Partner: Jędrzej Szymański

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

Recent publications
1.Walczak J., Dębska-Vielhaber G., Vielhaber S., Szymański J., Charzyńska A., Duszyński J., Szczepanowska J., Distinction of sporadic and familial forms of ALS based on mitochondrial characteristics, The FASEB Journal, ISSN: 0892-6638, DOI: 10.1096/fj.201801843R, Vol.33, No.3, pp.4388-4403, 2019
Abstract:

Bioenergetic failure, oxidative stress, and changes in mitochondrial morphology are common pathologic hallmarks of amyotrophic lateral sclerosis (ALS) in several cellular and animal models. Disturbed mitochondrial physiology has serious consequences for proper functioning of the cell, leading to the chronic mitochondrial stress. Mitochondria, being in the center of cellular metabolism, play a pivotal role in adaptation to stress conditions. We found that mitochondrial dysfunction and adaptation processes differ in primary fibroblasts derived from patients diagnosed with either sporadic or familial forms of ALS. The evaluation of mitochondrial parameters such as the mitochondrial membrane potential, the oxygen consumption rate, the activity and levels of respiratory chain complexes, and the levels of ATP, reactive oxygen species, and Ca2+ show that the bioenergetic properties of mitochondria are different in sporadic ALS, familial ALS, and control groups. Comparative statistical analysis of the data set (with use of principal component analysis and support vector machine) identifies and distinguishes 3 separate groups despite the small number of investigated cell lines and high variability in measured parameters. These findings could be a first step in development of a new tool for predicting sporadic and familial forms of ALS and could contribute to knowledge of its pathophysiology.—Walczak, J., Dębska-Vielhaber, G., Vielhaber, S., Szymański, J., Charzyńska, A., Duszyński, J., Szczepanowska, J. Distinction of sporadic and familial forms of ALS based on mitochondrial characteristics.

Keywords:

amyotrophic lateral sclerosis, neurodegeneration, primary fibroblasts, PCA

Affiliations:
Walczak J.-other affiliation
Dębska-Vielhaber G.-Otto-von-Guericke University, Magdeburg (DE)
Vielhaber S.-Otto-von-Guericke University, Magdeburg (DE)
Szymański J.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Charzyńska A.-University of Warsaw (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)
2.Malińska D., Więckowski M.R., Michalska B., Drabik K., Prill M., Patalas-Krawczyk P., Walczak J., Szymański J., Mathis C., Van der Toorn M., Luettich K., Hoeng J., Peitsch M.C., Duszyński J., Szczepanowska J., Mitochondria as a possible target for nicotine action, Journal of Bioenergetics and Biomembranes, ISSN: 0145-479X, DOI: 10.1007/s10863-019-09800-z, Vol.51, No.4, pp.259-276, 2019
Abstract:

Mitochondria are multifunctional and dynamic organelles deeply integrated into cellular physiology and metabolism. Disturbances in mitochondrial function are involved in several disorders such as neurodegeneration, cardiovascular diseases, metabolic diseases, and also in the aging process. Nicotine is a natural alkaloid present in the tobacco plant which has been well studied as a constituent of cigarette smoke. It has also been reported to influence mitochondrial function both in vitro and in vivo. This review presents a comprehensive overview of the present knowledge of nicotine action on mitochondrial function. Observed effects of nicotine exposure on the mitochondrial respiratory chain, oxidative stress, calcium homeostasis, mitochondrial dynamics, biogenesis, and mitophagy are discussed, considering the context of the experimental design. The potential action of nicotine on cellular adaptation and cell survival is also examined through its interaction with mitochondria. Although a large number of studies have demonstrated the impact of nicotine on various mitochondrial activities, elucidating its mechanism of action requires further investigation.

Keywords:

adaptation, mitochondria, nicotine, oxidative stress

Affiliations:
Malińska D.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Więckowski M.R.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Luettich K.-Philip Morris Products S.A. (CH)
Hoeng J.-Philip Morris Products S.A. (CH)
Peitsch M.C.-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)
Michalska B.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Drabik K.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Prill M.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Patalas-Krawczyk P.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Walczak J.-other affiliation
Szymański J.-Nencki Institute of Experimental Biology, Polish Academy of Sciences (PL)
Mathis C.-Philip Morris Products S.A. (CH)
Van der Toorn M.-Philip Morris Products S.A. (CH)
3.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)