Crystalline structure of pulverized dental calculus induces cell death in oral epithelial cells

Autor: Kanako Higuchi, Atsutoshi Yoshimura, Yoshitaka Hara, Takashi Kaneko, S.M. Ziauddin, Eicke Latz, J. L. Montenegro Raudales, Yukio Ozaki, Takashi Ukai, Toshihiro Miyazaki
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
Cell Membrane Permeability
Inflammasomes
Cell
metabolism [Tumor Necrosis Factor-alpha]
Interleukin-1beta
Apoptosis
Amino Acid Chloromethyl Ketones
chemistry.chemical_compound
Mice
drug effects [Cell Membrane Permeability]
Dental Calculus
drug effects [Macrophages]
pharmacology [Amino Acid Chloromethyl Ketones]
Cell Death
Caspase 1
Pyroptosis
Inflammasome
metabolism [L-Lactate Dehydrogenase]
medicine.anatomical_structure
Carcinoma
Squamous Cell

Periodontics
medicine.drug
pharmacology [NLR Family
Pyrin Domain-Containing 3 Protein]

Programmed cell death
benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone
Cytochalasin D
chemistry [Dental Calculus]
drug effects [Apoptosis]
drug effects [Epithelial Cells]
03 medical and health sciences
metabolism [Interleukin-1beta]
Cell Line
Tumor

NLR Family
Pyrin Domain-Containing 3 Protein

medicine
Animals
Humans
Propidium iodide
ddc:610
pharmacology [Inflammasomes]
L-Lactate Dehydrogenase
Tumor Necrosis Factor-alpha
Macrophages
Calculus (dental)
metabolism [Caspase 1]
Tooth surface
Epithelial Cells
drug effects [Cell Death]
medicine.disease
Molecular biology
Squamous carcinoma
Mice
Inbred C57BL

stomatognathic diseases
030104 developmental biology
chemistry
pharmacology [Cytochalasin D]
Zdroj: Journal of periodontal research 53(3), 353-361 (2017). doi:10.1111/jre.12520
DOI: 10.1111/jre.12520
Popis: Background and objective Dental calculus is a mineralized deposit attached to the tooth surface. We have shown that cellular uptake of dental calculus triggers nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation, leading to the processing of the interleukin-1β precursor into its mature form in mouse and human phagocytes. The activation of the NLRP3 inflammasome also induced a lytic form of programmed cell death, pyroptosis, in these cells. However, the effects of dental calculus on other cell types in periodontal tissue have not been investigated. The aim of this study was to determine whether dental calculus can induce cell death in oral epithelial cells. Material and methods HSC-2 human oral squamous carcinoma cells, HOMK107 human primary oral epithelial cells and immortalized mouse macrophages were exposed to dental calculus or 1 of its components, hydroxyapatite crystals. For inhibition assays, the cells were exposed to dental calculus in the presence or absence of cytochalasin D (endocytosis inhibitor), z-YVAD-fmk (caspase-1 inhibitor) or glyburide (NLRP3 inflammasome inhibitor). Cytotoxicity was determined by measuring lactate dehydrogenase (LDH) release and staining with propidium iodide. Tumor necrosis factor-α production was quantified by enzyme-linked immunosorbent assay. Oral epithelial barrier function was examined by permeability assay. Results Dental calculus induced cell death in HSC-2 cells, as judged by LDH release and propidium iodide staining. Dental calculus also induced LDH release from HOMK107 cells. Following heat treatment, dental calculus lost its capacity to induce tumor necrosis factor-α in mouse macrophages, but could induce LDH release in HSC-2 cells, indicating a major role of inorganic components in cell death. Hydroxyapatite crystals also induced cell death in both HSC-2 and HOMK107 cells, as judged by LDH release, indicating the capacity of crystal particles to induce cell death. Cell death induced by dental calculus was significantly inhibited by cytochalasin D, z-YVAD-fmk and glyburide, indicating NLRP3 inflammasome involvement. In permeability assays, dental calculus attenuated the barrier function of HSC-2 cell monolayers. Conclusion Dental calculus induces pyroptotic cell death in human oral epithelial cells and the crystalline structure plays a major role in this process. Oral epithelial cell death induced by dental calculus might be important for the etiology of periodontitis.
Databáze: OpenAIRE