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Biomedical subjects

E Bonanno

Publications and source records attributed to E Bonanno.

15 recordsLinked to original sources
PubMed1996

Age-related changes affecting atherosclerotic risk. Potential for pharmacological intervention.

The incidence of cardiovascular diseases that are related to the atherosclerotic process increases exponentially with age. Organ lesions, the clinical manifestation of atherosclerotic disease, are late events due to complications in the plaque (ulceration, thrombosis, calcification) which are the result of an increased vulnerability to disruption of a previously stable plaque. The higher incidence of age-related clinical events could be explained by a rising sensitivity of plaques to destabilising factors, both parietal and humoral. The increased probability that a plaque in an elderly patient will became vulnerable could be related to those destabilising factors that significantly increase with aging, such as advanced glycation end-products. For these reasons, it seems most important that the analysis of these age-related destabilising factors, rather than those factors that promote the development of early atherosclerotic plaques, should be undertaken. Taking the point of view of a pharmacological intervention, this should eventually lead to a more complete understanding of this process.

Age Factors↗
PubMed1996

Human immunodeficiency virus infection of human bone marrow stromal myoid cells.

In order to investigate the potential susceptibility of bone marrow stromal myoid cells to human immunodeficiency virus (HIV), a myoid cell population devoid of all other cellular components of marrow environment was isolated from 3 normal adult bone marrow samples. The bone marrow myoid cells were infected with 3 different strains of HIV-1, 2 strains isolated from patients with acquired immune deficiency syndrome (AIDS) and HTLV-IIIB strain. To demonstrate successful infection and HIV production, culture supernatants, harvested weekly until 2 months post-infection, were tested for the presence of p24 antigen and infectious virus. Myoid cell monolayers obtained from the 3 different bone marrow samples were shown to be susceptible to infection. In particular, infection led to the presence of p24 antigen and of infectious virus in culture supernatants up to day 49 post-infection. After day 49, it was not possible to demonstrate the presence of infectious virus in culture supernatants and HIV-DNA polymerase chain reaction (PCR) failed to show viral genome in any of the cultures assayed. Our results demonstrate the susceptibility of myoid stromal cells to HIV infection and may provide an in vitro model for studying the effects of HIV infection in disregulation of the haemopoietic function of bone marrow environment.

Bone Marrow↗
PubMed1996

[The immediate and midterm results of percutaneous mitral valvuloplasty in subjects over 60].

We have analyzed the immediate and mid-term (1 and 2 years) results of percutaneous mitral valvuloplasty (PMV) by Inoue's catheter in 97 patients < 60 years (Group A) compared with 34 patients > 60 years (Group B). In 61% Group A the patients were in NYHA functional class II, 36% in III, and 3% in I; in Group B, 56% of the patients were in NYHA functional class III, 38% in II, and 6% in IV. Mean mitral valve area was 1.1 cm2 before dilatation in both groups, and a significant (p < 0.0001) increase was obtained in both Group A (0.9 +/- 0.3 cm2) and Group B (0.8 +/- 0.3 cm2). No significant differences were observed between the two groups. Mean transvalvular gradient decreased significantly (p < 0.0001) from 13.6 +/- 5.7 to 7.2 +/- 3.1 mmHg in Group A, and from 9.9 +/- 4 to 6.5 +/- 2.3 mmHg in Group B (A vs B: p < 0.02). Optimal result was obtained in 94% and 88% of Group A and Group B patients, respectively. Suboptimal result was obtained in 2% and 6% of Group A and Group B patients, respectively. These differences were not significant. Failure of PMV occurred in 4% and 6%, respectively. At 1-year follow-up Group A 7 patients and 5 Group B patients showed restenosis; at 2-year follow-up one more restenosis was present in Group A (A vs B at 1 and 2 years: NS). We conclude that PMV is a safe and effective technique in young patients and in patients > 60 years.

Adult↗
PubMed1994

Modulation of angiogenesis in vitro by laminin-entactin complex.

Laminin is a cross-shaped glycoprotein whose inner cross-region binds to the glycoprotein entactin (nidogen) forming a stable complex extractable from basement membrane matrices with chelating agents. In this study we evaluated the effect of the laminin-entactin complex on angiogenesis in serum-free collagen gel culture of rat aorta. Laminin-entactin stimulated or inhibited angiogenesis depending on its concentration in the gel. Stimulatory concentrations of laminin-entactin (30 to 300 micrograms/ml) promoted an increase in the number and length of microvessels. A similar effect was observed with purified laminin. Elongation of microvessels was also obtained with the laminin fragments E1' and E8 and with entactin, all of which have binding sites for endothelial cells. By contrast the E4 fragment of laminin, which has no cellular binding sites, failed to promote microvascular elongation. Inhibitory concentrations of laminin-entactin (3000 micrograms/ml) allowed formation of only a few stubby endothelial sprouts. Laminin-entactin promoted dose-dependent stabilization of microvessels preventing their regression. Microvessels stabilized by laminin-entactin were surrounded by thick patches of basement membrane-like material, whereas untreated microvessels prone to regression had a highly attenuated basement membrane. The angiogenic effect of laminin-entactin was enhanced by exogenous bFGF. However, bFGF was unable to stimulate angiogenesis over control values when incorporated in gels containing a high concentration of laminin-entactin. Our results indicate that laminin and its supramolecular complex laminin-entactin play an important modulatory role in angiogenesis. The dose-dependent effects of the laminin-entactin complex suggest that the basement membrane is a dynamic regulator of angiogenesis whose function varies depending on the concentration of its molecular components.

Animals↗
PubMed1994

Homogeneous stromal cell population from normal human adult bone marrow expressing alpha-smooth muscle actin filaments.

BACKGROUND: Hematopoietic microenvironment has a crucial role homing and regulating precursor cell growth both in physiologic and pathologic conditions. Fibroblast, endothelial cells, macrophages, adipocytes, and myoid cells, are the cellular component recognized in human bone marrow cultures. The presence of myoid cells in human bone marrow has been observed during fatal life, whereas during adult life, it is strictly related to pathologic conditions. EXPERIMENTAL DESIGN: The aim of this study was to isolate a homogeneous stromal cell population. The mononuclear fraction obtained from the vertebral body of living humans was cultured without hydrocortisone and horse serum to inhibit foam cell differentiation. RESULTS: The immunocytochemistry and electron microscopy characterization indicate that the cellular population we isolated had an homogeneous "myoid" differentiation. Moreover, these cells were able to support blast cell colony formation in vitro. CONCLUSIONS: This method allowed the preparation of homogeneous myoid cell cultures depleted of other bone marrow stromal components. The isolation of a single stromal population is relevant in order to study the function of contractile filaments in allowing close-binding interactions with hematopoietic precursor cells.

Actins↗
PubMed1993

Fibronectin promotes the elongation of microvessels during angiogenesis in vitro.

Fibronectin is a component of the extracellular matrix of developing microvessels whose role in angiogenesis is poorly understood. This study evaluated the effect of plasma fibronectin on angiogenesis in serum-free collagen gel culture of rat aorta. Aortic explants embedded in collagen gels generated microvascular outgrowths. Fibronectin incorporated in the collagen gel promoted a selective dose-dependent elongation of the newly formed microvessels without stimulating vascular proliferation. The fibronectin-treated microvessels were longer due to a proportional increase in the number of microvascular cells. However, fibronectin had no effect on microvascular DNA synthesis and mitotic activity. Fibronectin stimulated microvascular length also in cultures in which mitotic activity was suppressed and angiogenesis was markedly reduced by pretreating the aortic explants with mitomycin C. The synthetic peptide Gly-Arg-Gly-Asp-Ser (GRGDS), which competes for the binding of fibronectin to its cell receptors and inhibits the adhesion of endothelial cells to substrates, arrested the elongation of developing microvessels causing regression and inhibition of angiogenesis. Conversely, Gly-Arg-Gly-Glu-Ser (GRGES), which lacks the RGD sequence, had no inhibitory effect. These data support the hypothesis that fibronectin promotes angiogenesis and suggest that developing microvessels elongate in response to fibronectin as a result of an adhesion-dependent migratory recruitment of endothelial cells that does not require increased cell proliferation.

Amino Acid Sequence↗
PubMed1992

Large-vessel endothelium switches to a microvascular phenotype during angiogenesis in collagen gel culture of rat aorta.

The purpose of this study was to investigate the vasoformative behavior in vitro of the native intimal endothelium of the rat aorta. To visualize the intimal surface directly, thoracic aortas were everted using a procedure that sequestered adventitial cells and possible remnant microvessels of periaortic soft tissues inside the aortic tube. Everted aortas embedded in collagen gel and cultured under serum-free conditions generated branching microvessels by a process of sprouting from the aortic intima. The newly formed microvessels originated from patches of activated intimal endothelial cells, which had survived the mechanical damage of the eversion procedure. Activated endothelial cells crawled over each other and engaged in lumen formation forming bilayers or multilayers of cells which became the source of sprouting histotypic microvessels. The endothelium of the newly formed microvessels was positive for factor VIII-related antigen and was partially surrounded by periendothelial cells which expressed alpha-smooth muscle actin. The results of this study indicate that the intimal endothelium of the rat aorta has considerable functional plasticity and can switch to a vasoformative phenotype in response to changes in the surrounding extracellular matrix environment.

Animals↗
PubMed1991

Regulation of angiogenesis in vitro by collagen metabolism.

The role of collagen in microvascular growth was investigated using the aortic ring model of angiogenesis. Collagen production by vasoformative outgrowths in plasma clot culture of rat aorta was either stimulated with ascorbic acid or inhibited with the proline analogue cis-hydroxyproline. Microvessels proliferating in the absence of ascorbic acid supplements became ecstatic and developed large lumina. In contrast, newly formed microvessels in the presence of ascorbic acid remained small and maintained thin lumina throughout the angiogenic process. Biochemical studies demonstrated enhanced collagen production and deposition in cultures treated with ascorbic acid. Ultrastructural studies of these cultures showed a marked increase in newly formed interstitial collagen in the perivascular matrix and in regions of the plasma clot containing nonendothelial mesenchymal cells. Small microvessels with thin lumina similar to the ones observed in ascorbic acid-treated plasma clot cultures were obtained by growing aortic explants in gels of interstitial collagen in the absence of ascorbic acid. Inhibition of collagen production with the proline analogue cis-hydroxyproline had a marked anti-angiogenic effect in both plasma clot and collagen gel cultures. The anti-angiogenic effect of cis-hydroxyproline was abolished by adding L-proline to the culture medium, thereby restoring normal metabolism. These results support the hypothesis that angiogenesis is regulated by collagen production and suggest that the size of newly formed microvessels is influenced by the degree of collagenization of the extracellular matrix.

Animals↗
PubMed1991

Inhibition of angiogenesis in vitro by Arg-Gly-Asp-containing synthetic peptide.

This study was designed to evaluate the effect of the synthetic peptide Gly-Arg-Gly-Asp-Ser (GRGDS) on angiogenesis in serum-free collagen gel culture of rat aorta. The GRGDS peptide contains the amino acid sequence Arg-Gly-Asp (RGD), which has been implicated as a recognition site in interactions between extracellular matrix (ECM) molecules and cell membrane receptors. RGD-containing synthetic peptides are known to inhibit attachment of endothelial cells to substrates, but their effect on angiogenesis has not been fully characterized. Aortic explants embedded in collagen gel in the absence of GRGDS generated branching microvessels through a process of endothelial migration and proliferation. Addition of GRGDS to the culture medium caused a marked inhibition of angiogenesis. In contrast, GRGES, a control peptide lacking the RGD sequence, failed to inhibit angiogenesis. The inhibitory effect of GRGDS was nontoxic and reversible. The angiogenic activity of aortic explants previously inhibited with GRGDS could be restored by incubating the cultures in GRGDS-free medium. These findings suggest that angiogenesis is an anchorage-dependent process that can be inhibited by interfering with the attachment of endothelial cells to the ECM. It also indicates that synthetic peptides can be used as probes to study the mechanisms by which the ECM regulates angiogenesis.

Amino Acid Sequence↗
PubMedDate not supplied

Echodensitometry: a methodologic approach to the non-invasive diagnosis of carotid atherosclerotic plaques.

The ultrasound image of the fibroatheromatous plaque has to date been unable to reveal the presence or absence of complications as shown by histology, such as thrombosis and intraplaque hemorrhage. We propose a novel densitometric method for determining the composition of the plaque at the echotomography, along with a new classification based on mathematical models drawn from the optical density distribution curve. This approach avails of an extremely high sensitivity. Percent areas occupied by thrombosis, intraplaque hemorrhage and atheroma in histologic sections have been shown to correspond to hyporeflecting areas in echotomographic images, whereas those occupied by calcium and fibrous tissue correspond to reflecting areas with or without acoustic shadow, respectively. This method may prove to have an important role in the non-invasive monitoring of even slight changes during progression or regression of the fibroatheromatous plaque.

Arteriosclerosis↗
PubMedDate not supplied

Histopathological characterization of carotid plaques echotomography.

The positive correlation between cerebral ischemia and carotid atherosclerosis of extracranial tract has been well established. The reliability of echotomography as diagnostic and prognostic tool in the evaluation of the carotid atherosclerotic lesions is now intensively investigated. Most of the attention has been payed to the accuracy in the determination of the carotid stenosis. A percentage of cerebrovascular accidents do not correlate to the vascular stenosis but to the other modifications induced by the atherosclerotic plaque, such as the release of emboli, acute stenosis for intraplaque haemorrhage or thrombosis. Thus the evaluation of the composition of the plaque may represent a good prognostic tool. In the present study, fifty-two carotid obtained at surgery from patients, who preoperatively underwent ultrasonographic scanning of both carotid arteries, were examined by histological methods. In calcified tissues a significant correlation between findings obtained with both techniques was observed. In the complicated plaques atheromasic gruel, intraplaque haemorrhages and thrombosis could not be discriminated by echotomography.

Carotid Arteries↗