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Notch signaling regulates expression of Mcl-1 andapoptosis in PPD-treated macrophages

Cellular & Molecular Immunology 2013年第5期10卷 444-452页

作者： Tanapat P alaga Siriluk Ratanabunyong Thitiporn Pattarakankul Naunpun Sangphech Wipawee Wongchana yukihiro hadae Patipark Kueanjinda Department of Microbiology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand Interdisciplinary Program in Medical Microbiology Graduate School Chulalongkorn University Bangkok 10330 Thailand Graduate Program in Industrial Microbiology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand Graduate Program in Biotechnology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand International Center for Biotechnology Osaka University Osaka 565-0871 Japan

Macrophages are cellular targets for infection by bacteria and viruses. The fate of infected macrophages plays a key role in determining the outcome of the host immune response. Apoptotic cell death of macrophages is considered to be a protective host defense that eliminates pathogens and infected cells. In this study, we investigated the involvement of Notch signaling in regulating apoptosis in macrophages treated with tuberculin purified protein derivative （PPD）. Murine bone marrow-derived macrophages （BMMs） treated with PPD or infected with Mycobacterium bovis Bacillus Calmette-Guerin （BCG） induced upregulation of Notch1. This upregulation correlated well with the upregulation of the anti-apoptotic gene mcl-1 both at the transcriptional and translational levels. Decreased levels of Notch I and Mcl- 1 were observed in BMM treated with PPD when a gamma secretase inhibitor （GSI）, which inhibits the processing of Notch receptors, was used. Moreover, silencing Notch1 in the macrophage-like cell line RAW264.7 decreased Mcl-1 protein expression, suggesting that Notch1 is critical for Mcl-1 expression in macrophages. A significant increase in apoptotic cells was observed upon treatment of BMM with PPD in the presence of GSI compared to the vehicle-control treated cells. Finally, analysis of the mcl-1 promoter in humans and mice revealed a conserved potential CSURBP-Jκ binding site. The association of Notch I with the mcl-1 promoter was confirmed by chromatin immunoprecipitation. Taken together, these results indicate that Notch I inhibits apoptosis of macrophages stimulated with PPD by directly controlling the mcl-1 promoter.

关键词： apoptosis BCG macrophage Mcl-1 Notch signaling PPD

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