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Quintessence Publishing: Journals: OHPD

 

Oral Health & Preventive Dentistry

Edited by Anton Sculean, Poul Erik Petersen, Avijit Banerjee

ISSN (print) 1602-1622 • ISSN (online) 1757-9996

Publication:

2022
Volume 20 , Issue 1



Pages: 263270
DOI: 10.3290/j.ohpd.b3147193
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Long Non-coding RNA PVT1 is Involved in the Pathological Mechanism of Pulpitis by Regulating miR-128-3p

Lin Xia / Jian Wang / Yue Qi / Yongjie Fei / Dongmei Wang

Purpose: Pulpitis is a common disease in stomatology, which is caused by dental pulp infection. It was found that long non-coding RNA regulates inflammation and repair responses through competitively sponging microRNAs. This study explored the expression and clinical significance of PVT1 in pulpitis patients, and further investigated the possible regulatory mechanism of PVT1 on pulpitis through in-vitro experiments. Materials and Methods: The expression of PVT1 and miR-128-3p was detected through RT-qPCR. An ROC curve was drawn to estimate the diagnostic significance of PVT1 and miR-128-3p for pulpitis. An in-vitro pulpitis cell model was constructed to evaluate the effects of PVT1 or miR-128-3p on cell proliferation, apoptosis, and inflammatory response. The Luciferase reporter gene explored the interaction between PVT1 and miR-128-3p. Results: The expression of PVT1 increased, while the miR-128-3p level decreased, in the saliva of pulpitis patients. ROC curves showed that both PVT1 and miR-128-3p had the potential to diagnose pulpitis. This in-vitro study revealed that the expression of PVT1 was increased in the pulpitis cell model. A low level of PVT1 suppressed the hDPCs injury induced by LPS. The Luciferase reporter gene verified the targeting relationship between PVT1 and miR-128-3p, and the latter was negatively regulated by PVT1. Further in-vitro studies showed that inhibition of miR-128-3p could reverse the effect of si-PVT1 on cell viability, cell apoptosis and inflammatory response. Conclusion: This study revealed that knockdown of PVT1 may suppress the damage in pulpitis cell models induced by LPS via targeting miR-128-3p.

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