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Modulation of Cell Growth and Apoptosis by Sex Hormones in Cultured Monocytic THP‐1 Cells
Author(s) -
CUTOLO MAURIZIO,
SULLI ALBERTO,
CRAVIOTTO CHIARA,
FELLI LAMBERTO,
PIZZORNI CARMEN,
SERIOLO BRUNO,
VILLAGGIO BARBARA
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04216.x
Subject(s) - thp1 cell line , apoptosis , cell culture , programmed cell death , hormone , oncogene , biology , peripheral blood mononuclear cell , microbiology and biotechnology , cell , cancer research , cell cycle , chemistry , endocrinology , in vitro , biochemistry , genetics
A bstract : Several authors have reported the regulation of apoptotic phenomena by sex hormones in different cell lines, including T lymphocytes and mononuclear cells. Since androgens can modulate the programmed cell death in responsive cell lines, we decided to investigate the induction of apoptosis in THP‐1 cells following their differentiation into macrophage‐like cells and exposure to sex hormones. In addition, we decided to evaluate the proto‐oncogene Bax and Fas (CD 95) and cleaved PARP (poly‐adp‐ribose‐polymerase) expression in the same cultured cells. The results showed for the first time the dose‐/time‐dependent regulation of the apoptotic event in human monocytic THP‐1 cells treated with different concentrations of androgens. No significant changes were observed for estrogen‐treated and unstimulated control cells. In particular, the cells, after stimulation with androgens but not with estrogens, were found to be positive for the proto‐oncogene Bax , Fas, and for cleaved subunits of PARP expression as demonstrated with different assays including immunocytochemical assay and Western blot analysis. In conclusion, these results support the possibility of sex hormone modulation of apoptosis in macrophage‐like cells, with interesting therapeutic perspectives in rheumatoid arthritis.