Recombinant Rv0753c Protein of Mycobacterium tuberculosis Induces Apoptosis Through Reactive Oxygen Species-JNK Pathway in Macrophages

ƒThis is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/ license/by-nc/3.0/). 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 (ΔΨm), 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.

• Publication year

  2020

• Venue

  Journal of Bacteriology and Virology

• Publication date

  2020-12-01

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  DOI 10.4167/JBV.2020.50.4.246
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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