Epithelial TRPV1 signaling accelerates gingival epithelial cell proliferation

Area of Science:

• Physiology
• Molecular Biology
• Oral Biology

Background:

• Transient Receptor Potential Vanilloid 1 (TRPV1) is a sensor for thermal and chemical stimuli, primarily known as a pain receptor on nociceptive fibers.
• TRPV1 expression has been identified in non-neuronal cells, including epithelial cells, but its presence in gingival epithelial cells (GECs) was previously unknown.

Purpose of the Study:

• To investigate the expression and function of TRPV1 in gingival epithelial cells (GECs).
• To determine if TRPV1 activation influences GEC proliferation and to explore the underlying molecular mechanisms.

Main Methods:

• Detection of TRPV1 mRNA and protein in GECs.
• Treatment of GEC cell line (epi 4) with capsaicin (TRPV1 agonist) and SB-366791 (TRPV1 antagonist).
• Measurement of intracellular Ca(2+) levels, cell proliferation, and apoptosis.
• cDNA microarray analysis to identify gene expression changes.

Main Results:

• TRPV1 mRNA and protein are expressed in GECs.
• Capsaicin stimulation increased intracellular Ca(2+) and promoted GEC proliferation, an effect blocked by a TRPV1 antagonist.
• In vivo studies showed increased GEC proliferation in capsaicin-treated mice.
• Microarray analysis revealed significant up-regulation of proliferation-related genes, including fibroblast growth factor-17 and neuregulin 2.

Conclusions:

• Functional TRPV1 is expressed in gingival epithelial cells.
• TRPV1 activation by capsaicin regulates GEC proliferation, suggesting a role in oral tissue homeostasis and repair.
• TRPV1 signaling in GECs does not affect apoptosis.