Journal
MARINE DRUGS
Volume 17, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/md17030138
Keywords
gingival recession; oral mucosa fibroblasts; extracellular matrix; mitochondria; oxidative phosphorylation
Categories
Funding
- Ministry of Science and Technology (Republic of China) [MOST106-2313-B-110-002]
- Zuoying Branch of Kaohsiung Armed Forces General Hospital [ZBH 107-20, ZBH 108-19]
- Kaohsiung Veterans General Hospital [VGHNSU107-005, VGHNSU108-004]
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Gingival recession (GR) potentially leads to the exposure of tooth root to the oral cavity microenvironment and increases susceptibility to dental caries, dentin hypersensitivity, and other dental diseases. Even though many etiological factors were reported, the specific mechanism of GR is yet to be elucidated. Given the species richness concerning marine biodiversity, it could be a treasure trove for drug discovery. In this study, we demonstrate the effects of a marine compound, (+)-rhodoptilometrin from crinoid, on gingival cell migration, wound healing, and oxidative phosphorylation (OXPHOS). Experimental results showed that (+)-rhodoptilometrin can significantly increase wound healing, migration, and proliferation of human gingival fibroblast cells, and it does not have effects on oral mucosa fibroblast cells. In addition, (+)-rhodoptilometrin increases the gene and protein expression levels of focal adhesion kinase (FAK), fibronectin, and type I collagen, changes the intracellular distribution of FAK and F-actin, and increases OXPHOS and the expression levels of complexes I similar to V in the mitochondria. Based on our results, we believe that (+)-rhodoptilometrin might increase FAK expression and promote mitochondrial function to affect cell migration and promote gingival regeneration. Therefore, (+)-rhodoptilometrin may be a promising therapeutic agent for GR.
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