ApoA1

Vanella, Luca; Li, Ming; Kim, Dong-Hyun; Malfa, Giuseppe Antonio; Bellner, Lars; Kawakami, Tomoko; Abraham, Nader G.

doi:10.4161/cc.11.4.19125

Cited by 23 publications

(12 citation statements)

References 62 publications

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“…22, 25 Wnt10b is an endogenous regulator of adipogenesis that functions as a ‘switch' that retards adipocyte differentiation and maturation into lipid-laden cells. Activation of Wnt10b contributes to the inactivation/phosphorylation of glycogen synthase kinase-3 β and, consequently, elevated level of β -catenin (Figure 8); it is the molecular node of the canonical Wnt signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: PPARδ binding to heme oxygenase 1 promoter prevents angiotensin II-induced adipocyte dysfunction in Goldblatt hypertensive rats

et al. 2013

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Objective:Renin–angiotensin system (RAS) regulates adipogenic response with adipocyte hypertrophy by increasing oxidative stress. Recent studies have shown the role of peroxisome proliferator-activated receptor-δ (PPARδ) agonist in attenuation of angiotensin II-induced oxidative stress. The aim of this study was to explore a potential mechanistic link between PPARδ and the cytoprotective enzyme heme oxygenase-1 (HO-1) and to elucidate the contribution of HO-1 to the adipocyte regulatory effects of PPARδ agonism in an animal model of enhanced RAS, the Goldblatt 2 kidney 1 clip (2K1C) model.Method:We first established a direct stimulatory effect of the PPARδ agonist (GW 501516) on the HO-1 gene by demonstrating increased luciferase activity in COS-7 cells transfected with a luciferase-HO-1 promoter construct. Sprague-Dawley rats were divided into four groups: sham-operated animals, 2K1C rats and 2K1C rats treated with GW 501516, in the absence or presence of the HO activity inhibitor, stannous mesoporphyrin (SnMP).Results:2K1C animals had increased visceral adiposity, adipocyte hypertrophy, increased inflammatory cytokines, increased circulatory and adipose tisssue levels of renin and Ang II along with increased adipose tissue gp91 phox expression (P<0.05) when compared with sham-operated animals. Treatment with GW 501516 increased adipose tissue HO-1 and adiponectin levels (P<0.01) along with enhancement of Wnt10b and β-catenin expression. HO-1 induction was accompanied by the decreased expression of Wnt5b, mesoderm specific transcript (mest) and C/EBPα levels and an increased number of small adipocytes (P<0.05). These effects of GW501516 were reversed in 2K1C animals exposed to SnMP (P<0.05).Conclusion:Taken together, our study demonstrates, for the first time, that increased levels of Ang II contribute towards adipose tissue dysregulation, which is abated by PPARδ-mediated upregulation of the heme-HO system. These findings highlight the pivotal role and symbiotic relationship of HO-1, adiponectin and PPARδ in the regulation of metabolic homeostasis in adipose tissues.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: PPARδ binding to heme oxygenase 1 promoter prevents angiotensin II-induced adipocyte dysfunction in Goldblatt hypertensive rats

et al. 2013

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“…Administration of L-4F to obese (B6V-Lep-ob/J) mice restored adipocyte function, increased adiponectin release and decreased levels of IL-1 and IL-6 and was associated with an increase in insulin sensitivity and decreased glucose levels [15*]. The mechanism appeared to be related to an L-4F-mediated increase in heme oxygenase 1 (HO-1) and Wnt10b activity [15*].…”

Section: Efficacy Of Apolipoprotein Mimetics In Models Of Diseasementioning

confidence: 99%

“…The mechanism appeared to be related to an L-4F-mediated increase in heme oxygenase 1 (HO-1) and Wnt10b activity [15*]. …”

Section: Efficacy Of Apolipoprotein Mimetics In Models Of Diseasementioning

confidence: 99%

Apolipoprotein A-I mimetics

Reddy

Navab²,

Anantharamaiah

et al. 2014

Current Opinion in Lipidology

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Purpose of Review To summarize recent publications in the field of apolipoprotein mimetics. Recent Findings Apolipoprotein mimetic peptides continue to show efficacy in a number of animal models of disease and demonstrate properties that make them attractive as potential therapeutic agents. A number of new apolipoprotein mimetics have been described recently. A major site of action of apolipoprotein mimetic peptides was found to be in the small intestine where they decrease the levels of pro-inflammatory bioactive lipids. A major problem related to the use of apolipoprotein mimetic peptides is their cost, particularly those that need to be generated by solid phase synthesis with chemical addition of end blocking groups. Novel approaches to apolipoprotein mimetic therapy have emerged recently that show promise in overcoming these barriers. Summary Despite the recent failure of therapies designed to raise HDL-cholesterol in humans, an approach to therapy using mimetics of HDL and its components continues to show promise.

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“…In addition, Vanella et al . showed that L‐4F increases adiponectin production and reverses adipocyte dysfunction via increasing HO‐1 expression both in vitro and in vivo 39. Kruger et al .…”

Section: Discussionmentioning

confidence: 99%

The apolipoprotein A‐I mimetic peptide, D‐4F, restrains neointimal formation through heme oxygenase‐1 up‐regulation

Liu

et al. 2017

J Cellular Molecular Medi

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D‐4F, an apolipoprotein A‐I (apoA‐I) mimetic peptide, possesses distinctly anti‐atherogenic effects. However, the biological functions and mechanisms of D‐4F on the hyperplasia of vascular smooth muscle cells (VSMCs) remain unclear. This study aimed to determine its roles in the proliferation and migration of VSMCs. In vitro, D‐4F inhibited VSMC proliferation and migration induced by ox‐LDL in a dose‐dependent manner. D‐4F up‐regulated heme oxygenase‐1 (HO‐1) expression in VSMCs, and the PI3K/Akt/AMP‐activated protein kinase (AMPK) pathway was involved in these processes. HO‐1 down‐regulation with siRNA or inhibition with zinc protoporphyrin (Znpp) impaired the protective effects of D‐4F on the oxidative stress and the proliferation and migration of VSMCs. Moreover, down‐regulation of ATP‐binding cassette transporter A1 (ABCA1) abolished the activation of Akt and AMPK, the up‐regulation of HO‐1 and the anti‐oxidative effects of D‐4F. In vivo, D‐4F restrained neointimal formation and oxidative stress of carotid arteries in balloon‐injured Sprague Dawley rats. And inhibition of HO‐1 with Znpp decreased the inhibitory effects of D‐4F on neointimal formation and ROS production in arteries. In conclusion, D‐4F inhibited VSMC proliferation and migration in vitro and neointimal formation in vivo through HO‐1 up‐regulation, which provided a novel prophylactic and therapeutic strategy for anti‐restenosis of arteries.

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ApoA1

Cited by 23 publications

References 62 publications

RETRACTED ARTICLE: PPARδ binding to heme oxygenase 1 promoter prevents angiotensin II-induced adipocyte dysfunction in Goldblatt hypertensive rats

RETRACTED ARTICLE: PPARδ binding to heme oxygenase 1 promoter prevents angiotensin II-induced adipocyte dysfunction in Goldblatt hypertensive rats

Apolipoprotein A-I mimetics

The apolipoprotein A‐I mimetic peptide, D‐4F, restrains neointimal formation through heme oxygenase‐1 up‐regulation

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