期刊
MOLECULAR MEDICINE
卷 24, 期 -, 页码 -出版社
SPRINGER
DOI: 10.1186/s10020-018-0064-z
关键词
-
资金
- Institute of Health Carlos III (ISCIII) [MPY-1038/14, MPY-1146/16]
- Ministry of Economy and Competitiveness (MINECO) [SAF-2015-71140-R]
Background: The multiple biological effects of vitamin D and its novel activities on inflammation and redox homeostasis have raised high expectations on its use as a therapeutic agent for multiple fibrogenic conditions. We have assessed the therapeutic effects of 1 alpha,25-Dihydroxyvitamin D-3, the biologically active form of vitamin D, in the context of lung fibrosis. Methods: We have used representative cellular models for alveolar type II cells and human myofibroblasts. The extension of DNA damage and cellular senescence have been assessed by immunofluorescence, western-blot and senescence-associated beta-galactosidase activity. We have also set up a murine model for lung fibrosis by intraperitoneal injections of bleomycin. Results: Vitamin D induces cellular senescence in bleomycin-treated alveolar epithelial type II cells and aggravates the lung pathology induced by bleomycin. These effects are probably due to an alteration of the cellular DNA double-strand breaks repair in bleomycin-treated cells. Conclusions: The detrimental effects of vitamin D in the presence of a DNA damaging agent might preclude its use as an antifibrogenic agent for pulmonary fibrosis characterized by DNA damage occurrence and cellular senescence.
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