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Busschaert, Nathalie,Park, Seong-Hyun,Baek, Kyung-Hwa,Choi, Yoon Pyo,Park, Jinhong,Howe, Ethan N. W.,Hiscock, Jennifer R.,Karagiannidis, Louise E.,Marques, Igor,Fé,lix, Ví,tor,Namkung, Wan Nature Publishing Group 2017 Nature chemistry Vol.9 No.7
<P>Perturbations in cellular chloride concentrations can affect cellular pH and autophagy and lead to the onset of apoptosis. With this in mind, synthetic ion transporters have been used to disturb cellular ion homeostasis and thereby induce cell death; however, it is not clear whether synthetic ion transporters can also be used to disrupt autophagy. Here, we show that squaramide-based ion transporters enhance the transport of chloride anions in liposomal models and promote sodium chloride influx into the cytosol. Liposomal and cellular transport activity of the squaramides is shown to correlate with cell death activity, which is attributed to caspase-dependent apoptosis. One ion transporter was also shown to cause additional changes in lysosomal pH, which leads to impairment of lysosomal enzyme activity and disruption of autophagic processes. This disruption is independent of the initiation of apoptosis by the ion transporter. This study provides the first experimental evidence that synthetic ion transporters can disrupt both autophagy and induce apoptosis.</P>
Immunoregulatory Effects of Extracts from the stem bark of Albizzia julibrissin Durazz
Kim, Jeong J,Lee, Byung E,Jung, Dong S,Kim, Se-Won,Ko, Seon-Yle,Baek, Dong-Heon,Chang, Sun-Hwa,Choi, Youngnim Korean Academy of Oral Biology and the UCLA Dental 2004 International Journal of Oral Biology Vol.29 No.4
Although there are many disease modifying anti-rheumatic drugs (DMARDs) available, more safe and effective reagents have yet to be developed. Activated T cells make good targets for DMARD therapy. Therefore, we screened over fifty herbal extracts, and identified that water extract from the stem bark of Albizzia julibrissin selectively killed activated T cells but not nai¨ve splenocytes, in vitro. Wb3-3, obtained by further extraction and column chromatography to maximize selective activity, was used for further investigation. Annexin-V and caspase activity assay revealed that WB3-3 killed activated T cells by inducing apoptosis, which was mediated through mainly caspase-8 rather than caspase-9. The effect of WB3-3 in vivo was confirmed by the elimination of Vβ8^(+)- but no Vβ6^(+)-T cells following activation with Streptococcal Enterotoxin B (SEB). Furthermore, WB3-3 inhibited neither CD25 up-regulation nor proliferative response, and rather increased IL-2 secretion during Con A activation of naive T cells. Our results imply the potential of WB3-3 to include a lead compound for a new immunoregulatory drug.