Apolipoprotein A-I mimetic peptide reverses impaired arterial healing after injury by reducing oxidative stress

Rosenbaum, Michael; Chaudhuri, Pinaki; Abelson, Benjamin; Cross, Brandy N.; Graham, Linda M.

doi:10.1016/j.atherosclerosis.2015.06.018

Cited by 21 publications

(17 citation statements)

References 36 publications

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“…Recent studies have reported a potential anti-inflammatory role for apoA-I in the regulation of monocyte/macrophage recruitment to local sites of inflammation, via modulation of lipid rafts in cellular membranes which resulted in suppression of PI3K/Akt signaling (Iqbal et al, 2016). It also displays anti-oxidant properties as shown by its ability to inhibit LDL oxidation, remove lipid hydroperoxides, and also protect endothelial cells from apoptosis (Suc et al, 1997; Podrez, 2010; Rosenbaum et al, 2015). Furthermore, its structural homology with PSF has contributed to its anti-clotting and anti-aggregation effects on platelets which has strengthened its cardioprotective role (Yui et al, 1988).…”

Section: Apolipoprotein Mimetic Peptidesmentioning

confidence: 99%

The Potential Therapeutic Application of Peptides and Peptidomimetics in Cardiovascular Disease

et al. 2017

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Cardiovascular disease (CVD) remains a leading cause of mortality and morbidity worldwide. Numerous therapies are currently under investigation to improve pathological cardiovascular complications, but yet, there have been very few new medications approved for intervention/treatment. Therefore, new approaches to treat CVD are urgently required. Attempts to prevent vascular complications usually involve amelioration of contributing risk factors and underlying processes such as inflammation, obesity, hyperglycaemia, or hypercholesterolemia. Historically, the development of peptides as therapeutic agents has been avoided by the Pharmaceutical industry due to their low stability, size, rate of degradation, and poor delivery. However, more recently, resurgence has taken place in developing peptides and their mimetics for therapeutic intervention. As a result, increased attention has been placed upon using peptides that mimic the function of mediators involved in pathologic processes during vascular damage. This review will provide an overview on novel targets and experimental therapeutic approaches based on peptidomimetics for modulation in CVD. We aim to specifically examine apolipoprotein A-I (apoA-I) and apoE mimetic peptides and their role in cholesterol transport during atherosclerosis, suppressors of cytokine signaling (SOCS)1-derived peptides and annexin-A1 as potent inhibitors of inflammation, incretin mimetics and their function in glucose-insulin tolerance, among others. With improvements in technology and synthesis platforms the future looks promising for the development of novel peptides and mimetics for therapeutic use. However, within the area of CVD much more work is required to identify and improve our understanding of peptide structure, interaction, and function in order to select the best targets to take forward for treatment.

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Section: Apolipoprotein Mimetic Peptidesmentioning

confidence: 99%

The Potential Therapeutic Application of Peptides and Peptidomimetics in Cardiovascular Disease

et al. 2017

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“…4F has also been shown to improve HDL function (40,41), reduce systemic inflammation (42), reduce oxidative stress (43), and increase the clearance of oxidized lipid species from the circulation (44). Given these effects, and given the nature and location of atherosclerosis itself, our laboratory had long assumed that the circulation was the site of action for 4F (45).…”

Section: D-k-v-a-e-k-f-k-e-a-f-nhmentioning

confidence: 99%

Transintestinal transport of the anti-inflammatory drug 4F and the modulation of transintestinal cholesterol efflux

Meriwether

Sulaiman

Wagner

et al. 2016

Journal of Lipid Research

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Increasing evidence, both direct and indirect, indicates that the small intestine (SI) may be an important modulator of atherosclerosis. As a result, the SI offers promising therapeutic targets for the prevention and treatment of this disease.The SI is linked to atherosclerosis in at least four respects. First, intestinal inflammation in the form of inflammatory bowel disease (IBD) has been linked to an increased prevalence of early stage vascular disease in patients without the classical cardiovascular risk factors (1-3). Second, our own recent research has established a link between aberrant levels of lipid signals in the SI and both dyslipidemia and atherosclerosis. Intestinally derived unsaturated lysophosphatidic acids (LPAs) and eicosanoids can both induce dyslipidemia as well as systemic inflammation in LDL receptor null (LDLR / ) mice (4, 5). Dietary LPA can also induce atherogenesis (6), and the levels of unsaturated LPAs in the SI correlate with the extent of atherosclerosis in LDLR / mice fed a Western diet (WD) (7). Third, the SI is an important source of apoAI (8), and at least in mice 30% of the steady-state plasma HDLcholesterol pool is derived from the SI (9). Moreover, while HDL can interrupt atherogenesis by preventing oxidative Abstract The site and mechanism of action of the apoA-I mimetic peptide 4F are incompletely understood. Transintestinal cholesterol efflux (TICE) is a process involved in the clearance of excess cholesterol from the body. While TICE is responsible for at least 30% of the clearance of neutral sterols from the circulation into the intestinal lumen, few pharmacological agents have been identified that modulate this pathway. We show first that circulating 4F selectively targets the small intestine (SI) and that it is predominantly transported into the intestinal lumen. This transport of 4F into the SI lumen is transintestinal in nature, and it is modulated by TICE. We also show that circulating 4F increases reverse cholesterol transport from macrophages and cholesterol efflux from lipoproteins via the TICE pathway. We identify the cause of this modulation of TICE either as 4F being a cholesterol acceptor with respect to enterocytes, from which 4F enhances cholesterol efflux, or as 4F being an intestinal chaperone with respect to TICE. Our results assign a novel role for 4F as a modulator of the TICE pathway and suggest that the anti-inflammatory functions of 4F may be a partial consequence of the codependent intestinal transport of both 4F and cholesterol.

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“…Alternatively, APOA1 has an important athero-protective function thanks to its anti-inflammatory role and its influence on the recruitment of monocytes/macrophages to local sites of inflammation 21 . It has also been proposed to have anti-oxidant activity 22 . APOA1 has been proposed as a potentially promising therapeutic targetto treat CV disease by augmenting HDL cholesterol efflux and hence, reducing the risk of CV disease 23 .…”

Section: Discussionmentioning

confidence: 99%

Potential role of new molecular plasma signatures on cardiovascular risk stratification in asymptomatic individuals

Baldán-Martín

López

Corbacho-Alonso

et al. 2018

Sci Rep

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The evaluation of cardiovascular (CV) risk is based on equations derived from epidemiological data in individuals beyond the limits of middle age such as the Framingham and SCORE risk assessments. Lifetime Risk calculator (QRisk®), estimates CV risk throughout a subjects’ lifetime, allowing those. A more aggressive and earlier intervention to be identified and offered protection from the consequences of CV and renal disease. The search for molecular profiles in young people that allow a correct stratification of CV risk would be of great interest to adopt preventive therapeutic measures in individuals at high CV risk. To improve the selection of subjects susceptible to intervention with aged between 30–50 years, we have employed a multiple proteomic strategy to search for new markers of early CV disease or reported CV events and to evaluate their relationship with Lifetime Risk. Blood samples from 71 patients were classified into 3 groups according to their CV risk (healthy, with CV risk factors and with a previously reported CV event subjects) and they were analyzed using a high through quantitative proteomics approach. This strategy allowed three different proteomic signatures to be defined, two of which were related to CV stratification and the third one involved markers of organ damage.

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Apolipoprotein A-I mimetic peptide reverses impaired arterial healing after injury by reducing oxidative stress

Cited by 21 publications

References 36 publications

The Potential Therapeutic Application of Peptides and Peptidomimetics in Cardiovascular Disease

The Potential Therapeutic Application of Peptides and Peptidomimetics in Cardiovascular Disease

Transintestinal transport of the anti-inflammatory drug 4F and the modulation of transintestinal cholesterol efflux

Potential role of new molecular plasma signatures on cardiovascular risk stratification in asymptomatic individuals

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