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RAGE mRNA expression and its correlation with nuclear factor kappa beta mRNA expression in inflamed human

Michael Crabtree1, Roberta Pileggi, Indraneel Bhattacharyya

  • 1Department of Endodontics, College of Dentistry, University of Florida, Gainesville, Florida 32610-3003, USA.

Journal of Endodontics
|May 24, 2008
PubMed

Insights

Advanced glycation end products (AGEs) and their receptor (RAGE) correlate with nuclear factor kappa beta (NF-κB) in periapical inflammation. African Americans showed higher RAGE expression, suggesting potential inflammatory markers.

Area of Science:

  • Oral Biology
  • Immunology
  • Pathology

Background:

  • Advanced glycation end products (AGEs) are implicated in inflammation and vascular issues.
  • The receptor for AGE (RAGE) is upregulated during inflammation and expressed on various cells.
  • RAGE and nuclear factor kappa beta (NF-κB) expression correlations are unestablished in inflammatory periapical lesions.

Purpose of the Study:

  • To investigate RAGE and NF-κB expression in inflammatory periapical lesions.
  • To determine the correlation between RAGE and NF-κB expression.
  • To explore patient variables as predictors for RAGE and NF-κB expression.

Main Methods:

  • Periapical tissue samples were obtained from 38 patients.
  • Reverse transcriptase polymerase chain reaction (RT-PCR) was used to assess RAGE and NF-κB expression.
  • Patient demographics were analyzed for correlations with protein expression.

Main Results:

  • A significant positive correlation was found between RAGE and NF-κB expression (P = .001).
  • African Americans exhibited significantly higher RAGE expression compared to white patients (ANOVA, P = .002).
  • A positive linear correlation was observed between RAGE and NF-κB in inflamed periradicular tissues.

Conclusions:

  • RAGE and NF-κB are positively correlated in inflamed periradicular tissues.
  • RAGE expression differs significantly between racial groups.
  • RAGE and NF-κB may serve as potential biomarkers for periapical inflammation.

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