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Updated: Jun 24, 2025

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates
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lncRNA CDKN2B-AS1 regulates collagen expression.

Weiwei Shi1, Jiahui Song1, January Mikolaj Weiner1

  • 1Dept. of Periodontology, Oral Medicine and Oral Surgery, Institute for Dental and Craniofacial Sciences, Charité - University Medicine Berlin, Berlin, Germany.

Human Genetics
|June 4, 2024
PubMed
Summary
This summary is machine-generated.

Long noncoding RNA CDKN2B-AS1 plays a role in periodontitis by repressing collagen gene expression in gingival fibroblasts. Dysregulated expression impacts tissue barrier and atherosclerotic plaque stability, linking it to coronary artery disease and myocardial infarction.

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Area of Science:

  • Genetics and Molecular Biology
  • Oral Biology
  • Cardiovascular Research

Background:

  • The long noncoding RNA (lncRNA) CDKN2B-AS1 is associated with coronary artery disease (CAD), myocardial infarction (MI), and periodontitis.
  • The precise molecular function of CDKN2B-AS1 in these conditions remains unclear, necessitating further investigation into its role in oral inflammatory diseases.

Purpose of the Study:

  • To investigate the role of CDKN2B-AS1 in gingival fibroblasts and elucidate its molecular mechanisms in the context of progressive periodontitis.
  • To understand how genetic variants within CDKN2B-AS1 influence its function and contribute to disease risk.

Main Methods:

  • Downregulation of CDKN2B-AS1 in primary gingival fibroblasts using LNA GapmeRs.
  • RNA-sequencing, differential gene expression analysis, and gene set enrichment analysis (GSEA).
  • Functional characterization of risk variants using luciferase-reporter assays, electrophoretic mobility shift assays (EMSA), and analysis of transcription factor binding sites.

Main Results:

  • Collagen biosynthesis was significantly upregulated upon CDKN2B-AS1 downregulation, with COL4A1 showing the most pronounced increase.
  • The inflammatory "TNFA signaling via NFKB" gene set was significantly downregulated.
  • The top upregulated protein-coding gene was CAPNS2, involved in extracellular matrix organization.
  • A CAD/MI risk variant (rs10757278) altered a STAT1 transcription factor binding site, affecting STAT1 binding and gene expression in a manner consistent with GTEx data.

Conclusions:

  • CDKN2B-AS1 acts as a repressor of collagen gene expression in gingival fibroblasts.
  • Allele-specific expression of CDKN2B-AS1, influenced by inflammatory factors, may dysregulate collagen biosynthesis.
  • This dysregulation can impact tissue barrier integrity and atherosclerotic plaque stability, providing a molecular link between genetic predisposition and disease phenotypes.