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Protease-activated receptor type 1 (PAR1) increases CEMP1 gene expression through MAPK/ERK pathway
Emanuel Silva Rovai1, Tomaz Alves2, Letícia Miquelitto Gasparoni2
1Universidade de Taubaté - Unitau, School of Dentistry, Periodontics Research Division, Taubaté, SP, Brazil.
Brazilian Oral Research
|April 20, 2022
Summary
The protease-activated receptor 1 (PAR1) enhances cementogenesis in human periodontal ligament stem cells (hPDLSCs). This process is dependent on the MAPK/ERK pathway, not PI3K, indicating PAR1
Area of Science:
- Cell Biology
- Stem Cell Research
- Periodontal Regeneration
Background:
- The protease-activated receptor 1 (PAR1) plays a role in cellular metabolism, including the differentiation and proliferation of osteogenic and cementogenic cells.
- Previous research has shown the regenerative potential of PAR1 in human periodontal ligament stem cells (hPDLSCs).
Purpose of the Study:
- To investigate the hypothesis that PAR1 regulates the cementogenic differentiation of hPDLSCs.
- To identify the intracellular signaling pathway involved in PAR1 activation during hPDLSC differentiation.
Main Methods:
- Human periodontal ligament stem cells (hPDLSCs) were isolated and cultured in osteogenic medium.
- Cells were treated with a PAR1 agonist and inhibitors of the MAPK/ERK and PI3K pathways.
- Cementogenesis gene expression (CEMP1) was analyzed using RT-qPCR.
Main Results:
- PAR1 activation by its agonist significantly increased CEMP1 gene expression compared to controls.
- Inhibition of the MAPK/ERK pathway abrogated the PAR1 agonist-induced increase in CEMP1 expression.
- Inhibition of the PI3K pathway did not affect CEMP1 gene expression.
Conclusions:
- PAR1 activation promotes cementogenesis in hPDLSCs.
- The MAPK/ERK signaling pathway is essential for PAR1-mediated CEMP1 gene expression.
- PAR1 regulates cementogenic differentiation of hPDLSCs in a PI3K-independent manner.
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