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Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

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Nicotine suppresses bone sialoprotein gene expression.

Y Nakayama¹, M Mezawa, S Araki

¹Department of Periodontology, Tianjin Medical University, Tianjin, China.

Journal of Periodontal Research

|December 5, 2008

Summary

Nicotine, a tobacco component, suppresses bone sialoprotein (BSP) gene transcription by interfering with key regulatory elements in osteoblast-like cells, impacting bone metabolism.

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Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration

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Published on: February 10, 2012

Area of Science:

Molecular Biology
Bone Metabolism
Cell Biology

Background:

Tobacco smoking is a known risk factor for periodontitis and osteoporosis.
Nicotine, a primary tobacco constituent, inhibits osteoblast proliferation and differentiation.
Bone sialoprotein (BSP) is crucial for initial bone mineralization, expressed by differentiated osteoblasts.

Purpose of the Study:

To investigate the effects of nicotine on bone metabolism.
To elucidate the molecular mechanisms by which nicotine influences BSP gene expression.

Main Methods:

Utilized rat osteoblast-like cell lines (UMR106, ROS 17/2.8) and rat bone marrow stromal cells (RBMC-D8).
Employed Northern hybridization to assess BSP mRNA levels.
Conducted transient transfection assays with BSP gene promoter-luciferase constructs.
Performed gel mobility shift assays to analyze nuclear protein binding to regulatory elements.

Main Results:

Nicotine significantly decreased BSP mRNA levels in UMR106 and ROS 17/2.8 cells.
Nicotine reduced luciferase activity in constructs containing the BSP promoter region (-116 to +60) in UMR106 and RBMC-D8 cells.
Nicotine inhibited nuclear protein binding to cAMP response element (CRE), fibroblast growth factor 2 response element (FRE), and homeodomain protein-binding site (HOX).

Conclusions:

Nicotine suppresses BSP transcription in rat osteoblast-like cells.
This suppression is mediated through interference with CRE, FRE, and HOX elements in the proximal BSP gene promoter.
Findings suggest a molecular mechanism linking nicotine exposure to altered bone metabolism.