathological processes, including cardiovascular function ( Wysocka et al, 2018 ; Esmaeili et al, 2019 ), cardiac contractility ( Zhong et al, 2017 ; Esmaeili et al, 2019 ), angiogenesis ( Wu et al, 2017 ; Cheng et al, 2019 ), energy metabolism ( Bertrand et al, 2015 ; Castan-Laurell et al, 2019 ), liver diseases ( Principe et al, 2008 ; Lv et al, 2017 ), ischemia/reperfusion injury ( Yang et al, 2015 ; Chen et al, 2016 ) and cancer ( Yang et al, 2016a ; Masoumi et al, 2020 ). Recent studies were focused on the role of apelin in psychosis and neuropathy ( Lv et al, 2020 ). Xiao et al (2018) demonstrated that intrahippocampal infusion of apelin-13 (1-4 μg/rat) exhibited an anti-depressive effect in forced swim test.…”

Section: Introductionmentioning

confidence: 99%

Intrathecally Administered Apelin-13 Alleviated Complete Freund’s Adjuvant-Induced Inflammatory Pain in Mice

Zhang

Zhou

et al. 2020

Front. Pharmacol.

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Apelin is the endogenous ligand for APJ, a G-protein-coupled receptor. Apelin gene and protein are widely distributed in the central nervous system and peripheral tissues. The role of apelin in chronic inflammatory pain is still unclear. In the present study, a mouse model of complete Freund’s adjuvant (CFA)-induced inflammatory pain was utilized, and the paw withdrawal latency/threshold in response to thermal stimulation and Von Frey ﬁlament stimulation were recorded after intrathecal (i.t.) injection of apelin-13 (0.1, 1, and 10 nmol/mouse). The mRNA and protein expression, concentration of glutamic acid (Glu), and number of c-Fos immunol staining in lumbar spinal cord (L4/5) were determined. The results demonstrated that Apln gene expression in the lumbar spinal cord was down-regulated in the CFA pain model. Apelin-13 (10 nmol/mouse, i.t.) alleviated CFA-induced inflammatory pain, and it exhibited a more potent antinociceptive effect than apelin-36 and (pyr)apelin-13. The antinociception of apelin-13 could be blocked by APJ antagonist apelin-13(F13A). I.T. apelin-13 attenuated the increased levels of Aplnr , Grin2b, Camk2d , and c-Fos genes expression, Glu concentration, and NMDA receptor 2B (GluN2B) protein expression caused by CFA. Apelin-13 significantly reduced the number of Fos-positive cells in laminae III and IV/V of the dorsal horn. This study indicated that i.t. apelin-13 exerted an analgesic effect against inflammatory pain, which was mediated by activation of APJ, and inhibition of Glu/GluN2B function and neural activity of the spinal dorsal horn.

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The Apelin/APJ System in Psychosis and Neuropathy

Cited by 42 publications

References 68 publications

Increased apelin receptor gene expression in the subfornical organ of spontaneously hypertensive rats

Increased apelin receptor gene expression in the subfornical organ of spontaneously hypertensive rats

Association of Apelin and Apelin Receptor Polymorphisms With the Risk of Comorbid Depression and Anxiety in Coronary Heart Disease Patients

Intrathecally Administered Apelin-13 Alleviated Complete Freund’s Adjuvant-Induced Inflammatory Pain in Mice

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