http://www.cnr.it/ontology/cnr/individuo/prodotto/ID14090
Haptoglobin binds the anti-atherogenic protein Apolipoprotein E- impairment of the apolipoprotein E stimulation of both the enzyme lecithin:cholesterol acyl-transferase activity and the cholesterol uptake by hepatocytes (Articolo in rivista)
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- Label
- Haptoglobin binds the anti-atherogenic protein Apolipoprotein E- impairment of the apolipoprotein E stimulation of both the enzyme lecithin:cholesterol acyl-transferase activity and the cholesterol uptake by hepatocytes (Articolo in rivista) (literal)
- Anno
- 2009-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1111/j.1742-4658.2009.07319.x (literal)
- Alternative label
Cigliano L., Pugliese C. R., Spagnuolo M. S., Palumbo R., Abrescia P (2009)
Haptoglobin binds the anti-atherogenic protein Apolipoprotein E- impairment of the apolipoprotein E stimulation of both the enzyme lecithin:cholesterol acyl-transferase activity and the cholesterol uptake by hepatocytes
in FEBS journal. S (Online)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Cigliano L., Pugliese C. R., Spagnuolo M. S., Palumbo R., Abrescia P (literal)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
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- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Università di Napoli; Università di Napoli; CNR; CNR; Università di Napoli (literal)
- Titolo
- Haptoglobin binds the anti-atherogenic protein Apolipoprotein E- impairment of the apolipoprotein E stimulation of both the enzyme lecithin:cholesterol acyl-transferase activity and the cholesterol uptake by hepatocytes (literal)
- Abstract
- Haptoglobin (Hpt) binds apolipoprotein A-I (ApoA-I), and impairs its stimulation of lecithin: cholesterol acyltransferase (LCAT). LCAT plays a major role in reverse cholesterol transport (RCT). Apolipoprotein E (ApoE), like ApoA-I, promotes different steps of RCT, including LCAT stimulation. ApoE contains amino acid sequences that are homologous with the ApoA-I region bound by Hpt and are involved in the interaction with LCAT. Therefore, Hpt was expected to also bind ApoE, and inhibit the ApoE stimulatory effect on LCAT. Western blotting and ELISA experiments demonstrated that the Hpt beta-subunit binds ApoE. The affinity of Hpt for ApoE was higher than that for ApoA-I. High ratios of Hpt with either apolipoprotein, such as those associated with the acute phase of inflammation, inhibited, in vitro, the stimulatory effect of ApoE on the cholesterol esterification activity of LCAT. Hpt also impaired human hepatoblastoma-derived cell uptake of [(3)H]cholesterol from proteoliposomes containing ApoE or ApoA-I. We suggest that the interaction between Hpt and ApoE represents a mechanism by which inflammation affects atherosclerosis progression. Hpt might influence ApoE function in processes other than RCT. (literal)
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