Immunosuppression and transplant vascular disease: benefits and adverse effects

Moien‐Afshari, Farzad; McManus, Bruce M.; Laher, Ismail

doi:10.1016/j.pharmthera.2003.08.002

Cited by 48 publications

(38 citation statements)

References 136 publications

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“…[12][13][14]16,[22][23][24] Endothelial injury that occurs after insults such as exposure to CNI results in decreased endothelial NO production, superoxide anion production, increased endothelin-1 production, and sensitivity to endothelin-1. [1][2][3][4][5]25 These disturbances, in turn, stimulate the expression of inflammatory cytokines such as interleukin-6 6,7 and cell adhesion molecules such as ICAM-1. These events allow circulating neutrophils to migrate to sites of endothelial injury, where they subject local tissues, including the endothelium, to further injury.…”

Section: Discussionmentioning

confidence: 99%

Epidermal Growth Factor–Like Domain 7 Is a Novel Inhibitor of Neutrophil Adhesion to Coronary Artery Endothelial Cells Injured by Calcineurin Inhibition

Badiwala

Guha²,

Tumiati³

et al. 2011

Circulation

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Background— We investigated the effect of epidermal growth factor–like domain 7 (Egfl7) on nuclear factor-κB activation, intercellular adhesion molecule-1 expression, and neutrophil adhesion to human coronary artery endothelial cells after calcineurin-inhibition–induced injury. Methods and Results— Human coronary endothelial cells were incubated with cyclosporine (CyA) 10 μg/mL with or without Egfl7 (100 ng/mL) or the Notch receptor activator Jagged1 (200 ng/mL) for 6 to 48 hours. CyA upregulated nuclear factor-κB (p65) activity (128±2% of control, P <0.001) in nuclear extracts, as determined with a DNA-binding activity ELISA. This activity was inhibited by Egfl7 (86±3% of control; P <0.001 versus CyA alone). Jagged1 blocked Egfl7-induced nuclear factor-κB inhibition (105±4% of control; P <0.05 versus CyA plus Egfl7). CyA upregulated cell-surface intercellular adhesion molecule-1 expression (215±13% of control; P <0.001), as determined by flow cytometry. This expression was suppressed by Egfl7 (148±5%; P <0.001 versus CyA alone). Jagged1 attenuated the intercellular adhesion molecule-1–suppressive effect of Egfl7 when administered with CyA (193±3% versus 148±5%; P <0.01). CyA increased neutrophil adhesion to human coronary endothelial cells (control 20±5%, CyA 37±3%; P <0.001 versus control) in a nonstatic neutrophil adhesion assay. This increase was attenuated by Egfl7 (22±6%; P <0.001 versus CyA alone). Jagged 1 attenuated the effect of Egfl7 on neutrophil adhesion (31±3%; P <0.001 versus Egfl7 plus CyA). Conclusions— Our study reveals that Egfl7 is a potent inhibitor of neutrophil adhesion to human coronary endothelial cells subsequent to calcineurin-inhibition–induced injury. Mechanistically, Egfl7 blocked nuclear factor-κB pathway activation and intercellular adhesion molecule-1 expression, which suggests that it may have significant antiinflammatory properties. Because Jagged1 blocked the effect of Egfl7, Notch receptor antagonism may contribute to the mechanism of action of Egfl7.

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Section: Discussionmentioning

confidence: 99%

Epidermal Growth Factor–Like Domain 7 Is a Novel Inhibitor of Neutrophil Adhesion to Coronary Artery Endothelial Cells Injured by Calcineurin Inhibition

Badiwala

Guha²,

Tumiati³

et al. 2011

Circulation

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show abstract

“…As is well known, calcineurin inhibitors such as cyclosporin A have been shown to interact with vasoactive metabolites, causing arterial hypertension and arteriosclerosis (2,3). Cyclosporin A is known to impair vascular vasodilatation and may induce vasoconstriction (4,5).…”

mentioning

confidence: 99%

Associations of Churg‐Strauss syndrome with the HLA–DRB1 locus, and relationship to the genetics of antineutrophil cytoplasmic antibody–associated vasculitides: Comment on the article by Vaglio et al

Wieczorek¹,

Hellmich²,

Gross³

et al. 2007

Arthritis & Rheumatism

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“…Instead of chest pain, more serious events, such as congestive heart failure, ventricular arrhythmias and sudden death, are commonly the first clinical manifestations (11).…”

Section: Hypothesis -19mentioning

confidence: 99%

“…By 5 years, diagnosis of CAV reaches 50% in heart transplant recipients (10,11). Patients with CAV have silent ischemia due to the denervated heart.…”

mentioning

confidence: 99%

Cardiac Allograft Vasculopathy: The silent, long-suffering enemy

Bishay¹

2008

HYP

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Immunosuppression and transplant vascular disease: benefits and adverse effects

Cited by 48 publications

References 136 publications

Epidermal Growth Factor–Like Domain 7 Is a Novel Inhibitor of Neutrophil Adhesion to Coronary Artery Endothelial Cells Injured by Calcineurin Inhibition

Epidermal Growth Factor–Like Domain 7 Is a Novel Inhibitor of Neutrophil Adhesion to Coronary Artery Endothelial Cells Injured by Calcineurin Inhibition

Associations of Churg‐Strauss syndrome with the HLA–DRB1 locus, and relationship to the genetics of antineutrophil cytoplasmic antibody–associated vasculitides: Comment on the article by Vaglio et al

Cardiac Allograft Vasculopathy: The silent, long-suffering enemy

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