Research Topics
Genomes and Genes | Howard S KruthSummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
Receptor-independent fluid-phase pinocytosis mechanisms for induction of foam cell formation with native low-density lipoprotein particlesHoward S Kruth
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland 20892 1422, USA
Curr Opin Lipidol 22:386-93. 2011..The purpose of this review is to discuss recent findings showing that native unmodified LDL can induce massive macrophage cholesterol accumulation mimicking macrophage foam cell formation that occurs within atherosclerotic plaques...
Macropinocytosis is the endocytic pathway that mediates macrophage foam cell formation with native low density lipoproteinHoward S Kruth
Section of Experimental Atherosclerosis, NHLBI, National Institutes of Health, Bethesda, Maryland 20892 1422, USA
J Biol Chem 280:2352-60. 2005..Macropinocytosis in macrophages and possibly other vascular cells is a new pathway to target for modulating foam cell formation in atherosclerosis...
Native low-density lipoprotein uptake by macrophage colony-stimulating factor-differentiated human macrophages is mediated by macropinocytosis and micropinocytosisJoshua J Anzinger
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 1422, USA
Arterioscler Thromb Vasc Biol 30:2022-31. 2010..To examine the pinocytotic pathways mediating native low-density lipoprotein (LDL) uptake by human macrophage colony-stimulating factor-differentiated macrophages (the predominant macrophage phenotype in human atherosclerotic plaques)...
Heterogeneity of human macrophages in culture and in atherosclerotic plaquesStephen W Waldo
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892 1422, USA
Am J Pathol 172:1112-26. 2008....
Extracellular cholesterol-rich microdomains generated by human macrophages and their potential function in reverse cholesterol transportDaniel S Ong
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 1422, USA
J Lipid Res 51:2303-13. 2010....
Protein kinase C beta and delta isoenzymes mediate cholesterol accumulation in PMA-activated macrophagesHong Tao Ma
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 1422, USA
Biochem Biophys Res Commun 349:214-20. 2006..Thus, our findings show that beta and some other PKC isoenzyme, most likely delta, mediate cholesterol accumulation when macropinocytosis of LDL is stimulated in PMA-activated human monocyte-derived macrophages...
Liver X receptors inhibit human monocyte-derived macrophage foam cell formation by inhibiting fluid-phase pinocytosis of LDLChiara Buono
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892 1422, USA
J Lipid Res 48:2411-8. 2007..The findings reveal an additional new mechanism by which LXR agonists may inhibit macrophage cholesterol accumulation and atherosclerosis, namely, by inhibiting macrophage uptake of LDL...
Murine bone marrow-derived macrophages differentiated with GM-CSF become foam cells by PI3Kγ-dependent fluid-phase pinocytosis of native LDLJoshua J Anzinger
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
J Lipid Res 53:34-42. 2012..These results show that GM-CSF-differentiated murine macrophages become foam cells by fluid-phase pinocytosis of LDL and identify PI3Kγ as contributing to this process...
PMA activation of macrophages alters macrophage metabolism of aggregated LDLWei Huang
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 10, Room 5N-113, 10 Center Drive MSC 1422, Bethesda, MD 20892, USA
J Lipid Res 43:1275-82. 2002..This results in more cholesterol to be stored in macrophages and less aggregated LDL to be available for plasmin-mediated release from macrophage SCCs...
Constitutive receptor-independent low density lipoprotein uptake and cholesterol accumulation by macrophages differentiated from human monocytes with macrophage-colony-stimulating factor (M-CSF)Bin Zhao
Section of Experimental Atherosclerosis, NHLBI, National Institutes of Health, Bethesda, Maryland 20892-1422, USA
J Biol Chem 281:15757-62. 2006..This mechanism of macrophage foam cell formation does not depend on LDL modification or macrophage receptors...
Retention of aggregated LDL by cultured human coronary artery endothelial cellsBin Zhao
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Biochem Biophys Res Commun 321:728-35. 2004..Thus, it is unlikely that endothelial cells can transport AgLDL out of atherosclerotic lesions, but it is likely that retention of AgLDL affects endothelial function...
Fluorescent pegylated nanoparticles demonstrate fluid-phase pinocytosis by macrophages in mouse atherosclerotic lesionsChiara Buono
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute NHLBI, NIH, Bethesda, Maryland 20892 1422, USA
J Clin Invest 119:1373-81. 2009..These results show that macrophages within atherosclerotic lesions can take up LDL-sized nanoparticles by fluid-phase pinocytosis and indicate that fluid-phase pinocytosis of LDL is a mechanism for macrophage foam cell formation in vivo...
Evaluation of transduction efficiency in macrophage colony-stimulating factor differentiated human macrophages using HIV-1 based lentiviral vectorsFrancisco J Leyva
Experimental Atherosclerosis Section, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, USA
BMC Biotechnol 11:13. 2011..The objective of this study was to determine transduction efficiency of two HIV-based lentiviral vector configurations as delivery systems for the transduction of primary human blood monocyte-derived macrophages...
UBIAD1 mutation alters a mitochondrial prenyltransferase to cause Schnyder corneal dystrophyMichael L Nickerson
Cancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA
PLoS ONE 5:e10760. 2010..We characterized lesions in the UBIAD1 gene in new SCD families and examined protein homology, localization, and structure...
Sequestration of aggregated low-density lipoproteins by macrophagesHoward S Kruth
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute NIH, Buiulding 10, Room 5N113, 10 Center Drive MSC 1422, Bethesda, MD 20892 1422, USA
Curr Opin Lipidol 13:483-8. 2002..This review discusses a novel endocytic pathway by which macrophages process aggregated LDL...
Macrophage foam cell formation with native low density lipoproteinHoward S Kruth
Section of Experimental Atherosclerosis, NHLBI National Institutes of Health, Bldg 10 Rm 5N 113, 10 Center Drive, MSC 1422, Bethesda, MD 20892, USA
J Biol Chem 277:34573-80. 2002..In addition, the findings direct attention to macrophage fluid phase endocytosis as a relevant pathway to target for modulating macrophage cholesterol accumulation in atherosclerosis...
Histopathology and regression of retinal hard exudates in diabetic retinopathy after reduction of elevated serum lipid levelsMichael Cusick
Division of Epidemiology and Clinical Research, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Ophthalmology 110:2126-33. 2003..The novel histopathologic findings of hard exudate and diabetic maculopathy are similar to the pathologic changes observed in larger atherosclerotic lesions, except that they occur in the intraretinal perivascular space...
