Metalloproteinase 14 (MMP-14) and hsa-miR-410-3p expression in human inflamed dental pulp and odontoblasts

Aniela Brodzikowska,Agnieszka Cudnoch-Jędrzejewska,Agata Gondek,Wiktor Paskal,Paweł Włodarski,Kacper Pełka,Beata Rak

doi:10.1007/s00418-019-01811-6

Aniela Brodzikowska, Agnieszka Cudnoch-Jędrzejewska + Show 5 more

Open Access

https://doi.org/10.1007/s00418-019-01811-6

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Abstract

The objective of this study is to evaluate MMP-14 expression in odontoblasts and in the bulk of dental pulp of teeth with pulpitis; to determine the expression of microRNA-410 (miR-410) in pulp tissue, since sequence analysis suggests that miR-410 has potential binding site on MMP-14’s 3′UTR, and hence, can regulate expression of the latter one. Tissue samples of dental pulp from teeth with pulpitis and healthy (control) were formalin fixed and paraffin embedded (FFPE). Samples were examined using immunohistochemical staining for MMP-14 and the expression of miR-410 was evaluated using qRT-PCR. In both, healthy and inflamed pulp odontoblasts stained more intensively than remaining pulp tissue, but this difference was not statistically significant. More positive staining was observed in inflamed pulps compared to healthy pulps. Expression of miR-410 was found significantly lower in inflamed pulps than in healthy ones. In the two examined zones, odontoblasts and remaining pulp, miR-410 was expressed on a similar level. No statistically significant correlation of miR-410 and MMP-14 expression was found. We showed that inflammation changes the MMP-14 expression in pulp tissue and odontoblasts. This study demonstrates for the first time miR-410 expression in human dental pulp and that expression of this microRNA was downregulated in inflamed dental pulp and odontoblasts.

Highlights

Pulpal inflammation is caused by microbes, and physical or chemical irritants
The assessment of expression of Matrix metalloproteinases (MMPs)-14 was performed on 12 tissue samples by immunohistochemical staining
The inflammation of the pulp usually results when bacterial toxins pass through dentin and reach the pulp (BirkedalHansen 1995)

Summary

Introduction

The pulp injury causes cellular damage and release of nonspecific proinflammatory mediators, e.g., histamine, bradykinin, neurokinins, and prostaglandins (Cooper et al 2010). These factors cause vasodilatation, increased blood flow, exudate formation, and edema. Carious enamel and dentin contain numerous bacteria capable of eliciting inflammatory reactions in pulp. These reactions are not often caused by direct exposure to bacteria, but instead to their toxins that penetrate via dentinal tubules into the pulp. Stimulation by black-pigmented Bacteroides elevates MMP-2 production (Chang et al 2002)

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