Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 107, Issue 2, Pages 316-327Publisher
WILEY-BLACKWELL
DOI: 10.1002/jcb.22127
Keywords
APOPTOSIS; p53; PHTHALATES; SIRNA; BONE
Categories
Funding
- Italian Ministry of University and Research
- University of Camerino, Fondazione Carima, Italy
Ask authors/readers for more resources
The role of two estrogen-mimicking compounds in regulating osteoblast activities were examined. Previously, our attention was focused on benzyl butyl phthalate (BBP) and di-n-butyl phthalate (DBP) since previous works showed that they enter the cytoplasm, bioaccumulate, modify actin cytoarchitecture and exert mitogenic effects involving microfilament disruption, and nuclear actin and lamin A regulation in Py1a rat osteoblasts. In this study we showed that BBP and DBP cause DNA base lesions both in MT3T3-E1 osteoblasts and in mouse primary calvarial osteoblasts (COBS). In addition, treatment with the above effectors caused an increase of p53 and phospho-p53 (ser-15 and ser-20) as well as an increase of apoptotic proteins with consequent decrease of cell viability. Moreover, treatment with phthalates did not modified p53 and phospho-p53 expression in Pyla rat osteoblasts. It is of relevance that in p53 knockdown mouse osteoblasts a proliferative effect of phthalates, similar to that observed in rat Py1a osteoblasts, was found. In conclusion, our data demonstrated that phthalates induce osteoblast apoptosis, which is, at least in part, mediated by p53 activation, suggesting that the proliferative effects could be due to p53 missing activation or p53 mutation. J. Cell. Biochem. 107: 316-327, 2009. (C) 2009 Wiley-Liss. Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available