scholarly journals Fibrinogen and fragment D-induced vascular constriction

2005 ◽  
Vol 288 (3) ◽  
pp. H1257-H1264 ◽  
Author(s):  
David Lominadze ◽  
Nina Tsakadze ◽  
Utpal Sen ◽  
Jeff C. Falcone ◽  
Stanley E. D'Souza
Keyword(s):  
Femoral Artery ◽  
Vascular Wall ◽  
Intercellular Adhesion Molecule ◽  
Cremaster Muscle ◽  
Sprague Dawley ◽  
Intercellular Adhesion Molecule 1 ◽  
High Risk Factor ◽  
Arterial Constriction ◽  
Bq 610

Elevated fibrinogen (Fg) concentration in blood is a high risk factor for many cardiovascular diseases. We hypothesize that Fg and its early degradation product, fragment D, may result in arterial constriction by binding endothelial intercellular adhesion molecule-1 (ICAM-1). The vasoconstriction induced by Fg and fragment D was studied in third- and second-order arterioles (3As and 2As, respectively) of Sprague-Dawley rat cremaster muscle in vivo, in aortic and femoral artery rings, and in the segments of first-order arterioles (1As) isolated from rat cremaster muscle. Intravascular infusion of Fg induced significant constriction of 3As and 2As (by 33.4 ± 3.4 and 23.7 ± 4.3%, respectively) in vivo and was abolished in the presence of the specific endothelin type A receptor blocker BQ-610. Fg and fragment D produced significant constriction of both aortic and femoral artery rings. Isolated 1As constricted in response to Fg (0.3 μM) and fragment D (3 μM) by 31 ± 1.4 and 12 ± 1.5%, respectively. Fluorescently labeled Fg and fragment D bound to the vascular wall, whereas albumin bound to a significantly lesser degree. The binding of Fg and fragment D to the arteriolar wall and constriction of aortic and femoral artery rings as well as isolated 1As were abolished in the presence of anti-Fg and anti-ICAM-1 antibodies. These results indicate that binding of Fg and fragment D to the vascular wall through ICAM-1 may contribute to the increased vascular tone and resistance that compromise circulation.

scholarly journals The potential of lunasin extract for the prevention of breast cancer progression by upregulating E-Cadherin and inhibiting ICAM-1

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 902
Author(s):  
Kusmardi Kusmardi ◽  
Elvan Wiyarta ◽  
Numlil Khaira Rusdi ◽  
Andi Muh. Maulana ◽  
Ari Estuningtyas ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Soybean Protein ◽  
Negative Control ◽  
Intercellular Adhesion Molecule ◽  
Sprague Dawley ◽  
Intercellular Adhesion Molecule 1 ◽  
Significant Difference ◽  
E Cadherin

Background: Research in natural substances for their anticancer potential has become increasingly popular. Lunasin, a soybean protein, is known to inhibit cancer progression via various pathways.  The aim of this study was to investigate the effect of Lunasin Extract (LE) on the expression of Intercellular Adhesion Molecule 1 (ICAM-1) and epithelial cadherins (E-Cadherin) in breast cancer. Methods: In this true-experimental in vivo study, 24 Sprague-Dawley rats that were induced by 7,12-Dimethylbenz[a]anthracene (DMBA), were used. Based on the therapy given, the groups were divided into, normal, positive control (PC), negative control (NC), adjuvant, curative, and preventive. Lunasin was extracted from soybean seeds of the Grobogan variety in Indonesia. Tissue samples were obtained, processed, stained with anti-ICAM-1 and anti-E-Cadherin antibodies, examined under a microscope, and quantified using H-score. The data were analyzed using ANOVA, which was then followed by Duncan's test. Results: Statistically significant difference in ICAM-1 expression was observed between the following groups: adjuvant and NC, normal and NC, PC and NC, adjuvant and preventive, normal and preventive, PC and preventive, adjuvant and curative, normal and curative, PC and curative. E-Cadherin expression was significantly different between preventive and NC, adjuvant and NC, PC and NC, normal and NC, adjuvant and curative, PC and curative, normal and curative, normal and preventive. Significant negative correlation was found between ICAM-1 and E-Cadherin [-0.616 (-0.8165; -0.283)] with p = 0.001. Conclusion: Preventive dose of LE was able to reduce ICAM-1 expression while increasing E-Cadherin expression.

scholarly journals Expression of intracellular adhesion molecule–1 linking superoxide to mobilization of granulocytes and macrophages after periarterial blood in rat femoral artery: effect of rebamipide

2000 ◽  
Vol 8 (5) ◽  
pp. 1-7 ◽  
Author(s):  
Jae Moon Choi ◽  
Chi Dae Kim ◽  
Ki Whan Hong
Keyword(s):  
Adhesion Molecule ◽  
Femoral Artery ◽  
Autologous Blood ◽  
In Vitro Study ◽  
High Expression ◽  
In Vivo Studies ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

Object To clarify the mechanism(s) involved in the perivascular mobilization of granulocytes and macrophages by periarterial autologous blood (PAAB) in the vicinity of the femoral artery (FA) in rats, superoxide production as well as expression of intercellular adhesion molecule–1 (ICAM-1) were determined by conducting both in vitro and in vivo experiments. Methods In an in vitro study, a significant amount of superoxide inhibited by diphenyleneiodonium (20 μM and 100 μM) was identified at 3 hours after application of 10% whole blood to the aortic segments, and these results were correlated with in vitro ICAM-1 expression. High expression of ICAM-1 was subsequently demonstrated in these segments at 24 hours in in vitro and in vivo studies. In the in vivo study, an increased mobilization of granulocytes paralleled with a high expression of ICAM-1 in the vessels at 24 hours after administration of PAAB to the FA and then declined. Subsequently, macrophage infiltration progressively increased at all layers throughout a period of 7 to 12 days. Pretreatment with rebamipide (100 and 300 mg kg−1 day−1, orally) significantly inhibited the expression of ICAM-1 with inhibition of mobilization of granulocyte/macrophage. Conclusions These findings suggest that application of PAAB to the rat FA causes superoxide-linked expression of ICAM-1 and mobilization of granulocyte and macrophages. Thus, the potential value in suppressing these variables stimulated by PAAB is indicated in therapeutic strategies for prevention and possible regression of vasospasm after subarachnoid hemorrhage.

ICAM-1 and P-selectin expression in a model of NSAID-induced gastropathy

1998 ◽  
Vol 274 (2) ◽  
pp. G246-G252 ◽  
Author(s):  
Z. Morise ◽  
S. Komatsu ◽  
J. W. Fuseler ◽  
D. N. Granger ◽  
M. Perry ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Critical Role ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
Intercellular Adhesion Molecule ◽  
Sprague Dawley ◽  
Intercellular Adhesion Molecule 1 ◽  
Mucosal Permeability

A growing body of experimental evidence suggests that neutrophilic polymorphonuclear leukocyte (PMN)-endothelial cell interactions play a critical role in the pathophysiology of nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy. The objective of this study was to directly determine whether the expression of endothelial cell adhesion molecules is enhanced in a model of NSAID-induced gastropathy. Gastropathy was induced in male Sprague-Dawley rats via oral administration of indomethacin (Indo, 20 mg/kg). Lesion scores, blood-to-lumen clearance of 51Cr-EDTA (mucosal permeability), and histological analysis (epithelial necrosis) were used as indexes of gastric mucosal injury. Gastric mucosal vascular expression of intercellular adhesion molecule 1 (ICAM-1) or P-selectin were determined at 1 and 3 h after Indo administration using the dual radiolabeled monoclonal antibody (MAb) technique. For some experiments, a blocking MAb directed at either ICAM-1 (1A29) or P-selectin (RMP-1) or their isotype-matched controls was injected intravenously 10 min before Indo administration. We found that P-selectin expression was significantly increased at 1 h but not 3 h after Indo administration, whereas ICAM-1 expression was significantly increased at both 1 and 3 h after Indo treatment. The blocking ICAM-1 and P-selectin MAbs both inhibited Indo-induced increases in lesion score, mucosal permeability, and epithelial cell necrosis. However, the Indo-induced gastropathy was not associated with significant PMN infiltration into the gastric mucosal interstitium, nor did Indo reduce gastric mucosal blood flow. We propose that NSAID-induced gastric mucosal injury may be related to the expression of P-selectin and ICAM-1; however, this mucosal injury does not appear to be dependent on the extravasation of inflammatory cells or mucosal ischemia.

Expression and self-regulatory function of cardiac interleukin-6 during endotoxemia

2000 ◽  
Vol 279 (5) ◽  
pp. H2241-H2248 ◽  
Author(s):  
Hiroshi Saito ◽  
Cam Patterson ◽  
Zhaoyong Hu ◽  
Marschall S. Runge ◽  
Ulka Tipnis ◽  
...  
Keyword(s):  
Feedback Mechanism ◽  
Intercellular Adhesion Molecule ◽  
Regulatory Function ◽  
Heart Cells ◽  
Intercellular Adhesion Molecule 1 ◽  
Negative Feedback Mechanism ◽  
Proinflammatory Mediators ◽  
Tnf Α

Interleukin (IL)-6 reportedly has negative inotropic and hypertrophic effects on the heart. Here, we describe endotoxin-induced IL-6 in the heart that has not previously been well characterized. An intraperitoneal injection of a bacterial lipopolysaccharide into C57BL/6 mice induced IL-6 mRNA in the heart more strongly than in any other tissue examined. Induction of mRNA for two proinflammatory cytokines, IL-1β and tumor necrosis factor (TNF)-α, occurred rapidly before the induction of IL-6 mRNA and protein. Although stimulation of isolated rat neonatal myocardial cells with IL-1β or TNF-α induced IL-6 mRNA in vitro, nonmyocardial heart cells produced higher levels of IL-6 mRNA upon stimulation with IL-1β. In situ hybridization and immunohistochemical analyses localized the IL-6 expression primarily in nonmyocardial cells in vivo. Endotoxin-induced expression of cardiac IL-1β, TNF-α, and intercellular adhesion molecule 1 was augmented in IL-6-deficient mice compared with control mice. Thus cardiac IL-6, expressed mainly by nonmyocardial cells via IL-1β action during endotoxemia, is likely to suppress expression of proinflammatory mediators and to regulate itself via a negative feedback mechanism.

scholarly journals Role of poly(ADP-ribose) synthetase in pulmonary leukocyte recruitment

2003 ◽  
Vol 285 (5) ◽  
pp. L996-L1005 ◽  
Author(s):  
Rainer Kiefmann ◽  
Kai Heckel ◽  
Martina Dörger ◽  
Sonja Schenkat ◽  
Mechthild Stoeckelhuber ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Leukocyte Recruitment ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Edema Formation ◽  
Pulmonary Microcirculation

During systemic inflammation, recruitment and activation of leukocytes in the pulmonary microcirculation may result in a potentially life-threatening acute lung injury. We elucidated the role of the poly(ADP-ribose) synthetase (PARS), a nucleotide-polymerizing enzyme, in the regulation of leukocyte recruitment within the lung with regard to the localization in the pulmonary microcirculation and in correlation to hemodynamics in the respective vascular segments and expression of intercellular adhesion molecule 1 during endotoxemia. Inhibition of PARS by 3-aminobenzamide reduced the endotoxin-induced leukocyte recruitment within pulmonary arterioles, capillaries, and venules in rabbits as quantified by in vivo fluorescence microscopy. Microhemodynamics and thus shear rates in all pulmonary microvascular segments remained constant. Simultaneously, inhibition of PARS with 3-aminobenzamide suppressed the endotoxin-induced adhesion molecules expression as demonstrated for intercellular adhesion molecule 1 by immunohistochemistry and Western blot analysis. We confirmed this result with the use of PARS knockout mice. The inhibitory effect of 3-aminobenzamide on leukocyte recruitment was associated with a reduction of pulmonary capillary leakage and edema formation. We first provide evidence that PARS activation mediates the leukocyte sequestration in pulmonary microvessels through upregulation of adhesion molecules. As reactive oxygen species released from leukocyte are supposed to cause an upregulation of adhesion molecules we conclude that PARS inhibition contributes to termination of this vicious cycle and inhibits the inflammatory process.

Contribution of adenosine to arteriolar autoregulation in striated muscle

1983 ◽  
Vol 244 (4) ◽  
pp. H567-H576 ◽  
Author(s):  
R. J. Morff ◽  
H. J. Granger
Keyword(s):  
Blood Flow ◽  
Striated Muscle ◽  
Perfusion Pressure ◽  
Cremaster Muscle ◽  
Sprague Dawley ◽  
Red Blood Cell Velocity ◽  
Myogenic Factors ◽  
Bath Medium ◽  
Arteriolar Diameter

The contribution of adenosine to blood flow autoregulation in striated muscle was evaluated by direct in vivo visualization of arterioles in the rat cremaster muscle. Male Sprague-Dawley rats were anesthetized with pentobarbital sodium, and the cremaster muscle was surgically exposed and maintained in a controlled tissue bath environment with pH 7.40, CO2 tension (PCO2) congruent to 40 mmHg, and O2 tension (PO2) at either a high (congruent to 70 mmHg) or a low (congruent to 10 mmHg) value. Local adenosine activity was blocked in some animals by the addition of theophylline (3 X 10(-5) M) to the bath medium. Individual second (2A)- and third (3A)-order arterioles were observed via closed-circuit television microscopy, and blood flow in each arteriole was calculated from simultaneous measurements of arteriolar diameter and red blood cell velocity. Perfusion pressure to the animal's hindquarters was altered by varying the degree of occlusion of the sacral aorta; arteriolar diameter, velocity, and blood flow responses were plotted as a function of the varying pressure. Both 2A and 3A arterioles exhibited vasodilation and substantial superregulation of blood flow (increased blood flow with decreased perfusion pressure) when bath PO2 was low and adenosine activity was not blocked. Addition of theophylline to the cremaster bath medium significantly reduced the dilation and abolished superregulation, although substantial autoregulation remained. When bath PO2 was high, the degree of arteriolar dilation and autoregulation was reduced compared with the low bath PO2 responses, and blocking adenosine activity had no effect on the responses. These results support the concept that changes in local adenosine levels are involved in the autoregulatory responses observed in the rat cremaster muscle and that the magnitude of adenosine's contribution is directly related to the degree of tissue hypoxia. However, blocking adenosine activity did not totally abolish autoregulation, suggesting that other metabolic and/or myogenic factors may also be contributing to blood flow regulation in this tissue.

scholarly journals Monoclonal antibody to the interferon-inducible protein Leu-13 triggers aggregation and inhibits proliferation of leukemic B cells

Blood ◽  
1990 ◽  
Vol 76 (12) ◽  
pp. 2583-2593 ◽  
Author(s):  
SS Evans ◽  
DB Lee ◽  
T Han ◽  
TB Tomasi ◽  
RL Evans
Keyword(s):  
B Cells ◽  
Dna Synthesis ◽  
Lymphocytic Leukemia ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Adhesive Properties ◽  
Prolymphocytic Leukemia ◽  
Ifn Alpha

Abstract Interferon (IFN)-alpha inhibits DNA synthesis stimulated by low molecular weight B-cell growth factor (BCGF) in hairy cells in vitro, suggesting that the therapeutic efficacy of IFN-alpha in hairy cell leukemia (HCL) involves growth inhibition of malignant B cells. Evidence that the 16-Kd cell surface protein Leu-13 mediates an antiproliferative signal in T lymphocytes and is IFN-inducible in endothelial cells prompted us to examine the expression and functional role of this molecule in leukemic B cells. Leu-13 density, determined by flow cytometry, was upregulated in vitro and in vivo by IFN-alpha on malignant B cells from patients with HCL, chronic lymphocytic leukemia, and prolymphocytic leukemia. Monoclonal anti-Leu-13 triggered homotypic aggregation of leukemic B cells via an adhesion pathway that was not inhibited by antibodies to leukocyte function associated antigen-1 (LFA- 1) or intercellular adhesion molecule-1 (ICAM-1). Moreover, anti-Leu-13 potentiated the inhibitory effects of IFN-alpha on BCGF-stimulated DNA synthesis, assessed by [3H]-thymidine and [3H]-deoxyadenosine incorporation into DNA. These results indicate that Leu-13 is part of a novel IFN-inducible signaling pathway which may modify the growth and adhesive properties of leukemic B cells under physiologic or therapeutic conditions.

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