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KMID : 0921620200500040246
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Journal of Bacteriology and Virology
2020 Volume.50 No. 4 p.246 ~ p.256
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Recombinant Rv0753c Protein of Mycobacterium tuberculosis Induces Apoptosis Through Reactive Oxygen Species-JNK Pathway in Macrophages
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Lee Kang-In
Choi Seung-A
Choi Han-Gyu
Kebede Sintayehu Gurmessa
Dang Thi Binh
Back Yong-Woo
Park Hye-Soo
Kim Hwa-Jung
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Abstract
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Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains one of the most important infectious diseases worldwide. Mtb and its culture filtrates or sonic extracts induce apoptosis in macrophages. However, there is a little known about Mtb components that modulate apoptosis and their regulating mechanism. We identified Rv0753c protein with apoptotic potential through searching the biologic active proteins from the multidimensional fractions of Mtb culture filtrate. Here, we investigated the apoptotic effects of Rv0753c on RAW264.7 cells. The recombinant Rv0753c induced RAW264.7 cells apoptosis in a caspase-9-dependent manner. Dissipation of the mitochondrial transmembrane potential (ΔΨ m ), mitochondrial translocation of Bax, and release of cytochrome c from mitochondria were observed in macrophages treated with Rv0753c. Enhanced reactive oxygen species (ROS) production was required for Rv0753c-mediated apoptosis. Furthermore, ROS-mediated JNK activation was major signaling pathway for Rv0753c-induced apoptosis. Moreover, Rv0753c-mediated apoptosis is dependent on TLR4. Altogether, these results suggest that Rv0753c induce apoptosis through ROS-JNK signaling pathway in RAW264.7 cells.
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KEYWORD
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Mycobacterium tuberculosis, RAW264.7 cells, Apoptosis, ROS, Rv0753c
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