Human Cell, Journal Year: 2024, Volume and Issue: 37(6), P. 1649 - 1662
Published: Aug. 27, 2024
Language: Английский
Human Cell, Journal Year: 2024, Volume and Issue: 37(6), P. 1649 - 1662
Published: Aug. 27, 2024
Language: Английский
Translational dental research., Journal Year: 2025, Volume and Issue: 1(1), P. 100008 - 100008
Published: Jan. 1, 2025
Language: Английский
Citations
0Journal of Dental Research, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 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
Language: Английский
Citations
0Biomolecules, Journal Year: 2025, Volume and Issue: 15(3), P. 316 - 316
Published: Feb. 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.
Language: Английский
Citations
0Journal of Evolutionary Biochemistry and Physiology, Journal Year: 2025, Volume and Issue: 61(1), P. 115 - 121
Published: Jan. 1, 2025
Language: Английский
Citations
0Journal of Dentistry, Journal Year: 2025, Volume and Issue: unknown, P. 105745 - 105745
Published: April 1, 2025
Language: Английский
Citations
0Frontiers in Physiology, Journal Year: 2022, Volume and Issue: 13
Published: Nov. 10, 2022
Vascular calcification (VC) is associated with a number of cardiovascular diseases, as well chronic kidney disease. The role smooth muscle cells (SMC) has already been widely explored in VC, the intracellular Ca2+ regulating SMC function. Increased calcium concentration ([Ca2+]i) vascular proposed to stimulate VC. However, contribution non-selective Piezo1 mechanosensitive cation channels elevation [Ca2+]i, and consequently process VC never examined. In this work essential arterial medial demonstrated. presence was proved on human aortic samples using immunohistochemistry. Quantitative PCR Western blot analysis confirmed expression channel cell line (HAoSMC). Functional measurements were done HAoSMC under control calcifying condition. Calcification induced by supplementing growth medium inorganic phosphate (1.5 mmol/L, pH 7.4) (CaCl2, 0.6 mmol/L) for 7 days. Measurement [Ca2+]i fluorescent Fura-2 dye upon stimulation (either hypoosmolarity, or Yoda1) demonstrated significantly higher transients calcified compared HAoSMCs. augmented SMCs leading influx stimulation. Activation Yoda1 (10 μmol/L) enhanced HAoSMCs, while Dooku1, which antagonizes effect Yoda1, reduced amplification. Application Dooku1 alone inhibited calcification. Knockdown siRNA suppressed evoked conditions. Our results demonstrate pivotal
Language: Английский
Citations
17International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(16), P. 12953 - 12953
Published: Aug. 19, 2023
Piezo1, a non-selective cation channel directly activated by mechanical forces, is widely expressed in the digestive system and participates biological functions physiologically pathologically. In this review, we summarized latest insights on Piezo1’s cellular effect across entire system, discussed role of Piezo1 various aspects including ingestion digestion, material metabolism, enteric nervous intestinal barrier, inflammatory response within system. The goal comprehensive review to provide solid foundation for future research about
Language: Английский
Citations
10Frontiers in Bioengineering and Biotechnology, Journal Year: 2024, Volume and Issue: 12
Published: Feb. 8, 2024
Piezo1 (2010) was identified as a mechanically activated cation channel capable of sensing various physical forces, such tension, osmotic pressure, and shear force. mediates mechanosensory transduction in different organs tissues, including its role maintaining bone homeostasis. This review aimed to summarize the function possible mechanism mechanical receptor cells tissue. We found that it is potential therapeutic target for treatment diseases.
Language: Английский
Citations
3Journal of Dental Research, Journal Year: 2024, Volume and Issue: 103(9), P. 889 - 898
Published: June 24, 2024
Located at the interface of dentin-pulp complex, odontoblasts are specialized cells responsible for dentin synthesis and nociceptive signal detection in response to external stimuli. Recent studies have shown that mechanosensitive ion channel PIEZO1 is involved bone formation remodeling through influx calcium ions, it abundantly expressed odontoblasts. However, specific role reactionary dentinogenesis underlying mechanisms remain elusive. In this study, we found intense expression plasma membrane cytoplasm healthy human third molars, mouse mandibular odontoblast-like (hOBLCs). hOBLCs, positively regulated DSPP, DMP1, COL1A1 Ca
Language: Английский
Citations
3British Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 181(23), P. 4714 - 4732
Published: Oct. 14, 2024
Abstract PIEZO1 is a eukaryotic membrane protein that assembles as trimers to form calcium‐permeable, non‐selective cation channels with exquisite capabilities for mechanical force sensing and transduction of into effect in diverse cell types include blood cells, endothelial epithelial fibroblasts stem cells systems bone, lymphatics muscle. The channel has wide‐ranging roles considered target novel therapeutics ailments spanning cancers cardiovascular, dental, gastrointestinal, hepatobiliary, infectious, musculoskeletal, nervous system, ocular, pregnancy, renal, respiratory urological disorders. identification modulators its infancy but useful experimental tools emerged activating, lesser extent inhibiting, the channels. Elementary structure–activity relationships are known Yoda series small molecule agonists, which show potential physicochemical pharmacological properties. Intriguing effects Yoda1 stimulated removal excess cerebrospinal fluid. Despite PIEZO1's broad expression, opportunities suggested selective positive or negative modulation without intolerable adverse effects. Here we provide focused, non‐systematic, narrative review progress this pharmacology discuss future directions research area.
Language: Английский
Citations
3