MicroRNA-155 expression is associated with pulpitis progression by targeting SHIP1

Abstract

Pulpitis is a commonly seen oral in ammation condition in clinical practice, it can cause much pain for the patient and may induce infections in other systems. Much is still unknown for the pathogenic mechanism of pulpitis. In this work, we discovered that the expression of miR-155 was associated with dental pulpal in ammation both in vivo and in vitro. Experiments on odontoblast cell line MDPC-23 showed miR-155 could act as a positive regulator by increasing the production of pro-in ammatory cytokines IL-1β and IL-6 during in ammatory responses, whereas knockdown of miR-155 can reverse the effects. Bioinformatics analysis demonstrated that SHIP1 is a direct target of miR-155 in odontoblasts, this result was further veri ed at both mRNA and protein level. Inhibition of miR-155 resulted in the downregulation of in ammation factors, while co-transfection of si-SHIP1 and miR-155 inhibitor promoted the in ammatory responses. Treatment with miR-155 mimic or si-SHIP1 up-regulated the protein level of p-PI3K and p-AKT. By contrast, miR-155 inhibitor exerted the opposite effects. miR-155 mimics could upregulate the gene expression of IL-1β and IL-6. Co-transfection of LY294002 and miR-155 mimic attenuated the in ammatory responses. Consistent with in vitro results, miR-155 −/− mice could alleviate in ammatory response, as well as decrease the activation of p-PI3K and p-AKT, whereas increase the activation of SHIP1. In conclusion, these data revealed a novel role for miR-155 in regulation of dental pulpal in ammatory response by targeting SHIP1 through PI3K/AKT signaling pathway.

Activation of GABAergic neurons in anterior cingulate cortex and their impacts on pulpitis-induced pain

“…Due to the absence of effective and harmless analgesia, pulpitis, characterized by a high morbidity rate and severe symptoms, imposes a signi cant physical and mental burden on affected patients 30 . Current clinical treatments for pulpitis pain are root canal therapies, although fairly effective, resulting in irreversible pulp damage and compromised long-term prognosis, underscoring the imperative need to comprehend the mechanism of pulpitis pain 1 .…”

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

“…Previous studies have shown that miR‐155 appears to regulate MSC immunoregulatory properties as pro‐inflammatory agent (Onodera et al, 2017; Xu et al, 2013) and miR‐155 showed a significant promoting effect on pulpitis (Ayadilord et al, 2021; Kim et al, 2018). But according to Li et al, the expression of miR‐155 in LPS‐MDPC23 was downregulated (Li et al, 2022). In addition, the expression of miR‐155 was downregulated in LPS‐gingival fibroblasts compared to normal gingival fibroblasts, and there appeared to be little change in dental pulp and periodontal ligament fibroblasts (Sipert et al, 2014).…”

The role of Semaphorin 3A in oral diseases

“…SEMA3A can interact with microRNA‐155 (miR‐155), which has been found to be significantly upregulated in AP (Yue et al, 2016). miR‐155 exerts a pro‐inflammatory function in various tissues (Bala et al, 2016; Jiang et al, 2019; Li et al, 2022). Excessive expression of miR‐155 may affect inflammatory progression in AP by directly restraining SEMA3A (Yue et al, 2016).…”