Whole Cigarette Smoke Condensates Induce Accumulation of Amyloid Beta Precursor Protein with Oxidative Stress in Murine Astrocytes

• Published in: Toxics (Basel) Vol. 9; no. 7; p. 150
• Main Authors: Park, Eun-Jung, Jin, Seung-Woo, Lim, Hyun-Ji, Kim, Hyeon-Young, Kang, Min-Sung, Yang, Siyoung
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 28-06-2021; MDPI
• Subjects: Alzheimer's disease; Amyloid precursor protein; Astrocytes; autophagy; Brain; Cell cycle; Cell proliferation; Cigarette smoke; Cigarette smoking; Cigarettes; Condensates; Damage accumulation; Dementia; Gene expression; immune response; Membranes; Mitochondria; Neurodegenerative diseases; Organelles; Oxidative stress; Precursors; Proteins; Reagents; Risk analysis; Risk factors; Signal transduction; Smoke; Smoking; Structural damage; Target recognition; Toxic diseases; United States > US; cigarette smoking; autophagy; astrocytes; Alzheimer’s disease; immune response
• ISSN: 2305-6304; 2305-6304
• DOI: 10.3390/toxics9070150

Although cigarette smoking has been postulated to be a potential risk factor for Alzheimer's disease (AD), the toxic mechanism is still unclear. Additionally, astrocytes have been identified as a potential target, given they play multiple roles in maintaining normal brain function. In this study, we explored the toxic mechanism of whole cigarette smoke condensates (WCSC) using murine astrocytes. Cell proliferation, the percentage of cells in the G2/M phase, and LDH concentrations in the cell supernatants were all reduced in WCSC-treated cells. In addition, oxidative stress was induced, together with shortening of processes, structural damage of organelles, disturbances in mitochondrial function, blockage of autophagic signals, accumulation of amyloid β precursor protein, and loss of chemotactic functions. Based on these results, we hypothesize that dysfunction of astrocytes may contribute to the occurrence of cigarette-smoking-induced AD.