Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously reported evidence that patients with periodontitis have serum antibodies to oral Gram positive bacteria that are cross-reactive with epithelial antigens, including CD24. High level expression of CD24 was confined to the reactive periodontal epithelium and inflamed gingival attachment. As a model for the reactive epithelium of chronic periodontitis, H413 epithelial cells derived from a human oral squamous cell carcinoma were cloned and lines expressing high levels of CD24 were selected. RNA interference protocols were designed to determine if CD24 could modulate intercellular interactions and regulate the biology of these epithelial cells. Knock-down of CD24 protein was demonstrated by Western blot and flow cytometry. The level of mRNA for CD24 was reduced 90% by RNAi treatment as assayed by real-time, reverse transcriptase (RT)-PCR. Gene products known to be important in epithelial biology, including E-cadherin and TGF-beta3 that were demonstrated to undergo altered expression patterns in the periodontal lesion, were investigated. Down-regulation of CD24 mRNA was associated with reduced e-cadherin expression and up-regulated expression of snail, twist, and tgf-beta3. The cells were treated with monoclonal antibodies to CD24 to mimic the action of auto-reactive antibodies to CD24 detected in affected patients. Relative to isotype control antibody, stimulation by anti-CD24 antibodies induced up-regulated expression of e-cadherin and down-regulation of tgf-beta3 as assessed by real-time RT-PCR. No consistent changes for expression of beta-catenin, connexins, integrins, icam-1, tgf-beta1 or tgf-beta2 were observed. CD24 could play an important role in modulating expression of genes that regulate epithelial differentiation in periodontal disease.
 ...
PMID:Regulation of E-cadherin and TGF-beta3 expression by CD24 in cultured oral epithelial cells. 1693 May 38

HPDLSCs derived from periodontal ligament tissues contribute to tooth development and tissue regeneration. Exploring the effects of long noncoding RNAs (lncRNAs) in the process of osteogenic differentiation of periodontal ligament stem cells would provide novel therapeutic strategies for tissue regeneration. The expression levels of lncRNA, which significantly changed during osteogenic differentiation, were observed by real-time quantitative PCR (q-PCR). Then, we screened for osteogenic-related lncRNA, which was initially named lncRNA-TWIST1. Moreover, we detected the mRNA expression levels of TWIST1 and osteogenesis-related genes after upregulating and downregulating lncRNA-TWIST1 in PPDLSCs (periodontal mesenchymal stem cells from periodontitis patients) and HPDLSCs (periodontal mesenchymal stem cells from healthy microenvironment), respectively. The osteogenic degree was verified by detecting ALP activity and alizarin red staining. LncRNA-TWIST1 decreased the mRNA levels of TWIST1 and promoted osteogenic differentiation in PPDLSCs, which was confirmed by the increase in osteogenesis-related gene levels (Runx2, ALP, and OCN), the increase in ALP activity, and the formation of more osteogenic nodules. In contrast, downregulating lncRNA-TWIST1 decreased the expression of osteogenesis-related genes, ALP activity, and osteogenic nodules both in PPDLSCs and in HPDLSCs. LncRNA-TWIST1 promoted osteogenic differentiation both in PPDLSCs and in HPDLSCs by inhibiting the TWIST1 expression. LncRNA-TWIST1 may be a novel therapeutic strategy to regenerate dental tissues.
 ...
PMID:LncRNA-TWIST1 Promoted Osteogenic Differentiation Both in PPDLSCs and in HPDLSCs by Inhibiting TWIST1 Expression. 3134 8