Abstract

BackgroundLncRNA PTCSC3 is a known tumor suppressor, while its roles in other human diseases are unclear.MethodsAll participants were admitted by The second Affiliated Hospital, School of Medicine, Zhejiang University from January 2016 to January 2018. RT-qPCR, Vectors, cell transfection, In vitro cell proliferation assay and western blot were using to carry out the experiment.ResultsIn this study we found that PTCSC3 was downregulated, while toll-like receptor 4 (TLR4) was upregulated in periodontal ligament stem cells (PDLSCs) isolated from periodontitis affected teeth that in PDLSCs isolated from healthy teeth. Expression levels of PTCSC3 and TLR4 were only significantly and inversely correlated in PDLSCs isolated from periodontitis affected teeth but not in PDLSCs isolated from healthy teeth. PTCSC3 overexpression led to the downregulation of TLR4 in PDLSCs isolated from periodontitis affected teeth, while TLR4 overexpression failed to significantly affect PTCSC3. PTCSC3 overexpression also led to the inhibited proliferation of periodontitis-affected PDLSCs.ConclusionsTherefore, lncRNA PTCSC3 may regulate the proliferation of PDLSCs and TLR4 expression to improve periodontitis.

Highlights

  • LncRNA PTCSC3 is a known tumor suppressor, while its roles in other human diseases are unclear

  • PTCSC3 and toll-like receptor 4 (TLR4) were dysregulated in periodontitisaffected periodontal ligament stem cells (PDLSCs) Expression of PTCSC3 and TLR4 mRNA in 34 cases of periodontitis-affected PDLSCs and 34 cases of healthy PDLSCs was detected by RT-qPCR

  • PTCSC3 mediated the downregulation of TLR4 in 2 cases of periodontitis-affected PDLSCs Due the fact that PTCSC3 was downregulated in periodontitis, to recover this downregulation, this study performed PTCSC3 overexpression

Read more

Summary

Introduction

LncRNA PTCSC3 is a known tumor suppressor, while its roles in other human diseases are unclear. During the development of periodontitis, cytokine production in gingival epithelium is accelerated by bacterial infections, leading to local or even systemic inflammatory responses and loss of tooth [3, 4]. Studies in past several years showed that the development of periodontitis is accompanied by changed in expression patterns of a large set of lncRNAs [11]. LncRNA PTCSC3 has been characterized as a tumor suppressor [14], while its roles in other human diseases are unclear. Our RNA-seq data showed that PTCSC3 was likely downregulated in periodontitis, and its expression levels were inversely correlated with toll-like receptor 4 (TLR4), which promotes periodontitis [15]. This study aimed to investigate the role of PTCSC3 in periodontitis and explored its interactions with TLR4 by performing overexpression experiments, which recovered the downregulation of PTCSC3

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call