Injury and repair of smaller muscular and elastic arteries

Abstract

Indirect immunoperoxidase staining for fibrinogen/fibrin and fibronectin was performed on normal and healing arterial tissue of muscular and smaller elastic arteries. Fibronectin was observed in the wall of the normal arteries, whereas fibrinogen/fibrin could not be demonstrated. Fibronectin was observed in the intima as well as the media deposited in a similar fashion in the femoral and carotid artery during repair. Apart from the early occurrence of fibrin/fibrinogen in the media of both arteries the distribution of fibrinogen/fibrin and degradation products differed. In the femoral artery a progressively weakening positive reaction for fibrinogen/fibrin and degradation products towards the lumen was observed in the intima and the media 7 and 14 days after the lesion. By 28 days the reaction in the media was negative. No thrombus formation was observed. In contrast, all the specimens examined from the common carotid arteries were obliterated by luminal thrombi 28 days after the lesion. The thrombus as well as the damaged intimal thickening and the compressed media were loaded with fibrinogen/fibrin and degradation products. The deposition of fibronectin, fibrinogen, and degradation products in the carotid artery was similar to that previously reported in experimental aortic arteriosclerosis in rabbits as well as in giant cell arteritis.

Fibronectin biosynthesis in the rat aorta in vitro. Changes due to experimental hypertension.

“…Histochemical studies have documented the presence of fibronectin in aortic tissue, and changes in fibronectin content have been reported in different disease states, such as diabetes and atherosclerosis (9)(10)(11)(12)(13), although quantitation has been difficult due to the insoluble nature of the cellular fibronectin (14). Recently, a study by Glukhova et al (15) showed that different alternately spliced forms of fibronectin are selectively localized in the intima and media, and following either balloon injury to the rat aorta or in human aortic atherosclerotic lesions, a selective accumulation ofan alternatively spliced form of fibronectin was found within the intimal lesion.…”

Monocyte adhesion to balloon-injured arteries: The influence of endothelial cell seeding

“…36 Fibrinogen is known to deposit rapidly and abundantly after deendothelializing injury and is not seen in appreciable amounts on the lumen of intact vessels. 16,17 Other potential mechanisms of monocyte recruitment to an injured artery that may be influenced by the extent of EC coverage include binding to activated platelets, 19 direct binding to exposed subendothelial matrix, 21 increased permeability of the denuded vessel wall to mitogenic or chemotactic factors (such as lipid-protein complexes), 2,37,38 or altered expression of adhesion molecules by cells in the vessel wall. 11,39,40 Another recent report suggests that circulating intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 may deposit at sites of injury and act as ligands for leukocyte recruitment.…”

“…Cells were passaged with 0.05% trypsin-EDTA (Gibco) and replated to gelatin-coated dishes at ratios between 1:4 and 1:6. Cultures were allowed to grow until sufficient cells were available for seeding (approximately 3 × 10 6 cells), which required a mean of 17 (range, [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] days in culture and a maximum of three passages.…”

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brinogen may be an important ligand for early cell adhesion events after arterial injury. Fibrinogen rapidly accumulates on the deendothelialized vessel surface, 15,16 and inhibition of integrin-mediated monocyte-fibrinogen binding (with the monoclonal antibody 7E3) has been shown to decrease monocyte adhesion to balloon-denuded vessels. 17 Other important mechanisms of monocyte adhesion to the balloon-injured surface may involve platelets, subendothelial components, or other deposited ligands.

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