Increased expression of thrombomodulin on the cultured human umbilical vein endothelial cells and mouse hemangioma cells by cyclic AMP
Autor: | William A. Dittman, Mitsuhiro Osame, Takahiko Ito, Hidehiko Saito, Yasuko Soejima, Ikuro Maruyama, Kohei Ogawa, Shuji Yamamoto |
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Rok vydání: | 1991 |
Předmět: |
Umbilical Veins
Endothelium medicine.medical_treatment Receptors Cell Surface Biology Thrombomodulin Umbilical vein Mice chemistry.chemical_compound Thrombin 1-Methyl-3-isobutylxanthine medicine Animals Humans Drug Interactions RNA Messenger Cells Cultured Forskolin Dose-Response Relationship Drug Tumor Necrosis Factor-alpha Colforsin Hematology Molecular biology Endothelial stem cell Cytokine medicine.anatomical_structure Bucladesine chemistry Cell culture Immunology cardiovascular system Receptors Thrombin Endothelium Vascular Hemangioma Interleukin-1 medicine.drug |
Zdroj: | Thrombosis Research. 61:301-310 |
ISSN: | 0049-3848 |
DOI: | 10.1016/0049-3848(91)90107-8 |
Popis: | We previously reported that the expression of thrombomodulin on the MEG-01, a cell line from human megakaryoblastic leukemia, was increased by agents that increase intracellular cAMP. In this paper we examine the effect of these agents on cultured human umbilical vein endothelial cells (HUVEC) and mouse hemangioma cells. Incubation of the cells with 3 mM dibutyryl cAMP (dbcAMP) increased functionally active thrombomodulin by about 2-fold on HUVEC and 4-fold on hemangioma cells. This effect was observed from 1 hour after the incubation and continued up to 24 hours. Dot hybridization of mRNA demonstrated a dose dependent increase in thrombomodulin mRNA in response to dbcAMP. Treatment of HUVEC with 20 microM forskolin or 100 microM isobutylmethylxanthine (IBMX) also increased cell-surface thrombomodulin on HUVEC. These agents prevented the interleukin I (IL-I) or tumor necrosis factor (TNF)-induced decrease in thrombomodulin on HUVEC. These data suggest that the expression of thrombomodulin on HUVEC and mouse hemangioma cells may be regulated by intracellular cAMP level. |
Databáze: | OpenAIRE |
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