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Serum amyloid A and lipoprotein retention in murine models of atherosclerosis.
Arterioscler Thromb Vasc Biol. 2005 Apr; 25(4):785-90.AT

Abstract

OBJECTIVE

Elevated serum amyloid A (SAA) levels are associated with increased cardiovascular risk in humans. Because SAA associates primarily with lipoproteins in plasma and has proteoglycan binding domains, we postulated that SAA might mediate lipoprotein retention on atherosclerotic extracellular matrix.

METHODS AND RESULTS

Immunohistochemistry was performed for SAA, apolipoprotein A-I (apoA-I), apolipoprotein B (apoB), and perlecan on proximal aortic lesions from chow-fed low-density lipoprotein receptor (LDLR)-/- and apoE-/- mice euthanized at 10, 50, and 70 weeks. SAA was detected on atherosclerotic lesion extracellular matrix at all time points in both strains. SAA area correlated highly with lesion areas (apoE-/-, r=0.76; LDLR-/-, r=0.86), apoA-I areas (apoE-/-, r=0.88; LDLR-/-, r=0.80), apoB areas (apoE-/-, r=0.74; LDLR-/-, r=0.89), and perlecan areas (apoE-/-, r=0.83; LDLR-/-, r=0.79) (all P<0.0001). In vitro, SAA enrichment increased high-density lipoprotein (HDL) binding to heparan sulfate proteoglycans, and immunoprecipitation experiments using plasma from apoE-/- and LDLR-/- mice demonstrated that SAA was present on both apoA-I-containing and apoB-containing lipoproteins.

CONCLUSIONS

In chow-fed apoE-/- and LDLR-/- mice, SAA is deposited in murine atherosclerosis at all stages of lesion development, and SAA immunoreactive area correlates highly with lesion area, apoA-I area, apoB area, and perlecan area. These findings are consistent with a possible role for SAA-mediated lipoprotein retention in atherosclerosis.

Authors+Show Affiliations

Division of Cardiology, University of Washington, Seattle, WA 98195-6422, USA. cardiac@u.washington.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15692094

Citation

O'Brien, Kevin D., et al. "Serum Amyloid a and Lipoprotein Retention in Murine Models of Atherosclerosis." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 25, no. 4, 2005, pp. 785-90.
O'Brien KD, McDonald TO, Kunjathoor V, et al. Serum amyloid A and lipoprotein retention in murine models of atherosclerosis. Arterioscler Thromb Vasc Biol. 2005;25(4):785-90.
O'Brien, K. D., McDonald, T. O., Kunjathoor, V., Eng, K., Knopp, E. A., Lewis, K., Lopez, R., Kirk, E. A., Chait, A., Wight, T. N., deBeer, F. C., & LeBoeuf, R. C. (2005). Serum amyloid A and lipoprotein retention in murine models of atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 25(4), 785-90.
O'Brien KD, et al. Serum Amyloid a and Lipoprotein Retention in Murine Models of Atherosclerosis. Arterioscler Thromb Vasc Biol. 2005;25(4):785-90. PubMed PMID: 15692094.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Serum amyloid A and lipoprotein retention in murine models of atherosclerosis. AU - O'Brien,Kevin D, AU - McDonald,Thomas O, AU - Kunjathoor,Vidya, AU - Eng,KimLi, AU - Knopp,Eleanor A, AU - Lewis,Katherine, AU - Lopez,Roland, AU - Kirk,Elizabeth A, AU - Chait,Alan, AU - Wight,Thomas N, AU - deBeer,Frederick C, AU - LeBoeuf,Renee C, Y1 - 2005/02/03/ PY - 2005/2/5/pubmed PY - 2005/11/1/medline PY - 2005/2/5/entrez SP - 785 EP - 90 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 25 IS - 4 N2 - OBJECTIVE: Elevated serum amyloid A (SAA) levels are associated with increased cardiovascular risk in humans. Because SAA associates primarily with lipoproteins in plasma and has proteoglycan binding domains, we postulated that SAA might mediate lipoprotein retention on atherosclerotic extracellular matrix. METHODS AND RESULTS: Immunohistochemistry was performed for SAA, apolipoprotein A-I (apoA-I), apolipoprotein B (apoB), and perlecan on proximal aortic lesions from chow-fed low-density lipoprotein receptor (LDLR)-/- and apoE-/- mice euthanized at 10, 50, and 70 weeks. SAA was detected on atherosclerotic lesion extracellular matrix at all time points in both strains. SAA area correlated highly with lesion areas (apoE-/-, r=0.76; LDLR-/-, r=0.86), apoA-I areas (apoE-/-, r=0.88; LDLR-/-, r=0.80), apoB areas (apoE-/-, r=0.74; LDLR-/-, r=0.89), and perlecan areas (apoE-/-, r=0.83; LDLR-/-, r=0.79) (all P<0.0001). In vitro, SAA enrichment increased high-density lipoprotein (HDL) binding to heparan sulfate proteoglycans, and immunoprecipitation experiments using plasma from apoE-/- and LDLR-/- mice demonstrated that SAA was present on both apoA-I-containing and apoB-containing lipoproteins. CONCLUSIONS: In chow-fed apoE-/- and LDLR-/- mice, SAA is deposited in murine atherosclerosis at all stages of lesion development, and SAA immunoreactive area correlates highly with lesion area, apoA-I area, apoB area, and perlecan area. These findings are consistent with a possible role for SAA-mediated lipoprotein retention in atherosclerosis. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/15692094/Serum_amyloid_A_and_lipoprotein_retention_in_murine_models_of_atherosclerosis_ L2 - https://www.ahajournals.org/doi/10.1161/01.ATV.0000158383.65277.2b?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -