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17β -Estradiol promotes the synthesis and the secretion of annexin I in the CCRF-CEM human cell line
AIMS: Annexin I (ANXA1), a 37 kDa member of the annexin family of Ca^(2+)-binding and phospholipidbinding proteins, is particularly abundant in various populations of peripheral blood leukocytes. Since this protein modulates the anti-inflammatory actions of the steroid hormones, the purpose of this...
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Published in: | Mediators of Inflammation 2001, Vol.2001 (5), p.245-251 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | AIMS: Annexin I (ANXA1), a 37 kDa member of the annexin family of Ca^(2+)-binding and phospholipidbinding proteins, is particularly abundant in various populations of peripheral blood leukocytes. Since this protein modulates the anti-inflammatory actions of the steroid hormones, the purpose of this study was to investigate the effects of the female sex steroid hormone, 17β -estradiol (E_2β), on the synthesis and secretion of ANXA1 in the human CCRF-CEM acute lymphoblastic leukemia cell line. Methods: Complementary reverse transcription-polymerase chain reaction and Western blot assays were performed to study the effect of E2 b on the expression of mRNA and protein ANXA1, respectively. Results and discussion: Treatment of CCRF-CEM cells with E_2β, for 30 min, stimulated the synthesis of ANXA1 mRNA molecules, and increased the cellular level of ANXA1 protein. Moreover, when the cells were incubated with E_2β, under the same experimental conditions, a significant increase in the amount of ANXA1 secreted from the cells was also detected. ICI 182,780, a selective inhibitor of the intracellular estrogen receptor, had no effect on the E_2β-stimulated expression and externalisation of ANXA1. Taken together, these results indicate that E_2βinduces de novo synthesis of ANXA1 and stimulates its secretion in the CCRF-CEM cell line, apparently through a mechanism independent of the intracellular estrogen receptor. |
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ISSN: | 0962-9351 1466-1861 |
DOI: | 10.1080/09629350120093713 |