International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(11), С. 5642 - 5642
Опубликована: Май 22, 2024
It is remarkable how teeth maintain their healthy condition under exceptionally high levels of mechanical loading. This suggests the presence inherent adaptation mechanisms within structure to counter constant stress. Dentin, situated between enamel and pulp, plays a crucial role in mechanically supporting tooth function. Its intermediate stiffness viscoelastic properties, attributed its mineralized, nanofibrous extracellular matrix, provide flexibility, strength, rigidity, enabling it withstand loading without fracturing. Moreover, dentin’s unique architectural features, such as odontoblast processes dentinal tubules spatial compartmentalization odontoblasts dentin sensory neurons contribute distinctive perception external stimuli while acting defensive barrier for dentin-pulp complex. Since architecture governs functions nociception repair response stimuli, understanding mechanobiology developing treatments pain management dentin-associated diseases regeneration. review discusses physical features regulate mechano-sensing, focusing on mechano-sensitive ion channels. Additionally, we explore advanced vitro platforms that mimic providing deeper insights into fundamental mechanobiological phenomena laying groundwork effective mechano-therapeutic strategies diseases.
Язык: Английский
Процитировано
4Journal of Dental Research, Год журнала: 2025, Номер unknown
Опубликована: Фев. 4, 2025
Odontoblasts are terminally differentiated cells that exhibit mechanosensitivity and mineralization capacity. Mechanosensitive ion channels such as Piezo1 present in odontoblasts associated with their physiological functions via Ca 2+ signaling. Both signals influx from mechanosensitive release stores function secondary messenger systems for various biological phenomena. The endoplasmic reticulum (ER) serves an intracellular store mobilizes . Changes concentration inside the ER among factors cause stress. Perivascular located around dental pulp. Although formation indicates perivascular interact odontoblasts, detailed profiles under developmental pathological conditions remain unclear. In this study, we revealed pericyte marker, neural/glial antigen 2 (NG2)–positive cells, cell-rich zones (CZs) can differentiate into Piezo1-positive following genetic odontoblast depletion mice, modeled death after severe dentin injury reparative formation. NG2-positive pericytes faster than glial cells. To determine how focused on ER-stress sensor protein, activating transcription factor 6a (ATF6a). After depletion, regenerated layer were capable of acting functional odontoblasts. presence extracellular , application a sarco/ER -ATPase (SERCA) inhibitor, thapsigargin, known inducer, increased lineage (OLCs). increase was significantly inhibited by pharmacologic indicating stress SERCA inhibition augmented Piezo1-induced responses progenitor However, activation G q -coupled receptors adenosine diphosphate did not induce activation. Gene silencing ATF6a and/or NG2 impaired OLCs. Overall, orchestrates differentiation act sensory receptor dentin-forming
Язык: Английский
Процитировано
0Biomolecules, Год журнала: 2025, Номер 15(3), С. 316 - 316
Опубликована: Фев. 20, 2025
This study explored the role of Piezo1 in odontogenic differentiation dental papilla cells (DPCs) and tissue, focusing on a mechanism involving family with sequence similarity 83, member G (FAM83G). Here, we found Piezo1, mechanosensitive cation channel, was upregulated during odontogenesis DPCs tissues. Knockdown impaired differentiation, while its activation by Yoda1 enhanced process. Using 3D culture model an ectopic transplantation model, confirmed Piezo1’s vivo. RNA sequencing (RNA-seq) analysis revealed that FAM83G Piezo1-knockdown cells, silencing DPCs. These findings indicate positively regulates inhibiting both vitro vivo, representing potential target for tissue regeneration.
Язык: Английский
Процитировано
0Chemical Engineering Journal, Год журнала: 2024, Номер 501, С. 157483 - 157483
Опубликована: Ноя. 7, 2024
Язык: Английский
Процитировано
1Revista de la Asociación Dental Mexicana, Год журнала: 2024, Номер 81(6), С. 341 - 348
Опубликована: Янв. 1, 2024
Процитировано
0Опубликована: Янв. 1, 2024
Язык: Английский
Процитировано
0