Effects of all- retinoic acid on orphan receptor APJ signaling in spontaneously hypertensive rats

Zhong, Jiuchang; Huang, Dongyang; Liu, Gefei; Huang, Jin; Yang, Yanmei; Li, Yifan; Song, Xuhong; Du, Kun

doi:10.1016/j.cardiores.2004.10.020

Cited by 54 publications

(46 citation statements)

References 26 publications

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“…Spontaneously hypertensive rats have decreased cardiovascular apelin receptor and apelin mRNA and protein compared with control rats. Exercise training or long-term all-trans retinoic acid treatment improves hypertension in line with an increase in apelin receptor and apelin expression (Zhong et al, 2005;Zhang et al, 2006), consistent with the predominantly hypotensive effect seen in healthy individuals and animals. Spontaneously hypertensive rats have increased apelin expression in the rostral ventrolateral medulla, and overexpression of apelin in this area causes chronic hypertension in normotensive rats (Zhang et al, 2009b).…”

Section: A Cardiovascular Diseasesupporting

confidence: 57%

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

Pitkin

Maguire²,

Bonner³

et al. 2010

Pharmacol Rev

166

133

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Section: A Cardiovascular Diseasesupporting

confidence: 57%

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

Pitkin

Maguire²,

Bonner³

et al. 2010

Pharmacol Rev

166

133

View full text Add to dashboard Cite

“…Genes encoding these proteins are reported to be regulated by RA (32)(33)(34)(35) and were more highly expressed in NOD-derived than NOD.Idd3-derived CD11b + cells, as determined by microarray and confirmed by real-time PCR ( Figure 5, A and C). Interestingly, the expression of Irf4, Ephx1, Fcna, and Aplnr in NOD.Il21r KO CD11b + cells showed a similar pattern to that observed in NOD.Idd3-derived CD11b + cells (Figure 5D), suggesting a possible connection between the RA and IL-21 signaling pathways.…”

Section: Il-21 Signaling Both In T Cells and Apcs Contributes To The mentioning

confidence: 86%

Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice

Liu¹,

Lee²,

Sullivan³

et al. 2011

J. Clin. Invest.

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Type 1 diabetes (T1D) is an autoimmune disease that shows familial aggregation in humans and likely has genetic determinants. Disease linkage studies have revealed many susceptibility loci for T1D in mice and humans. The mouse T1D susceptibility locus insulin-dependent diabetes susceptibility 3 (Idd3), which has a homologous genetic interval in humans, encodes cytokine genes Il2 and Il21 and regulates diabetes and other autoimmune diseases; however, the cellular and molecular mechanisms of this regulation are still being elucidated. Here we show that T cells from NOD mice produce more Il21 and less Il2 and exhibit enhanced Th17 cell generation compared with T cells from NOD.Idd3 congenic mice, which carry the protective Idd3 allele from a diabetes-resistant mouse strain. Further, APCs from NOD and NOD.Idd3 mice played a central role in this differential Th17 cell development, and IL-21 signaling in APCs was pivotal to this process. Specifically, NOD-derived APCs showed increased production of pro-Th17 mediators and dysregulation of the retinoic acid (RA) signaling pathway compared with APCs from NOD.Idd3 and NOD.Il21r-deficient mice. These data suggest that the protective effect of the Idd3 locus is due, in part, to differential RA signaling in APCs and that IL-21 likely plays a role in this process. Thus, we believe APCs provide a new candidate for therapeutic intervention in autoimmune diseases.

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“…Transcription of apelin is reduced during angiotensin II elevation, 16 whereas inhibition of angiotensin II type-1 receptor transcription results in increased APJ expression. 17 In APJ-deficient animal models, there is an exaggerated pressor response to angiotensin II, whereas double angiotensin II type I and APJ knock out animals have elevated blood pressure relative to angiotensin II type I-deficient mice. 26 Moreover, angiotensin II-induced myocardial fibrosis can be prevented by apelin through inhibition of plasminogen activator inhibitor type-1 production.…”

Section: Discussionmentioning

confidence: 99%

Sustained Cardiovascular Actions of APJ Agonism During Renin–Angiotensin System Activation and in Patients With Heart Failure

Barnes

Alam

Carter

et al. 2013

Circ: Heart Failure

106

100

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Background— To assess cardiovascular actions of APJ agonism during prolonged (Pyr 1 )apelin-13 infusion and renin–angiotensin system activation. Methods and Results— Forty-eight volunteers and 12 patients with chronic stable heart failure attended a series of randomized placebo–controlled studies. Forearm blood flow, cardiac index, left ventricular dimensions, and mean arterial pressure were measured using bilateral venous occlusion plethysmography, bioimpedance cardiography, transthoracic echocardiography, and sphygmomanometry, respectively, during brief local (0.3–3.0 nmol/min) and systemic (30–300 nmol/min) or prolonged systemic (30 nmol/min) (Pyr 1 )apelin-13 infusions in the presence or absence of renin–angiotensin system activation with sodium depletion or angiotensin II coinfusion. During sodium depletion and angiotensin II coinfusion, (Pyr 1 )apelin-13–induced vasodilatation was preserved ( P <0.02 for both). Systemic intravenous (Pyr 1 )apelin-13 infusion increased cardiac index, whereas reducing mean arterial pressure and peripheral vascular resistance index ( P <0.001 for all) irrespective of sodium depletion or angiotensin II (0.5 ng/kg per minute) coinfusion ( P >0.05 for all). Prolonged 6-hour (Pyr 1 )apelin-13 infusion caused a sustained increase in cardiac index with increased left ventricular ejection fraction in patients with chronic heart failure (ANOVA; P <0.001 for all). Conclusions— APJ agonism has sustained cardiovascular effects that are preserved in the presence of renin–angiotensin system activation or heart failure. APJ agonism may hold major promise to complement current optimal medical therapy in patients with chronic heart failure. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifiers: NCT00901719, NCT00901888, NCT01049646, NCT01179061.

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Effects of all- retinoic acid on orphan receptor APJ signaling in spontaneously hypertensive rats

Cited by 54 publications

References 26 publications

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice

Sustained Cardiovascular Actions of APJ Agonism During Renin–Angiotensin System Activation and in Patients With Heart Failure

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