Role of ascorbic acid in the regulation of epigenetic processes induced by Porphyromonas gingivalis in endothelial-committed oral stem cells.
Histochem Cell Biol
; 156(5): 423-436, 2021 Nov.
Article
en En
| MEDLINE
| ID: mdl-34370052
ABSTRACT
Periodontitis is a common inflammatory disease that affects the teeth-supporting tissue and causes bone and tooth loss. Moreover, in a worldwide population, periodontal disease is often associated with cardiovascular diseases. Emerging studies have reported that one of the major pathogens related to periodontitis is Porphyromonas gingivalis (P. gingivalis), which triggers the inflammatory intracellular cascade. Here, we hypothesized a possible protective effect of ascorbic acid (AA) in the restoration of the physiological molecular pathway after exposure to lipopolysaccharide derived from P. gingivalis (LPS-G). In particular, human gingiva-derived mesenchymal stem cells (hGMSCs) and endothelial-differentiated hGMSCs (e-hGMSCs) exposed to LPS-G showed upregulation of p300 and downregulation of DNA methyltransferase 1 (DNMT1), proteins associated with DNA methylation and histone acetylation. The co-treatment of AA and LPS-G showed a physiological expression of p300 and DNMT1 in hGMSCs and e-hGMSCs. Moreover, the inflammatory process triggered by LPS-G was demonstrated by evaluation of reactive oxygen species (ROS) and their intracellular localization. AA exposure re-established the physiological ROS levels. Despite the limitations of in vitro study, these findings collectively expand our knowledge regarding the molecular pathways involved in periodontal disease, and suggest the involvement of epigenetic modifications in the development of periodontitis.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Ácido Ascórbico
/
Porphyromonas gingivalis
/
Sustancias Protectoras
/
Células Endoteliales
/
Células Madre Mesenquimatosas
Límite:
Humans
Idioma:
En
Revista:
Histochem Cell Biol
Asunto de la revista:
CITOLOGIA
/
HISTOCITOQUIMICA
Año:
2021
Tipo del documento:
Article
País de afiliación:
Italia