Yahiro, K., Akazawa, Y., Nakano, M., Suzuki, H., Hisatune, J., Isomoto, H., Sap, J., Noda, M., Moss, J. and Hirayama, T. (2015) Helicobacter pylori VacA Induces Apoptosis by Accumulation of Connexin 43 in Autophagic Vesicles via a Rac1/Erk-Dependent Pathway. Cell Death Discovery, 1, Article No. 15035.
https://doi.org/10.1038/cddiscovery.2015.35

has been cited by the following article:

• TITLE: Restoration of Mitochondrial Structure and Function within Helicobacter pylori VacA Intoxicated Cells

  AUTHORS: Robin L. Holland, Kristopher D. Bosi, Ami Y. Seeger, Steven R. Blanke

  KEYWORDS: Helicobacter pylori, VacA, Vacuolating Cytotoxin, Mitochondria, Mitochondrial Dysfunction, Mitochondrial Fission, Mitochondrial Transmembrane Potential, ATP, Mitochondrial Dynamics, Oxidative Phosphorylation

  JOURNAL NAME: Advances in Microbiology, Vol.13 No.8, August 14, 2023

  ABSTRACT: The Helicobacter pylori vacuolating cytotoxin (VacA) is an intracellular, mitochondrial-targeting exotoxin that rapidly causes mitochondrial dysfunction and fragmentation. Although VacA targeting of mitochondria has been reported to alter overall cellular metabolism, there is little known about the consequences of extended exposure to the toxin. Here, we describe studies to address this gap in knowledge, which have revealed that mitochondrial dysfunction and fragmentation are followed by a time-dependent recovery of mitochondrial structure, mitochondrial transmembrane potential, and cellular ATP levels. Cells exposed to VacA also initially demonstrated a reduction in oxidative phosphorylation, as well as increase in compensatory aerobic glycolysis. These metabolic alterations were reversed in cells with limited toxin exposure, congruent with the recovery of mitochondrial transmembrane potential and the absence of cytochrome c release from the mitochondria. Taken together, these results are consistent with a model that mitochondrial structure and function are restored in VacA-intoxicated cells.