Mast cell-mediated induction of ICAM-1, VCAM-1 and E-selectin in endothelial cells in vitro: constitutive release of inducing mediators but no effect of degranulation

Haaster, Charles M.C.J. van; Derhaag, Josien G.; Engels, W.; Lemmens, P. J. M. R.; Gijsen, Annemie P.; Hornstra, Gerard; Vusse, Ger J.; Duijvestijn, A. M.

doi:10.1007/s004240050493

Cited by 15 publications

(12 citation statements)

References 35 publications

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“…These pro-inf lammator y mediator and vasoactive substances attack vessels from outside [40] , promote the expression of VCAM-1 and E-selectin on endothelial cells [41] , increase the rolling and adhesion of leukocytes, and enhance the albumin leakage [39,41,42] . In the present study, the degranulation of mast cells induced by LPS infusion was found to be markedly inhibited by the treatment with compound Danshen injection in terms of the degranulated mast cell ratio, sug gesting that compound Danshen injection is also capable of protecting the microvessels by blockage of vasoactive substances from outside.…”

Section: Discussionmentioning

confidence: 99%

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Han

Horie²,

Miura³

et al. 2007

WJG

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stained with Monastral blue B, rolling and adhesion of leukocytes, production of oxygen radical in venular wall, albumin efflux and enhanced mast cell degranulation in vivo , all of which, except for the leukocyte rolling, were attenuated by the treatment with compound Danshen injection. Experiments performed in vitro further revealed that the expression of CD11b/CD18 and the production of oxygen free radical in neutrophils, and the expression of ICAM-1 in HUVECs were increased by exposure to LPS, and they were attenuated by compound Danshen injection. CONCLUSION: These results suggest that compoundDanshen injection is an efficient drug with multi-targeting potential for improving the microcirculatory disturbance. INTRODUCTIONIt is now well-recognized that stimulation with lipopolysaccharide (LPS) leads to a number of responses in microcirculation, such as endothelial cell damage, an increase in rolling, adhesion and emigration of leukocytes in post-capillary venules, enhanced oxygenfree radical production, mast cell degranulation and protein efflux [1][2][3][4][5][6] . Furthermore, it is demonstrated that LPS stimulation evokes an increase in the expression of adhesion molecules, including L-selectin [7] and CD11b/CD18 in leukocytes, E-selectin and intercellular adhesion molecule 1 (ICAM-1) in endothelial cells [7][8][9][10][11][12][13] . In addition, LPS stimulation can cause the release of proinflammatory mediators and vasoactive substances, such Abstract AIM: To investigate the effect of compound Danshen injection on lipopolysaccharide (LPS)-induced rat mesenteric microcirculatory dysfunctions and the underlying possible mechanism by an inverted intravital microscope and high-speed video camera system. METHODS:LPS was continuously infused through the jugular artery of male Wistar rats at the dose of 2 mg/kg per hour. Changes in mesenteric microcirculation, such as diameters of arterioles and venules, velocity of RBCs in venules, leukocyte rolling, adhesion and emigration, free radicals released from post-capillary venules, FITCalbumin leakage and mast cell degranulation, were observed through an inverted intravital microscope assisted with CCD camera and SIT camera. Meanwhile, the expression of adhesion molecules CD11b/CD18 and the production of free radical in neutrophils, and the expression of intercellular adhesion molecule 1 (ICAM-1) in human umbilical vein endothelial cells (HUVECs) were quantified by flow cytometry (FACS) in vitro . RESULTS:The continuous infusion with LPS resulted in a number of responses in microcirculation, including a significant increase in the positive region of venule

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Section: Discussionmentioning

confidence: 99%

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Han

Horie²,

Miura³

et al. 2007

WJG

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“…Mouse TNF‐α appears to be released from MC upon transcription, but also from cytoplasmatic stores, 17 the latter having a major impact on the leucocyte recruitment activity in experimental inflammation 18 . In addition, recent data suggest that the release of rat MC‐prestored mediators (possibly histamine and TNF‐α) hardly has any effect on ICAM‐1 expression upon activation 19 …”

Section: Introductionmentioning

confidence: 99%

Mast cells induce upregulation of P‐selectin and intercellular adhesion molecule 1 on carotid endothelial cells in a new in vitro model of mast cell to endothelial cell communication

et al. 2002

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Summary It is suggested that mast cells contribute to cell recruitment in inflammation through the upregulation of endothelial adhesion molecules. P-selectin and intercellular adhesion molecule (ICAM)-1 are two key adhesion molecules that have been associated indirectly with mast cell activity. The canine C 2 mastocytoma cell line and primary cultures of canine carotid endothelial cells were used to establish a new in vitro model to help study the interaction between mast cells and endothelial cells. Carotid endothelial cells were incubated with mast cell mediators to uncover their effect on endothelial ICAM-1 and P-selectin expression. To assess the relative contributions of tumour necrosis factor (TNF)-α and histamine to such effect, an H 1 antihistamine and a TNF-α blocking antibody were used. Prior to activation by mast cell mediators, P-selectin was expressed only within the cytoplasm, and ICAM-1 was constitutively expressed on the surface of the canine carotid endothelial cells. Both adhesion molecules were enhanced significantly and strongly upon mast cell activation at various time points. Unstored TNF-α was fully responsible for ICAM-1 upregulation. P-selectin was up-regulated by both preformed and newly synthesized mast cell mediators, but neither histamine nor TNF-α accounted for such an effect. Therefore, a new model is proposed in which the pro-inflammatory effect of mast cells on endothelial cells can be studied in vitro. In this model, it has been demonstrated that only TNF-α accounts for the overexpression of ICAM-1 induced by mast cells, and that mast cells up-regulate P-selectin expression through a histamine-independent mechanism.

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“…When degranulated, mast cells release histamine and TNF-α, and initiate the cytokine cascade, which leads to the expression of vascular cell adhesion molecule-1 (VCAM-1) and E-selectin on endothelial cells and subsequent neutrophil-induced injury (Frangogiannis et al, 1998;van Haaster et al, 1997). The inhibitory effect of PNS on mast cell degranulation was previously identified from the results of experiments with the compound Myakuryu .…”

Section: Discussionmentioning

confidence: 87%

Protective effects of ginsenoside Rb1, ginsenoside Rg1, and notoginsenoside R1 on lipopolysaccharide-induced microcirculatory disturbance in rat mesentery

et al. 2007

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Mast cell-mediated induction of ICAM-1, VCAM-1 and E-selectin in endothelial cells in vitro: constitutive release of inducing mediators but no effect of degranulation

Cited by 15 publications

References 35 publications

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Mast cells induce upregulation of P‐selectin and intercellular adhesion molecule 1 on carotid endothelial cells in a new in vitro model of mast cell to endothelial cell communication

Protective effects of ginsenoside Rb1, ginsenoside Rg1, and notoginsenoside R1 on lipopolysaccharide-induced microcirculatory disturbance in rat mesentery

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