Serum amyloid A (SAA): influence on HDL-mediated cellular cholesterol efflux.

Banka, Carole L.; Yuan, Ting; Beer, Maria C. de; Kindy, Mark S.; Curtiss, Linda K.; Beer, Frederick C. de

doi:10.1016/s0022-2275(20)39863-1

Cited by 179 publications

(21 citation statements)

References 25 publications

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“…Although it was suggested that the presence of SAA in acute-phase HDL might be related to the decreased cholesterol efflux, no experimental data to support such a hypothesis were provided. Another study found no difference in cholesterol efflux from monocytic THP-1 cells between normal and acute-phase HDL (43). When normal HDL was markedly remodeled in vitro such that the HDL contained an amount of SAA greater than 50% of its total protein, this resulted in decreases in cholesterol efflux (43).…”

Section: Discussionmentioning

confidence: 99%

“…Another study found no difference in cholesterol efflux from monocytic THP-1 cells between normal and acute-phase HDL (43). When normal HDL was markedly remodeled in vitro such that the HDL contained an amount of SAA greater than 50% of its total protein, this resulted in decreases in cholesterol efflux (43). However, this degree of remodeling does not typically occur during the APR.…”

Section: Discussionmentioning

confidence: 99%

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Cholesterol efflux by acute-phase high density lipoprotein: role of lecithin:cholesterol acyltransferase

Khovidhunkit

Shigenaga

Moser

et al. 2001

Journal of Lipid Research

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HDL plays an initial role in reverse cholesterol transport by mediating cholesterol removal from cells. During infection and inflammation, several changes in HDL composition occur that may affect the function of HDL; therefore, we determined the ability of acute-phase HDL to promote cholesterol removal from cells. Acute-phase HDL was isolated from plasma of Syrian hamsters injected with lipopolysaccharide. Cholesterol removal from J 774 murine macrophages by acute-phase HDL was less efficient than that by control HDL because of both a decrease in cholesterol efflux and an increase in cholesterol influx. LCAT activity of acute-phase HDL was significantly lower than that of control HDL. When LCAT activity of control HDL was inactivated, cholesterol efflux decreased and cholesterol influx increased to the level observed in acute-phase HDL. Inactivation of LCAT had little effect on acute-phase HDL. In GM 3468A human fibroblasts, the ability of acute-phase HDL to remove cholesterol from cells was also lower than that of normal HDL. The impaired cholesterol removal, however, was primarily a result of an increase in cholesterol influx without changes in cholesterol efflux. When control HDL in which LCAT had been inactivated was incubated with fibroblasts, cholesterol influx increased to a level comparable to that of acute-phase HDL, without any change in cholesterol efflux.These results suggest that the ability of acutephase HDL to mediate cholesterol removal was impaired compared with that of control HDL and the lower LCAT activity in acute-phase HDL may be responsible for this impairment. The decreased ability of acute-phase HDL to remove cholesterol from cells may be one of the mechanisms that account for the well-known relationship between infection/inflammation and atherosclerosis.-Khovidhunkit, W.,

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cholesterol efflux by acute-phase high density lipoprotein: role of lecithin:cholesterol acyltransferase

Khovidhunkit

Shigenaga

Moser

et al. 2001

Journal of Lipid Research

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“…This is an Open Access article under the CC BY license. (33). Some SAA isoforms are expressed in atherosclerotic plaques (34,35) and SAA induces the migration, adhesion, and tissue infiltration of monocytes (36), cells strongly implicated in the pathogenesis of atherosclerosis.…”

mentioning

confidence: 99%

SAA-only HDL formed during the acute phase response in apoA-I+/+ and apoA-I–/– mice

Cabana

Reardon

Wei

et al. 1999

Journal of Lipid Research

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Serum amyloid A (SAA) is an acute phase protein of unknown function that is involved in systemic amyloidosis and may also be involved in atherogenesis. The precise role of SAA in these processes has not been established. SAA circulates in plasma bound to high density lipoprotein-3 (HDL 3 ). The pathway for the production of SAA-containing HDL is not known. To test whether apolipoprotein (apo)A-I-HDL is required in the production of SAA-HDL, we analyzed the lipopolysaccharide (LPS)-induced changes in apoA-I ؉ / ؉ and apoA-I ؊ / ؊ mice. In apoA-I ؉ / ؉ mice, after injection of LPS, remodeling of HDL occurred: total cholesterol increased and apoA-I decreased slightly and shifted to lighter density. Dense (density of HDL 3 ) but large (size of HDL 2 ) SAA-containing particles were formed. Upon fast phase liquid chromatography fractionation of plasma, Ͼ 90% of SAA eluted with HDL that was enriched in cholesterol and phospholipid and shifted "leftward" to larger particles. Non-denaturing immunoprecipitation with anti-mouse apoA-I precipitated all of the apoA-I but not all of the SAA, confirming the presence of SAA-HDL devoid of apoA-I. In the apoA-I ؊ / ؊ mice, which normally have very low plasma lipid levels, LPS injection resulted in significantly increased total and HDL cholesterol. Greater than 90% of the SAA was lipid associated and was found on dense but large, spherical HDL particles essentially devoid of other apolipoproteins. We conclude that serum amyloid A (SAA) is able to sequester lipid, forming dense but large HDL particles with or without apoA-I or other apolipoproteins. The capacity to isolate lipoprotein particles containing SAA as the predominant or only apolipoprotein provides an important system to further explore the biological function of SAA. -Cabana, V. G., C. A. Reardon, B. Wei, J. R. Lukens, and G. S. Getz. SAA-only HDL formed during the acute phase response in apoA-I ؉ / ؉ and apoA-I ؊ / ؊ mice.

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“…Τα οξειδωμένα λιπίδια επηρεάζουν και τα τρία στάδια της προσκόλλησης των μονοκυττάρων: προσέγγιση, ενεργοποίηση και σύνδεση. Η MM-LDL αλλά και η οξειδωμένη LDL απελευθερώνει Ρ-σελεκτίνη, η οποία και έχει βρεθεί αυξημένη σε ανθρώπινες αθηροσκληρωτικές βλάβες [184][185][186] Επιπλέον, η MM-LDL προκαλεί την παραγωγή από τα ενδοθηλιακά κύτταρα των ισχυρών μονοκυτταρικων ενεργοποιητων, όπως της χημειοτακτικής πρωτεΐνης των μονοκυττάρων 1(MCP-1) και του διεγερτικού παράγοντα των αποικιών των μονοκυττάρων (M-CSF) [187][188][189] . Με τη βοήθεια αυτών των μορίων τα μονοκύτταρα προσκολλώνται στα ενδοθηλιακά κύτταρα και μεταναστεύουν ανάμεσα από αυτά στο υπενδοθήλιο.…”

Section: αθηροσκλήρωση: ένα φλεγμονώδες φαινόμενοunclassified

Μελέτη Των Μηχανισμών Δράσης Φυσικών Αντιοξειδωτικών Στην Οξείδωση Των Λιποπρωτεϊνών

Φεσληκίδης¹

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Πρόλογος 1. ΕΙΣΑΓΩΓΗ 8.1. Εισαγωγή. 8.2. Μηχανισμοί δράσης των αντιοξειδωτικών. 8.3. Αντιοξειδωτικά που αναστέλλουν την παραγωγή ελευθέρων ριζών που προκαλείται από Cu 2+ . 8.3.1. Αντιοξειδωτικά που συνδέονται με τα ιόντα χαλκού και σχηματίζουν σύμπλοκα που είναι οξειδοαναγωγικά ανενεργά. 8.3.2. Αντιοξειδωτικά που αναστέλλουν τη σύνδεση των ιόντων χαλκού στις απολιποπρωτεΐνες. 8.3.3. Αντιοξειδωτικά που ελαττώνουν τη συγκέντρωση των υδροϋπεροξειδίων με αποσύνθεση. 8.3.4.Αντιοξειδωτικά που παρεμποδίζουν τη μεταφορά οξειδωμένων λιπιδίων. 8.4. Αντιοξειδωτικά που εξουδετερώνουν ή σταθεροποιούν τις ελεύθερες ρίζες. 8.4.1. Αντιοξειδωτικά που είναι σταθερές ελεύθερες ρίζες αντιδρούν με τις ρίζες και τις εξουδετερώνουν. 8.4.2. Αναγωγικά αντιδραστήρια τα οποία μπορούν να εξουδετερώσουν μέχρι δύο ελεύθερες ρίζες ανά μόριο. 8.4.3. Αντιοξειδωτικά που αλληλεπιδρούν με τις ελεύθερες ρίζες και σχηματίζουν ελεύθερες ρίζες λιγότερο δραστικές (σταθεροποιούν τις ελεύθερες ρίζες). 8.4.4. Αντιοξειδωτικά με μικτό μηχανισμό. 8.5. Προγραμματισμός και αξιολόγηση του τρόπου δράσης των αντιοξειδωτικών από τα αποτελέσματά τους στις κινητικές της υπεροξείδωσης . 8.5.1. Yπεροξείδωση που προκαλείται από το χαλκό. 8.5.2. Yπεροξείδωση που προκαλείται από το ΑΑΡΗ ΠΕΙΡΑΜΑΤΙΚΟ ΜΕΡΟΣ 1. ΥΛΙΚΑ 1.1 Αντιδραστήρια Πίνακας 1.3 Γενικά χαρακτηριστικά των λιποπρωτεϊνών του πλάσματος. Είδος λιποπρωτεΐνης Μέγεθος Πυκνότητα (g/ml) Αναλογία τριγλυκερολώνχοληστερεστέρων Αναλογία λιπιδίωνπρωτεϊνών Αποπρωτεΐνες που συσχετίζονται Χυλομικρά

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Serum amyloid A (SAA): influence on HDL-mediated cellular cholesterol efflux.

Cited by 179 publications

References 25 publications

Cholesterol efflux by acute-phase high density lipoprotein: role of lecithin:cholesterol acyltransferase

Cholesterol efflux by acute-phase high density lipoprotein: role of lecithin:cholesterol acyltransferase

SAA-only HDL formed during the acute phase response in apoA-I+/+ and apoA-I–/– mice

Μελέτη Των Μηχανισμών Δράσης Φυσικών Αντιοξειδωτικών Στην Οξείδωση Των Λιποπρωτεϊνών

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