Partner: Małgorzata Partyka

Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)

Recent publications
1.Malińska D., Szymański J., Patalas-Krawczyk P., Michalska B., Wojtala A., Prill M., Partyka M., Drabik K., Walczak J., Sewer A., Johne S., Luettich K., Peitsch M.C., Hoeng J., Duszyński J., Szczepanowska J., van der Toorn M., Więckowski M.R., Assessment of mitochondrial function following short- and long-term exposure of human bronchial epithelial cells to total particulate matter from a candidate modified-risk tobacco product and reference cigarettes, Food and Chemical Toxicology, ISSN: 0278-6915, DOI: 10.1016/j.fct.2018.02.013, Vol.115, pp.1-12, 2018
Abstract:

Mitochondrial dysfunction caused by cigarette smoke is involved in the oxidative stress-induced pathology of airway diseases. Reducing the levels of harmful and potentially harmful constituents by heating rather than combusting tobacco may reduce mitochondrial changes that contribute to oxidative stress and cell damage. We evaluated mitochondrial function and oxidative stress in human bronchial epithelial cells (BEAS 2B) following 1- and 12-week exposures to total particulate matter (TPM) from the aerosol of a candidate modified-risk tobacco product, the Tobacco Heating System 2.2 (THS2.2), in comparison with TPM from the 3R4F reference cigarette. After 1-week exposure, 3R4F TPM had a strong inhibitory effect on mitochondrial basal and maximal oxygen consumption rates compared to TPM from THS2.2. Alterations in oxidative phosphorylation were accompanied by increased mitochondrial superoxide levels and increased levels of oxidatively damaged proteins in cells exposed to 7.5 μg/mL of 3R4F TPM or 150 μg/mL of THS2.2 TPM, while cytosolic levels of reactive oxygen species were not affected. In contrast, the 12-week exposure indicated adaptation of BEAS-2B cells to long-term stress. Together, the findings indicate that 3R4F TPM had a stronger effect on oxidative phosphorylation, gene expression and proteins involved in oxidative stress than TPM from the candidate modified-risk tobacco product THS2.2.

Keywords:

Mitochondria, Mitochondrial respiratory chain, Oxidative stress, BEAS-2B cells, Cigarette, Tobacco heating system

Affiliations:
Malińska D.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Szymański J.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Johne S.-Philip Morris Products S.A. (CH)
Luettich K.-Philip Morris Products S.A. (CH)
Peitsch M.C.-Philip Morris Products S.A. (CH)
Hoeng J.-Philip Morris Products S.A. (CH)
Duszyński J.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Szczepanowska J.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
van der Toorn M.-Philip Morris Products S.A. (CH)
Więckowski M.R.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Patalas-Krawczyk P.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Michalska B.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Wojtala A.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Prill M.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Partyka M.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Drabik K.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Walczak J.-other affiliation
Sewer A.-Philip Morris Products S.A. (CH)
2.Walczak J., Partyka M., Duszyński J., Szczepanowska J., Implications of mitochondrial network organization in mitochondrial stress signalling in NARP cybrid and Rho0 cells, Scientific Reports, ISSN: 2045-2322, DOI: 10.1038/s41598-017-14964-y, Vol.7, No.14864, pp.1-14, 2017
Abstract:

Mitochondrial dysfunctions lead to the generation of signalling mediators that influence the fate of that organelle. Mitochondrial dynamics and their positioning within the cell are important elements of mitochondria-nucleus communication. The aim of this project was to examine whether mitochondrial shape, distribution and fusion/fission proteins are involved in the mitochondrial stress response in a cellular model subjected to specifically designed chronic mitochondrial stress: WT human osteosarcoma cells as controls, NARP cybrid cells as mild chronic stress and Rho0 as severe chronic stress. We characterized mitochondrial distribution in these cells using confocal microscopy and evaluated the level of proteins directly involved in the mitochondrial dynamics and their regulation. We found that the organization of mitochondria within the cell is correlated with changes in the levels of proteins involved in mitochondrial dynamics and proteins responsible for regulation of this process. Induction of the autophagy/mitophagy process, which is crucial for cellular homeostasis under stress conditions was also shown. It seems that mitochondrial shape and organization within the cell are implicated in retrograde signalling in chronic mitochondrial stress.

Affiliations:
Walczak J.-other affiliation
Partyka M.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Duszyński J.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Szczepanowska J.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)