Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells

Leyla Tahrani Hardin; David Vang; Der Thor; Xiaoyuan Han; Fatima Mashkoor; Tamer Alpagot; David M Ojcius; Nan Xiao

doi:10.18332/tid/168125

Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells

Tob Induc Dis. 2023 Aug 1:21:101. doi: 10.18332/tid/168125. eCollection 2023.

Authors

Leyla Tahrani Hardin¹, David Vang¹, Der Thor¹, Xiaoyuan Han¹, Fatima Mashkoor², Tamer Alpagot³, David M Ojcius¹, Nan Xiao¹

Affiliations

¹ Department of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
² Department of Oral and Maxillofacial Surgery, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
³ Department of Periodontics, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.

Abstract

Introduction: Smoking is known to alter the regenerative and immunomodulatory properties of many types of mesenchymal stem cells (MSCs). This study investigates the impact of cigarette smoke exposure on the regenerative potential of dental pulp stem cells (DPSCs).

Methods: DPSCs were treated with various doses of cigarette smoke condensate (CSC) or nicotine. Cell proliferation and survival were evaluated by a water-soluble tetrazolium salt (WST-1) and a survival assay. DPSC migration, cytokine expression, mutagenesis, and the signaling pathway were also measured during CSC and nicotine treatment.

Results: Low concentrations of CSC and nicotine did not impair cell proliferation, but higher concentrations reduced cell proliferation. CSC and nicotine could impede DPSC survival and migration in a dose-dependent manner. In addition, the cytokine secretion expression profile was altered with CSC or nicotine treatments. In particular, secretion of IL-6, TNF-α, and IL-10 significantly increased, while TGF-β1 levels showed different patterns after exposure to CSC or nicotine, as shown by ELISA and quantitative PCR. Nicotine treatment increased AKT (also known as protein kinase B) and extracellular signal-regulated kinase (ERK) phosphorylation. Finally, CSC induced higher levels of mutagenicity than nicotine, as shown by the Ames test.

Conclusions: These findings suggest that cigarette smoke exposure alters the regenerative abilities of DPSCs in various ways. Future studies are warranted to further characterize the underlying molecular mechanisms of smoking-mediated damage to DPSCs, which will guide the personalized stem cell treatment plan for smoking patients.

Keywords: DPSCs; inflammation; nicotine; regeneration; smoking.