Lipoprotein inflammatory properties and serum amyloid A levels but not cholesterol levels predict lesion area in cholesterol-fed rabbits

Lenten, Brian J. Van; Wagner, Alan C.; Navab, Mohamad; Anantharamaiah, G.M.; Hama, Susan; Reddy, Srinivasa T.; Fogelman, Alan M.

doi:10.1194/jlr.m700138-jlr200

Cited by 98 publications

(110 citation statements)

References 49 publications

(61 reference statements)

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“…Other studies show that D-4F treatment in hyperlipidemic rabbits reduces arterial lesion formation. This response was associated with a reduction in the HDL inflammatory index but not total cholesterol or HDL cholesterol [64]. These data provide further evidence that the quality and function of HDL is a better predictor of lesion formation than HDL concentration, in agreement with the proposal by Ansell et al [63].…”

Section: Apoa-i Mimetic Peptides and Atherogenic Lesion Formation In supporting

confidence: 81%

“…This observation suggested that functional properties of HDL, rather than absolute serum HDL concentration, may dictate its atheroprotective actions [63]. An HDL inflammatory index has recently been developed as a means to assess the functional quality of HDL [64]. This measurement is based on the ex vivo capacity of HDL to inhibit monocyte chemotactic activity in cultured endothelial cells [64].…”

Section: Pro-inflammatory Hdlmentioning

confidence: 99%

“…This measurement is based on the ex vivo capacity of HDL to inhibit monocyte chemotactic activity in cultured endothelial cells [64]. Assessment of HDL isolated from atherosclerotic rabbits revealed an increase in the inflammatory index that positively correlated with circulating levels of the acute phase reactant serum amyloid A [64].…”

Section: Pro-inflammatory Hdlmentioning

confidence: 99%

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Vasculoprotective Effects of Apolipoprotein Mimetic Peptides: An Evolving Paradigm in HDL Therapy

White¹,

Datta²,

Mochon³

et al. 2009

VDP

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Anti-atherogenic effects of high density lipoprotein (HDL) and its major protein component apolipoprotein A-I (apoA-I) are principally thought to be due to their ability to mediate reverse cholesterol transport. These agents also possess anti-oxidant properties that prevent the oxidative modification of low density lipoprotein (LDL) and anti-inflammatory properties that include inhibition of endothelial cell adhesion molecule expression. Results of the Framingham study revealed that a reduction in HDL levels is an independent risk factor for coronary artery disease (CAD). Accordingly, there has been considerable interest in developing new therapies that specifically elevate HDL cholesterol. However, recent evidence suggests that increasing circulating HDL cholesterol levels alone is not sufficient as a mode of HDL therapy. Rather, therapeutic approaches that increase the functional properties of HDL may be superior to simply raising the levels of HDL per se. Our laboratory has pioneered the development of synthetic, apolipoprotein mimetic peptides which are structurally and functionally similar to apoA-I but possess unique structural homology to the lipid-associating domains of apoA-I. The apoA-I mimetic peptide 4F inhibits atherogenic lesion formation in murine models of atherosclerosis. This effect is related to the ability of 4F to induce the formation of pre-β HDL particles that are enriched in apoA-I and paraoxonase. 4F also possesses anti-inflammatory and anti-oxidant properties that are independent of its effect on HDL quality per se. Recent studies suggest that 4F stimulates the expression of the antioxidant enzymes heme oxygenase and superoxide dismutase and inhibits superoxide anion formation in blood vessels of diabetic, hypercholesterolemic and sickle cell disease mice. The goal of this review is to discuss HDL-dependent and -independent mechanisms by which apoA-I mimetic peptides reduce vascular injury in experimental animal models.

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Section: Apoa-i Mimetic Peptides and Atherogenic Lesion Formation In supporting

confidence: 81%

Section: Pro-inflammatory Hdlmentioning

confidence: 99%

Section: Pro-inflammatory Hdlmentioning

confidence: 99%

See 1 more Smart Citation

Vasculoprotective Effects of Apolipoprotein Mimetic Peptides: An Evolving Paradigm in HDL Therapy

White¹,

Datta²,

Mochon³

et al. 2009

VDP

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“…Several recent animal studies have proposed that SAA promotes increased atherosclerosis development, [15][16][17] although the mechanism is unknown. To date there are no data suggesting a pro-atherogenic role for CRP, but CRP is not an acute phase reactant in mice, which limits the interpretation of this data.…”

mentioning

confidence: 99%

Serum Amyloid A, but Not C-Reactive Protein, Stimulates Vascular Proteoglycan Synthesis in a Pro-Atherogenic Manner

Wilson

Thompson

Webb

et al. 2008

The American Journal of Pathology

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Inflammatory markers serum amyloid A (SAA) and C-reactive protein (CRP) are predictive of cardiac disease and are proposed to play causal roles in the development of atherosclerosis, in which the retention of lipoproteins by vascular wall proteoglycans is critical. The purpose of this study was to determine whether SAA and/or CRP alters vascular proteoglycan synthesis and lipoprotein retention in a pro-atherogenic manner. Vascular smooth muscle cells were stimulated with either SAA or CRP (1 to 100 mg/L) and proteoglycans were then isolated and characterized. SAA, but not CRP, increased proteoglycan sulfate incorporation by 50 to 100% in a dose-dependent manner (P < 0.0001), increased glycosaminoglycan chain length, and increased low-density lipoprotein (LDL) binding affinity (K d , 29 g/ml LDL versus 90 g/ml LDL for SAA versus control proteoglycans; P < 0.005). Furthermore, SAA up-regulated biglycan via the induction of endogenous transforming growth factor (TGF)-␤. To determine whether SAA stimulated proteoglycan synthesis in vivo, ApoE ؊/؊ mice were injected with an adenovirus expressing human SAA-1, a null virus, or saline. Mice that received adenovirus expressing SAA had increased TGF-␤ concentrations in plasma and increased aortic biglycan content compared with mice that received either null virus or saline. Thus, SAA alters vascular proteoglycans in a pro-atherogenic manner via the stimulation of TGF-␤ and may play a causal role in the development of atherosclerosis.

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“…The efficacy of these peptides was recently also demonstrated in a rabbit model of atherosclerosis (Van Lenten 2007).…”

Section: Apolipoprotein Mimetic Peptides In Animal Models Of Atheroscmentioning

confidence: 99%

The Effect of Apolipoprotein Mimetic Peptides in Inflammatory Disorders Other Than Atherosclerosis

Navab

Anantharamaiah

Fogelman

2008

Trends in Cardiovascular Medicine

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Lipoprotein inflammatory properties and serum amyloid A levels but not cholesterol levels predict lesion area in cholesterol-fed rabbits

Cited by 98 publications

References 49 publications

Vasculoprotective Effects of Apolipoprotein Mimetic Peptides: An Evolving Paradigm in HDL Therapy

Vasculoprotective Effects of Apolipoprotein Mimetic Peptides: An Evolving Paradigm in HDL Therapy

Serum Amyloid A, but Not C-Reactive Protein, Stimulates Vascular Proteoglycan Synthesis in a Pro-Atherogenic Manner

The Effect of Apolipoprotein Mimetic Peptides in Inflammatory Disorders Other Than Atherosclerosis

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