Intermediate filament proteins in developing human arteries

 The distribution of intermediate filament proteins in adult human blood vessels and in human fetal elastic arteries is relatively well-known. However, the distribution of these proteins in the course from neonate to adult has not been established. In this investigation, human postnatal arteries were studied with immunohistochemistry, using antibodies targeted on the intermediate filament proteins desmin, vimentin and cytokeratins 8, 18 and 19. Vimentin was present in most smooth muscle cells in all vessels and at all ages. The proportions of desmin-expressing cells increased in the elastic arteries during the first year of life and was higher in the pulmonary trunk than in the aorta. In the muscular arteries, the proportion of desmin-labelled cells increased in the coronary and the deep femoral arteries, but remained constant in the renal and the cerebral arteries. Cytokeratins were detected in the pulmonary trunk earlier than in the aorta. Cytokeratins were present throughout the wall of the ductus arteriosus, but desmin was present only in some cells. Thus, there are postnatal changes in the distribution of intermediate filament proteins in the elastic arteries and in some muscular arteries, whereas the intermediate filament pattern remains unchanged in other muscular arteries. Accepted: 31 July 1998     

Structural organization of pulmonary arteries in the rat lung

The structure of the normal pulmonary arteries in the rat was studied with light and electron microscopy after use of a newly devised technique of perfusion fixation and tissue preparation. We distinguished two main types of artery in the rat lung on the basis of the structure of the media, an elastic artery and a muscular artery. The elastic artery was characterized by an abundance of extracellular matrix in the media and by an oblique arrangement of smooth muscle cells to connect neighboring elastic laminae. It was subdivided into two segments, a classical elastic and a transitional elastic segment. The muscular artery was distinguished by a paucity of extracellular matrix in the media and by a circumferential arrangement of smooth muscle cells (or pericytes) enclosing the lumina, and was subdivided into four segments, a thick muscular, an ordinary muscular, a partially muscular and a nonmuscular segment. The smooth muscle cells in the muscular artery contained well-developed microfilament bundles compared with those in the elastic artery. Structural differences in smooth muscle cells and in extracellular matrix in the media between the elastic and muscular arteries may reflect the functional heterogeneity of pulmonary arteries in response to hypoxic pulmonary vasoconstriction and to vasoactive substances such as endothelium-derived relaxing and hyperpolarizing factors, and endothelin.     

Human postnatal pulmonary arterial remodeling. Ultrastructural studies of smooth muscle cell and connective tissue maturation

A quantitative light and electron microscopic study of the elastic conducting, small muscular resistance arteries (accompanying or just proximal to the terminal bronchioli) and respiratory unit pulmonary arteries was carried out on the autopsy specimens of 12 children (newborn to 2 years) and three adults, who died without cardiopulmonary disease. Between birth and 1 month, in muscular and respiratory unit arteries, wall thickness decreased due to a reduction in mean smooth muscle cell diameter (p less than 0.01) and a reduction in overlap between adjacent cells. In the elastic arteries, the distance between adjacent elastic lamellae decreased as smooth muscle cell diameter decreased (p less than 0.01 for both). At birth, smooth muscle cells appeared immature, synthetic rather than contractile organelles predominating. Smooth muscle cell filament (thick, thin, and intermediate) volume density increased by 12 to 13% by 6 months in the small muscular arteries and by 2 years in the elastic arteries (p less than 0.001 for both). Surface and cytoplasmic dense bodies increased in a similar manner (p less than 0.001). The findings indicate a postnatal increase in contractile myofilament and surface dense bodies. The amount of connective tissue in the subendothelium and media increased between 1 month and adulthood, collagen finally predominating in small muscular arteries and elastin in the conducting arteries. Collagen fibrils showed regional differences in size within the media, between media and adventitia, and between different types of artery, and increased in size with age (p less than 0.001). Thus, the intrapulmonary arteries from hilum to precapillary bed adapted structurally to extrauterine life. It is suggested that the high fetal pulmonary vascular resistance is due to the shape and arrangement of smooth muscle cells within the vessel wall, rather than to an excessive contractility of each cell. After 1 month, remodeling occurred more slowly with growth, involving an increase in wall thickness, connective tissue deposition, and smooth muscle cell maturation.     

Arteries and veins of the normal dog lung: Qualitative and quantitative structural differences

As a necessary preliminary step to the study of pulmonary hypertension and edema, the structure of the pulmonary vasculature of seven normal dogs was examined in detail to distinguish arteries and veins. For light microscopy and morphometry, the left lung was injected from the arterial and venous sides with pigmented gelatin masses of different colors. The right lung was fixed for electron microscopy. The percentage of medial muscle thickness of arteries was greater (P < 0.05) than that of veins, for vessels over 200 μm diameter. Smooth muscle cells extended more peripherally into arteries (including in vessels less than 50 μm) than into veins. The larger arteries were elastic or transitional in type, whereas larger veins were muscular. The arteries branched with the airways. Fifty percent of arteries under 50 μm and more than 50% of veins under 200 μm were surrounded by alveoli. Muscular arteries had a thick media between distinct internal and external elastic laminae, whereas veins had no internal lamina but had a thin media separated from a thick adventitia by an external elastic lamina. By electron microscopy, the muscular arteries had tightly packed smooth muscle cells with few myoendothelial junctions; the venous smooth muscle cells were arranged loosely, and more numerous myoendothelial junctions were seen. No definite differences were noted between nonmuscular arteries and veins. The functional implications of these morphological findings (differential reactions to pharmacological agents, distensibility of pulmonary arteries and veins, and responses of small vessels to alveolar pressure) are discussed.     

Immunohistochemical detection of macrophage-derived foam cells and macrophage colony-stimulating factor in pulmonary atherogenesis of cholesterol-fed rabbits

In order to investigate the role of monocyte/macrophages and their relationship to the expression of macrophage colony-stimulating factor (MCSF) in pulmonary atherosclerosis, lungs were excised from rabbits that had been fed for 60 and 90 days on a diet containing 0.5% cholesterol. In the lungs, fatty streaks and elevated foam cell lesions predominated in the large or medium-sized elastic pulmonary arteries, while massive accumulation of foam cells in the intima of muscular arteries produced marked luminal narrowing and nearly complete occlusion. In these lesions, most of the foam cells were reactive with RbM2, a monoclonal antibody (mAb) against rabbit macrophages, while smooth muscle cell-derived foam cells were detected by mAb against smooth muscle actin in the deeper area of elevated foam cell lesions of elastic arteries. Ultrastructural observation confirmed the presence of monocytes in the intima, their differentiation into macrophages, and their transformation into foam cells in the atherosclerotic lesions. lmmunohistochemical expression of MCSF was demonstrated in the endothelial cells, smooth muscle cells and foam cells. A minor macrophagederived foam cell population was demonstrated to possess a prolif-erative capacity. These data suggest that MCSF is involved in the differentiation of monocytes into macrophages, their transformation into foam cells, and their proliferation during pulmonary atherogenesis.     

Remodelling of the pulmonary arteries during recovery from pulmonary hypertension induced by neonatal hypoxia

Little is understood of the mechanisms involved in reducing pulmonary arterial wall thickness on recovery from pulmonary hypertension and the present study sought to clarify the events that occur. Piglets were exposed to hypobaric hypoxia for 3 days, either from birth or from 3 days of age, and others were exposed for 11 days starting at 3 days. All recovered in room air for up to 6 days. Using light and electron microscopy, the pulmonary artery wall thickness, the relative contribution of smooth muscle and matrix, smooth muscle cell replication, and apoptosis were assessed after hypoxic exposure and during recovery from hypoxic exposure. In elastic arteries, after 6 days' recovery in room air, a reduction in wall thickness to normal was associated with a similar reduction in proportional area of smooth muscle cells and matrix (p < 0.05), increased apoptosis (p < 0.05), and an abnormally low replication rate (p < 0.05). In peripheral muscular arteries, an increase in external diameter, and wall thinning on recovery, was achieved by smooth muscle cell remodelling and a reduction in cell replication (p < 0.05). Apoptosis did not contribute. Thus, different mechanisms are involved in recovery from hypoxia-induced pulmonary hypertension in elastic and muscular pulmonary arteries. Recovery is slower in animals exposed from birth rather than from 3 days of age.     

Heterogeneity of myosin antigenic expression in vascular smooth muscle in vivo

Rabbit antisera elicited against purified human nonmuscle (platelet) and smooth muscle (uterine myometrium) myosins identified distinct species of myosin when frozen sections of a variety of mammalian tissues were examined by immunofluorescence microscopy. Antiplatelet myosin antiserum specifically stained several nonmuscle cell types including epithelial, some connective tissue, and all vascular endothelial (arterial, venous, capillary) cells. Antismooth muscle myosin antiserum stained only smooth muscle and no other cell types. Neither antiserum reacted with rat cardiac (ventricular) or skeletal muscle cells. Antismooth muscle myosin antiserum staining was detectable in medial vascular smooth muscle in all vessels examined from rat, bovine, human, and guinea pig sources (including elastic and muscular arteries, arterioles, venules, and veins). Although antiplatelet myosin antiserum did not stain nonvascular smooth muscle or vascular smooth muscle in muscular arteries, arterioles, venules, or veins, it did uniformly and specifically stain medial vascular smooth muscle in elastic arteries. This staining of elastic arteries was abolished by absorption of antiplatelet myosin antiserum with purified platelet myosin but not uterine myosin. Similarly, the reactivity of antismooth muscle myosin antiserum was abolished by incubation with uterine but not platelet myosin. The differences in staining patterns observed with antiplatelet myosin antiserum and antismooth muscle myosin antiserum in elastic arteries versus other blood vessels suggests a heterogeneity of antigenic expression in vascular smooth muscle myosin. The most likely explanations for this heterogeneity are the presence of different gene products (myosin isozymes) or a posttranslational alteration (possibly conformational) of a single myosin species. Heterogeneity in this important component of the contractile apparatus of vascular smooth muscle may have significant implications for the physiology and pathophysiology of the vessel wall.     

Blue rubber bleb nevus syndrome and pulmonary hypertension: an unusual association

INTRODUCTION: Blue rubber bleb nevus syndrome (BRBNS) is a rare congenital systemic angiodysplasia with multiple vascular malformations in the skin, gastrointestinal tract and, less often, in other internal organs and the brain. CASE REPORT: A 36-year-old man with past history of BRBNS was admitted to our hospital for progressive dyspnea and fatigue. Primary pulmonary hypertension (PPH) was diagnosed. He then developed acute abdominal pain and dyspnea, dying in a few hours due to sudden cardiac arrest. Postmortem examination demonstrated angiomatous lesions located in the skin, small bowel, heart, lungs, liver and thyroid. The lesions were slightly raised, soft and compressible and microscopically consisted of dilated vascular channels lined by a flattened endothelium. The vascular wall was formed by several layers of smooth muscle cells, intermixed with abundant aggregates of elastic lamellae and thin collagen fibers. Luminal thrombi were a frequent finding. In the small bowel, we identified the presence of an abnormally large artery directly opening into a thin-walled venous channel. The most striking finding in the lungs was the presence of thrombi of varying age in the lumen of segmental and elastic arteries, as well as muscular arteries and arterioles. Severe medial hypertrophy of muscular arteries and muscolarization of arterioles were also present. Intimal proliferative lesions and plexiform lesions were never observed. CONCLUSION: The pulmonary findings are consistent with recurrent thromboembolic events from shunts in the visceral lesions. To our knowledge, this is the first report of BRBNS with visceral arterovenous (AV) fistulae complicated by thromboembolic pulmonary hypertension (PH).     

Structural relationships between the endothelial actin system and the underlying elastic layer in the distal interlobular artery of the rat kidney

Summary The structure of the intracellular actin filaments and the extracellular matrices was studied in the distal interlobular arteries in the rat kidney, employing three different morphological techniques, including rhodamin-phalloidin staining of cryosections, resorcin-fuchsin staining of paraffin sections, and a cold dehydration procedure for electron microscopy. The endothelial cells possess longitudinally running stress fibers. The inner elastic layer is composed of meshworks of elastic fibers encompassing numerous pores. The smooth muscle cells containing abundant actin filaments are arranged circumferentially around the vascular axis. The endothelial stress fibers are found mainly in the basal half of the endothelial cells, and anchor onto the basal cell membranes. The elastic meshworks send off longitudinal branch fibers to contact the endothelial cell membranes at the anchoring sites of stress fibers. In addition circumferential branches run toward the smooth muscle cells. The functional significance of the intracellular contractile apparatus and the extracellular tensile component in small arteries was discussed.     

Ultrastructure of early plexogenic pulmonary arteriopathy

A lung biopsy specimen from a young woman with the clinical features of primary pulmonary hypertension showed grade 2 plexogenic pulmonary arteriopathy. Electron microscopy revealed 'dark', electron-dense smooth muscle cells in the inner part of the media of muscular pulmonary arteries. Many of these transformed myocytes had migrated into the lumens of pulmonary arteries and arterioles which they occluded. This migration of smooth muscle cells was associated with a substantial increase in the number of pulmonary endocrine cells in the bronchioles containing bombesin and calcitonin.     

Active collagen synthesis by pulmonary arteries in human primary pulmonary hypertension.

Immunohistochemistry was performed on lung tissue obtained from patients with severe unexplained pulmonary hypertension using an antibody to the amino-terminal end of the procollagen type I propeptide. This antibody identifies newly synthesized alpha I(I) procollagen before cleavage of the amino-terminal propeptide following secretion and, therefore, can identify sites of active collagen deposition. Procollagen was detected in the media, media and neointima, or neointima alone of a large number of small muscular arteries from hypertensive lungs. Normal adult lungs were negative. Neointimal cells in remodeled small muscular arteries stained positively for alpha-smooth muscle actin and desmin consistent with a smooth muscle lineage. These data suggest smooth muscle-like cells in small muscular arteries are actively synthesizing collagen in patients with severe unexplained pulmonary hypertension.     

SOST expression is restricted to the great arteries during embryonic and neonatal cardiovascular development.

Spatial-temporal regulation of bone morphogenetic protein (BMP) and Wnt activity is essential for normal cardiovascular development, and altered activity of these growth factors causes maldevelopment of the cardiac outflow tract and great arteries. In the present study, we show that SOST, a Dan family member reported to antagonize BMP and Wnt activity, is expressed within the medial vessel wall of the great arteries containing smooth muscle cells. The ascending aorta, aortic arch, brachiocephalic artery, common carotids, and pulmonary trunk were all associated with SOST expressing smooth muscle cells, while the heart itself, including the valves, and more distal arteries, that is, pulmonary arteries, subclavian arteries, and descending aorta, were negative. SOST was expressed from embryonic day 15.5 up to the neonatal period. SOST expression, however, did not correspond with inhibition of Smad-dependent BMP activity or beta-catenin-dependent Wnt activity in the great arteries. Activity of both signaling pathways was already down-regulated before induction of SOST expression.     

VEGF和PCNA在慢性低氧性肺动脉及高压大鼠主动脉、肺动脉平滑肌细胞中表达

目的研究慢性低氧性肺动脉高压(PAH)发生过程中,血管内皮生长因子(VEGF)及细胞核增殖抗原(PCNA)在体循环血管、肺循环血管平滑肌细胞中的表达。方法利用低压缺氧舱建立大鼠缺氧性肺动脉高压模型。实验分为3组即正常氧组、缺氧2wk组和缺氧3wk组。用免疫组化染色和图像分析,检测主动脉、肺动脉主干及肺内小动脉平滑肌细胞中VEGF及PCNA的表达量。结果VEGF在正常氧组大鼠的主动脉、肺动脉主干及肺内小动脉平滑肌内均有表达;缺氧组大鼠肺动脉主干及肺内小动脉平滑肌细胞内VEGF的表达明显增强并随着缺氧时间的延长而增加;主动脉平滑肌内VEGF的表达量无明显变化。PCNA在正常氧组大鼠的主动脉、肺动脉主干及肺内小动脉平滑肌内均有微弱表达;但缺氧时只有肺小动脉平滑肌内其表达量增加;主动脉、肺动脉主干平滑肌内PCNA的表达量无明显差别。结论在缺氧性肺动脉高压的发生过程中,VEGF在体循环血管、肺循环血管平滑肌细胞中的表达量具有差异性,提示其可能在肺动脉高压形成过程中起重要作用。     

Scanning electron microscopic studies of the vascular smooth muscle cells and pericytes in the rat heart

The cytoarchitecture of smooth muscle cells and pericytes in the rat cardiac vessels was studied by scanning electron microscopy after the removal of connective tissue matrices using a modified KOH-collagenase digestion method. The initial stem of the coronary arteries had groups of smooth muscle cells which ran in various directions on the outermost layer of the media. Although smooth muscle cells in coronary arteries of more than 100 microm in the outer diameter were arranged in a rough circle around the vessel axis, oblique and/or longitudinal muscle bundles were often present in the medio-adventitial border of the vessels. The presence of irregularly oriented muscular bundles is probably connected with resistance against the stretching force induced by the beating of the heart. As the vessel size decreased toward the periphery, almost all of the smooth muscle cells became spindle-shaped with several tiny processes and ran circularly or helicaly to the vessel axis. In the precapillary arterioles (6-12 microm), smooth muscle cells acquired various cytoplasmic processes which helicaly surrounded endothelial cells. Unmyelinated nerves were often associated with arterioles. Blood capillaries were morphologically divided into three segments: arterial capillaries which had pericytes with wide and circularly oriented processes, true capillaries whose pericytes extended long and thin primary processes bilaterally along the vessel axis, and venous capillaries surrounded irregularly and loosely by wide pericytic processes. The stellate pericytes in the postcapillary venules (10-30 microm) gradually changed into flat tape-like smooth muscle cells, which ran circularly in the collecting venules and veins (30-200 microm). The large collecting veins were finally overwhelmed by superficial thin layer of the myocardium, their own smooth muscle cells being very sparse. This suggests that large veins have poor ability to contract by themselves but are influenced by the surrounding myocardial cells.     

Segmentation features and structural organization of the intrapulmonary artery of the yak

This study aims to systematically investigate intrapulmonary artery segmentation, blood vessel wall characteristics and structure organization, and the interrelation between intrapulmonary artery structure and plateau hypoxia adaptation in yak. The normal intrapulmonary artery structure of the yak had been studied using histological methods and transmission electron microscopy. The intrapulmonary artery of the yak was also examined using morphometric analysis and angiography. Results showed that the elastic intrapulmonary artery is divided into two types, namely, classical and transitional elastic segments. The muscular intrapulmonary artery is divided into three types, namely, transitional, classical muscular, and muscular arteriole segments. In the transitional elastic artery, elastic fibers and smooth muscles are linked through three models of ends, lateral branches, and branch tops. Two phenomena are possible for the transition from the elastic intrapulmonary artery to the muscular artery. One phenomenon postulates that a less elastic membrane is first increased and then suddenly decreased, and another supposes that the elastic membrane is gradually reduced and assembled in one to two layers before entering the transitional muscular artery. The smooth muscle of the intrapulmonary artery tunica media had more apophysis; it was physically connected with elastic membrane or fiber and composed of functionally resilient unit of the intrapulmonary arterial wall. Glycogenosomes increased in the muscular intrapulmonary artery smooth muscle cells. It exist one to two layers intact smooth muscle in intrapulmonary arteriole, the presence of intact smooth muscle in the intrapulmonary arteriole of the yak is a kind of structure adaptation to low‐oxygen environment. Anat Rec, 296:1775–1788, 2013. © 2013 Wiley Periodicals, Inc.     

Contact guidance in the subendothelial space. Repair of rat aorta in vitro.

The regeneration of cells was observed on the surface of pieces of rat aorta partially denuded of endothelium and grown for several days in organ culture. Persisting endothelial cells did not contribute significantly to the population of cells that covered the denuded area; these were principally very enlongated smooth muscle cells. Except where the aorta had been transected, they were invariably parallel to the original long axis of the aorta. Similarly, chick embryo cells and Earle's L strain fibroblasts assumed a longitudinal orientation when seeded from suspension cultures onto devitalized, bare subendothelium. Scanning electron microscopic observation of the exposed subendothelium showed a longitudinal fibrillary pattern. The longitudinal orientation of cells on the subendothelium in organ cultures is thought to be comparable to that seen during the repair of arteries in situ, when longitudinal smooth muscle cells form layers under the endothelium. It is considered to be caused by contact guidance provided by the fibrillary structures of the subendothelial space.     

Restricted expression of the gap junctional protein connexin 43 in the arterial system of the rat

Connexin 43 (Cx43) has been reported to be expressed in vascular smooth muscle cells and endothelial cells. Evidence for possible variations in Cx43 distribution within different parts of the vascular system is limited. We have therefore investigated the expression of Cx43 in the endothelia and media of 11 vessels of different size and function in the rat, using immunofluorescence and confocal laser scanning microscopy. The results showed that punctate Cx43 staining was abundant in the endothelia and media of all of the 5 elastic arteries examined. In the media, the amount of Cx43 staining decreased as the size of the elastic arteries became smaller. In the 6 muscular arteries examined, 2 different patterns of Cx43 staining were observed. In the first type, Cx43 expression was high in the endothelium but virtually absent from the media. Mesenteric resistance, hepatic and tail arteries were examples. In the second type, Cx43 staining was absent from both the media and the endothelia. The coronary, basilar, and middle cerebral arteries showed this appearance. The results suggest that expression of Cx43 is largely restricted to elastic arteries in the arterial system of the rat. The lack of immunodetectable Cx43 from the media of all muscular arteries examined, and from the endothelia of some of these arteries, raises the possibility of significant differences in the form of expression of Cx43 in these vessels or the presence of other connexins.     

The histopathology of 36 cases of plexogenic pulmonary arteriopathy

A detailed histopathological study was made of the lungs of 36 cases of plexogenic pulmonary arteriopathy coming to combined heart-lung transplantation. It revealed two dissimilar processes involved in the pathogenesis of this disease. One comprised histological appearances consistent with constriction of muscular pulmonary arteries, a condition that would be likely to be reversed by pulmonary vasodilators. The other was the proliferation of myofibroblasts in the intima and lumen of pulmonary arteries, a disorder of growth unlikely to be influenced by this type of therapy. In previous ultrastructural studies we have shown that the source of these cells of muscular pedigree is muscle cells from the inner half of the media which migrate into the intima through gaps in the inner elastic lamina. In the present study we found a similar proliferation of myofibroblasts in the intima, not only of pulmonary arteries, but also of pulmonary veins, in plexogenic pulmonary arteriopathy. Arterial thrombi found were considered to be a complication rather than a cause of plexogenic pulmonary arteriopathy. Siderophages, cholesterol granulomas and focal fibrosis in the lung were considered to be a consequence of intrapulmonary haemorrhage early in the course of the disease. It is concluded that, while plexogenic pulmonary arteriopathy has an important vasoconstrictive element, it is also based on a disorder of growth of cells of muscular pedigree. This view has clear implications for the therapy of primary plexogenic pulmonary arteriopathy.     

Ultrastructure of arteries in rats fed a high-fat cholesterol diet. Intimal thickening of a small muscular artery

Focal nodular intimal thickening developed in a small muscular artery (tarsal pedis) of rats fed a diet containing 28% neutral fat and 2% cholesterol for three months. Examination by electron microscopy showed the main cellular component of these intimal lesions to be a smooth muscle cell. Single unidentified cells were present in the subendothelial region. The internal elastic membrane was fragmented and a few smooth muscle cells were seen between the fragments, extending from the media into the intima. Numerous vesicles were present in the intercellular space, a cluster being enclosed within a basement membrane in places. No lipid accumulation was found. The findings point to an important role for smooth muscle cells in the initiation of atherosclerosis, and suggest that lipid accumulation is a secondary event in the development of this process in muscular arteries in this animal model.     

Characterization of nonmuscle cells present in the intima of normal adult bovine pulmonary artery

In this study, the presence of cells in the intimal region of normal adult bovine pulmonary artery (BPA) was examined by analysis of longitudinal sections at the level of light and transmission electron microscopy. In addition, the morphological and immunohistochemical phenotype of these cells as well as the presence of particular extracellular matrix (ECM) components in this region were also determined. Since ECM production and cell proliferation have been demonstrated to be regulated by locally released growth factors such as transforming growth factor beta (TGFbeta), the presence of TGFbeta-1 in this region was also investigated. Our findings reveal the presence of immature or "nonmuscle" cells into the subendothelial space of normal adult BPA. These cells were characterized by the presence of abundant cytoplasmic organelles and scanty microfilaments. Such cells were negative to antibodies against smooth muscle alpha actin (SM alpha-actin), 1E12, and vWf, but not to vimentin. Similar cells have recently been detected in normal adult BPA and canine carotid arteries, but in the medial region. Because of their location in these elastic arteries, the nonmuscle cells are involved not only in the remodeling of the medial region, but also in the neointima or intimal thickening formation by migration from the media to the subendothelial space, where they proliferate and secrete ECM components. However, a limited number of morphological studies and the current investigation describe the presence of scattered nonmuscle cells within the intima of some normal elastic arteries. This would suggest an important role for these resident cells within the intima in normal and pathological processes as well. In addition, our results show the presence, in this region, of TGFbeta-1 and of ECM components that include collagen, elastin, fibronectin, and laminin which are present in normal conditions and during the intima formation in vivo.