Fibronectin stimulates macrophage uptake of low density lipoprotein-heparin-collagen complexes.

Falcone, Domenick J.; Salisbury, Brian

doi:10.1161/01.atv.8.3.263

Cited by 38 publications

(22 citation statements)

References 50 publications

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“…Aggregates of LDL have also been found to produce foam cells both in vitro and in vivo (5,7). Aggregation can occur via a variety of processes, including oxidation, interaction with phospholipase A 2 and C, sphingomyelinase, glycosylation, interactions with extracellular matrix, and mechanical processes (5,(36)(37)(38)(39)(40)(41)(42)(43)(44). These various aggregation methods all result in different manipulations of the LDL molecule with varying sizes and molecular arrangement.…”

Section: Discussionmentioning

confidence: 99%

Aggregated LDL and lipid dispersions induce lysosomal cholesteryl ester accumulation in macrophage foam cells

Griffin

Ullery

Cox

et al. 2005

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

Aggregated LDL and lipid dispersions induce lysosomal cholesteryl ester accumulation in macrophage foam cells

Griffin

Ullery

Cox

et al. 2005

Journal of Lipid Research

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“…Cellular fibronectin is important in wound healing and scar formation in the dermis (18) and plays a role in the scarring that characterizes liver cirrhosis (8,9). Plasma fibronectin, which is produced primarily in hepatocytes, plays an important role in clot formation (19), opsonization of bacteria (3), and opsonization of circulating collagenous degradation products (2). The antibody used in this study was raised against a plasma-derived immunogen, but it appears to recognize both cellular and plasma forms of fibronectin based on the staining of nonhepatocyte cell types (endothelial cells, Kupffer cells, macrophages) that are known to produce cellular fibronectin but are not known to produce plasma fibronectin (1,17).…”

Section: Discussionmentioning

confidence: 99%

“…Fibronectin is important in a wide variety of fundamental cell processes including cell-to-cell adhesion, cell-to-extracellular matrix adhesion, and cell migration (1). Fibronectin is also found in the plasma, where it is involved in blood clot formation and opsonization (2,3). This functional diversity of the fibronectin gene results from alternative splicing of pre-mRNA, leading to multiple protein isoforms with unique biological properties (4,5).…”

mentioning

confidence: 99%

Hepatocellular Carcinomas Show Abnormal Expression of Fibronectin Protein

et al. 2002

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Fibronectin plays an important role in cell-to-cell adhesion, cell migration, and cell signaling. In the liver, fibronectin expression has been studied primarily as a component of the extracellular matrix, but little information is available on the expression of fibronectin protein in the neoplastic cells of hepatocellular carcinomas (HCCs). Twenty-four surgically resected HCCs were immunostained with fibronectin. Tumor and normal liver tissues were concurrently analyzed in all cases, and expression in the tumor was evaluated in comparison to the nonneoplastic liver. The average age at resection was 54 ؎ 18 years for the 18 men and 6 women. Twenty-one of the cases were classic HCCs including 6 cases that were well differentiated, 12 cases moderately differentiated, and 3 cases poorly differentiated. The remaining 3 cases were moderately differentiated fibrolamellar carcinomas. In the normal liver, fibronectin labeled the sinusoids and weakly to moderately stained the cytoplasm of hepatocytes. In HCCs, 15/24 showed overexpression of fibronectin in the cytoplasm, 8/24 showed no change from the nonneoplastic liver, and one case showed decreased cytoplasmic staining. In addition, an abnormal membranous staining pattern was noted in 16/24 HCCs. In contrast to the HCCs, none of the three fibrolamellar carcinomas showed increased cytoplasmic or membranous staining. Excluding fibrolamellar carcinoma, increased cytoplasmic staining and/or an abnormal membranous staining was noted in 19/21 (90%) of HCCs. Fibronectin shows abnormal cytoplasmic and/or membranous staining in the majority of HCCs. The implications of fibronectin overexpression are uncertain but may reflect a critical step in tumor genesis.

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“…Subsequent in vitro studies showed the affinity of lipoproteins for matrix proteoglycans and collagen fibrils. 11,12 Studies with freeze-etch morphology produced the first clear images of the complex structure of the intima and captured the association of retained lipid with the matrix filaments, including collagen fibrils, first in rabbit models 8 and now in the present study in the apoE-deficient mouse model. Still unclear are the mechanisms by which the matrix filaments and associated collagen fibrils bind lipoproteins or facilitate their transformation and/or oxidation.…”

Section: Discussionmentioning

confidence: 67%

Ultrastructure of Early Lipid Accumulation in ApoE-Deficient Mice

Tamminen

Mottino

Qiao

et al. 1999

ATVB

111

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Abstract-Apolipoprotein (apo) E-deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques distributed in lesion-prone areas throughout the aorta. Lesions develop in apoE-deficient mice on a regular chow diet and will occur faster on a diet higher in cholesterol. Examination of the aortas from these mice on a chow diet by high-resolution, freeze-etch electron microscopy demonstrated lipid retention in the intima by 3 weeks of age. Lipid was retained in the matrix as individual particles between 33 and 48 nm in diameter, aligned along the collagen fibrils and in aggregates consisting of lipid particles with average diameters of 33 and 68 nm. Larger particles seemed to have formed from fusion of smaller particles. Lipid retention was more widespread in 5-and 9-week-old mice. Monocyte attachment to endothelial cells was observed by electron microscopy at 5 weeks of age. The appearance of the intimal lipid was similar to that previously described in rabbit models and suggests that lipid interaction with matrix filaments and subsequent aggregation of lipid particles are critical first steps in the process of foam cell formation. T he creation of apoE-deficient mice by homologous recombination of embryonic stem cells has provided a murine model of atherosclerosis. 1,2 The mice have severe hypercholesterolemia and have lesions that progress with age from fatty streaks to fibrous plaques distributed in lesionprone areas. Lesions develop even on a low-cholesterol, low-fat chow diet but occur sooner and become larger on a high-cholesterol, high-fat, Western-type diet.Two studies have provided detailed histological observations on the morphology of the development of atherosclerotic lesions in apoE-deficient mice. Nakashima et al 3 studied animals between 6 and 40 weeks of age fed Western-and chow-type diets. These authors showed that these animals developed the full range of lesions from fatty streaks to fibrous plaques and, most important, that the lesions were similar in their inflammatory-fibroproliferative features to those seen in rabbit models, nonhuman primates, and humans. Reddick et al 4 studied mice from 11 to 64 weeks of age fed solely a chow diet. Their morphological studies, at the light-microscope level of resolution, also showed that the progression of atherosclerotic lesions in mice lacking apoE paralleled that described in Watanabe heritable hyperlipidemic rabbits. These histological studies established that the light-microscopic appearance, cellular composition, and distribution of the lesions are typical of lesion development in animal models and similar in some respects to lesions in humans. However, these studies were at the light-microscope level of resolution, and the observations occurred after fatty streaks had begun to form. Given the importance of the apoE-knockout mouse model as an excellent system to study the pathogenesis and progression of atherosclerosis, the objective of the present study was to extend the structural observations...

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Fibronectin stimulates macrophage uptake of low density lipoprotein-heparin-collagen complexes.

Cited by 38 publications

References 50 publications

Aggregated LDL and lipid dispersions induce lysosomal cholesteryl ester accumulation in macrophage foam cells

Aggregated LDL and lipid dispersions induce lysosomal cholesteryl ester accumulation in macrophage foam cells

Hepatocellular Carcinomas Show Abnormal Expression of Fibronectin Protein

Ultrastructure of Early Lipid Accumulation in ApoE-Deficient Mice

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