Modulation of U937 cell adhesion to vascular endothelial cells by cyclic AMP
| Autor: | Giora Z. Feuerstein, Cheng-Po Sung, Barbara Storer, Anthony J. Arleth |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Cholera Toxin
Endothelium Biology medicine.disease_cause General Biochemistry Genetics and Molecular Biology Cell Line Cell Adhesion Cyclic AMP Dibutyryl Cyclic GMP Leukocytes medicine Humans General Pharmacology Toxicology and Pharmaceutics Cell adhesion U937 cell Cell adhesion molecule Monocyte Cholera toxin General Medicine Adhesion Adrenergic beta-Agonists Up-Regulation Cell biology Endothelial stem cell medicine.anatomical_structure Bucladesine Immunology cardiovascular system Cytokines Endothelium Vascular |
| Zdroj: | Life Sciences. 49:375-382 |
| ISSN: | 0024-3205 |
| DOI: | 10.1016/0024-3205(91)90445-h |
| Popis: | Adhesion of leukocytes to the endothelium is an essential event in inflammatory cell emigration from intravascular to extravascular compartment. While many mediators (e.g. cytokines) enhance cell adhesion through expression of adhesion molecules on endothelial cells the mechanism of this phenomenon is not known. In this study we examined the role of cAMP in mediation of the adhesion of monocytic cell line, U937 to human umbilical vein endothelial cells (HUVEC). Incubation of HUVEC with cholera toxin (10-500 ng/ml) for 4 hrs greatly enhanced the adhesiveness of HUVEC for U937 cells. The magnitude of adhesion stimulation produced by cholera toxin was comparable to that produced by the cytokines TNF alpha or IL-1 (2-3 folds). Upregulation of U937 cells adhesion to HUVEC was also achieved by short incubation (less than 1 hr) of HUVEC with cAMP elevating agents such as forskolin (10 microM), isoproterenol (0.3-30 microM), epinephrine (10-100 microM), norepinephrine (100 microM) as well as by endogenously added dibutyryl cAMP (0.05-2.0 mM). Dibutyryl cyclic GMP (0.05-2.0 mM) was ineffective in promoting adhesion. These data suggest that cAMP might be an important intracellular modulator of leukocyte adhesion to endothelium and therefore promoter of pro-inflammatory processes. |
| Databáze: | OpenAIRE |
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