http://www.cnr.it/ontology/cnr/individuo/prodotto/ID184540
Apolipoprotein A-I (ApoA-I) Mimetic Peptide P2a by Restoring Cholesterol Esterification Unmasks ApoA-I Anti-Inflammatory Endogenous Activity In Vivo (Articolo in rivista)
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- Label
- Apolipoprotein A-I (ApoA-I) Mimetic Peptide P2a by Restoring Cholesterol Esterification Unmasks ApoA-I Anti-Inflammatory Endogenous Activity In Vivo (Articolo in rivista) (literal)
- Anno
- 2012-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1124/jpet.111.189308 (literal)
- Alternative label
Bucci, M; Cigliano, L; Vellecco, V; D'Andrea, LD; Ziaco, B; Rossi, A; Sautebin, L; Carlucci, A; Abrescia, P; Pedone, C; Ianaro, A; Cirino, G; (2012)
Apolipoprotein A-I (ApoA-I) Mimetic Peptide P2a by Restoring Cholesterol Esterification Unmasks ApoA-I Anti-Inflammatory Endogenous Activity In Vivo
in The Journal of pharmacology and experimental therapeutics (Print); American Society Of Pharmacology And Experimental Therapeutics, Bethesda (Stati Uniti d'America)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Bucci, M; Cigliano, L; Vellecco, V; D'Andrea, LD; Ziaco, B; Rossi, A; Sautebin, L; Carlucci, A; Abrescia, P; Pedone, C; Ianaro, A; Cirino, G; (literal)
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- Univ Naples Federico 2, Dept Expt Pharmacol, Fac Pharm, I-80131 Naples, Italy
Univ Naples Federico 2, Dept Biol Sci, I-80131 Naples, Italy
CNR, Biostruct & Bioimaging Inst, Naples, Italy (literal)
- Titolo
- Apolipoprotein A-I (ApoA-I) Mimetic Peptide P2a by Restoring Cholesterol Esterification Unmasks ApoA-I Anti-Inflammatory Endogenous Activity In Vivo (literal)
- Abstract
- The acute-phase protein haptoglobin (Hpt) binds apolipoprotein A-I (ApoA-I) and impairs its action on lecithin-cholesterol acyltransferase, an enzyme that plays a key role in reverse cholesterol transport. We have previously shown that an ApoA-I mimetic peptide, P2a, displaces Hpt from ApoA-I, restoring the enzyme activity in vitro. The aim of this study was to evaluate whether P2a displaces Hpt from ApoA-I in vivo and whether this event leads to anti-inflammatory activity. Mice received subplantar injections of carrageenan. Paw volume was measured before the injection and 2, 4, 6, 24, 48, 72, and 96 h thereafter. At the same time points, concentrations of HDL cholesterol (C) and cholesterol esters (CEs) were measured by high-performance liquid chromatography, and Hpt and ApoA-I plasma levels were evaluated by enzyme-linked immunosorbent assay. Western blotting analysis for nitric-oxide synthase and cyclooxygenase (COX) isoforms was also performed on paw homogenates. CEs significantly decreased in carrageenan-treated mice during edema development and negatively correlated with the Hpt/ApoA-I ratio. P2a administration significantly restored the CE/C ratio. In addition, P2a displayed an anti-inflammatory effect on the late phase of edema with a significant reduction in COX2 expression coupled to an inhibition of prostaglandin E 2 synthesis, implying that, in the presence of P2a, CE/C ratio rescue and edema inhibition were strictly related. In conclusion, the P2a effect is due to its binding to Hpt with consequent displacement of ApoA-I that exerts anti-inflammatory activity. Therefore, it is feasible to design drugs that, by enhancing the physiological endogenous protective role of ApoA-I, may be useful in inflammation-based diseases. (literal)
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