# MicroRNA-210 Suppresses NF-κB Signaling in Lipopolysaccharide-Stimulated Dental Pulp Cells Under Hypoxic Conditions

## TL;DR

This study shows that miR-210 reduces inflammation in dental pulp cells under low oxygen conditions by suppressing a key inflammatory pathway.

## Contribution

The novel finding is that miR-210 acts as a negative regulator of inflammation via the TAB1–NF-κB pathway in hypoxic dental pulp cells.

## Key findings

- miR-210 is upregulated in human dental pulp cells under hypoxic conditions.
- miR-210 suppresses LPS-induced cytokine production and NF-κB activity by targeting TAB1.
- miR-210 inhibition increases TAB1 and inflammatory cytokine expression under hypoxia.

## Abstract

Dental pulp tissue, enclosed within rigid dentin, is susceptible to bacterial invasion via dentinal tubules, often leading to severe pulpal inflammation. This condition is typically associated with a hypoxic microenvironment, yet the mechanistic link between hypoxia and inflammation remains unclear. We identified a marked upregulation of microRNA-210 (miR-210) in human dental pulp cells (hDPCs) cultured under hypoxic conditions. This study investigated the role of miR-210 in modulating inflammation in lipopolysaccharide (LPS)-stimulated hDPCs. Hypoxic conditions and enforced expression of hypoxia-inducible factor 1α (HIF1α) significantly increased miR-210 levels. While LPS stimulation elevated proinflammatory cytokines (Interleukin-6, Monocyte Chemoattractant Protein-1, and Tumor Necrosis Factor Alpha) and activated nuclear factor-kappa B (NF-κB) signaling, miR-210 overexpression suppressed LPS-mediated cytokine production and NF-κB activity. Luciferase assays revealed that miR-210 targets and negatively regulates TGF-beta activated kinase 1 binding protein 1 (TAB1), a key upstream regulator of NF-κB. Transfection with an miR-210 mimic reduced TAB1 expression, NF-κB activation, and cytokine output in both LPS-stimulated hDPCs and rat pulp tissue ex vivo. Conversely, miR-210 inhibition enhanced TAB1 levels and inflammatory cytokine expression under hypoxic conditions. These findings suggest that miR-210 mitigates inflammation via the TAB1–NF-κB pathway, functioning as a negative feedback regulator. miR-210 may represent a promising therapeutic target for pulpal inflammation.