Melatonin promoted osteogenesis of human periodontal ligament cells by regulating mitochondrial functions through the translocase of the outer mitochondrial membrane 20

Sun, Haoyun; Zheng, Miaomiao; Liu, Jiawei; Fan, Wenguo; He, Hongwen; Huang, Fang

doi:10.1111/jre.13068

Cited by 10 publications

(8 citation statements)

References 81 publications

(158 reference statements)

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“…Because of their potential to enhance the mechanical characteristics of metals, these technologies have attracted a lot of interest in the field of material science. ECAP, a prominent SPD technique that has been shown to substantially increase both strength and ductility, can be used to refine the particle size of multiple metals, including CP Ti [ 22 , 23 , 24 , 25 , 26 ]. During the ECAP process, extremely severe plastic deformation is induced in the billet by passing it through an angular channel die [ 19 , 27 , 28 ].…”

Section: Introductionmentioning

confidence: 99%

Improving Pure Titanium’s Biological and Mechanical Characteristics through ECAP and Micro-Arc Oxidation Processes

Alemayehu,

Todoh,

Hsieh

et al. 2023

Micromachines

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Pure titanium is limited to be used in biomedical applications due to its lower mechanical strength compared to its alloy counterpart. To enhance its properties and improve medical implants feasibility, advancements in titanium processing technologies are necessary. One such technique is equal-channel angular pressing (ECAP) for its severe plastic deformation (SPD). This study aims to surface modify commercially pure titanium using micro-arc oxidation (MAO) or plasma electrolytic oxidation (PEO) technologies, and mineral solutions containing Ca and P. The composition, metallography, and shape of the changed surface were characterized using X-ray diffraction (XRD), digital optical microscopy (OM), and scanning electron microscope (SEM), respectively. A microhardness test is conducted to assess each sample’s mechanical strength. The weight % of Ca and P in the coating was determined using energy dispersive spectroscopy (EDS), and the corrosion resistance was evaluated through potentiodynamic measurement. The behavior of human dental pulp cell and periodontal cell behavior was also studied through a biomedical experiment over a period of 1-, 3-, and 7-days using culture medium, and the cell death and viability can be inferred with the help of enzyme-linked immunosorbent assay (ELISA) since it can detect proteins or biomarkers secreted by cells undergoing apoptosis or necrosis. This study shows that the mechanical grain refinement method and surface modification might improve the mechanical and biomechanical properties of commercially pure (CP) titanium. According to the results of the corrosion loss measurements, 2PassMAO had the lowest corrosion rate, which is determined to be 0.495 mmpy. The electrode potentials for the 1-pass and 2-pass coated samples are 1.44 V and 1.47 V, respectively. This suggests that the coating is highly effective in reducing the corrosion rate of the metallic CP Ti sample. Changes in the grain size and the presence of a high number of grain boundaries have a significant impact on the corrosion resistance of CP Ti. For ECAPED and surface-modified titanium samples in a 3.6% NaCl electrolyte solution, electrochemical impedance spectroscopy (EIS) properties are similar to Nyquist and Bode plot fitting. In light of ISO 10993-5 guidelines for assessing in vitro cytotoxicity, this study contributes valuable insights into pulp and periodontal cell behavior, focusing specifically on material cytotoxicity, a critical factor determined by a 30% decrease in cell viability.

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Section: Introductionmentioning

confidence: 99%

Improving Pure Titanium’s Biological and Mechanical Characteristics through ECAP and Micro-Arc Oxidation Processes

Alemayehu,

Todoh,

Hsieh

et al. 2023

Micromachines

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“…One can also assume an increased proportion of adipogenic cells during in vitro differentiation, since dexamethasone is also used to induce adipogenic differentiation. In addition, previous studies showed that the inductive effect of melatonin on the osteogenic differentiation is based on an inhibition of the accumulation of triglycerides and the induction of oxidative phosphorylation, which is associated with β oxidation of fatty acids [102,103]. A strongly controlled synthesis of new lipids can therefore be assumed, which also suggests a constant expression of the acyl-CoA synthetase during the differentiation of DFCs [74].…”

Section: Lipidomementioning

confidence: 95%

Evaluation of Current Studies to Elucidate Processes in Dental Follicle Cells Driving Osteogenic Differentiation

Morsczeck,

De Pellegrin,

Reck

et al. 2023

Biomedicines

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When research on osteogenic differentiation in dental follicle cells (DFCs) began, projects focused on bone morphogenetic protein (BMP) signaling. The BMP pathway induces the transcription factor DLX3, whichh in turn induces the BMP signaling pathway via a positive feedback mechanism. However, this BMP2/DLX3 signaling pathway only seems to support the early phase of osteogenic differentiation, since simultaneous induction of BMP2 or DLX3 does not further promote differentiation. Recent data showed that inhibition of classical protein kinase C (PKCs) supports the mineralization of DFCs and that osteogenic differentiation is sensitive to changes in signaling pathways, such as protein kinase B (PKB), also known as AKT. Small changes in the lipidome seem to confirm the participation of AKT and PKC in osteogenic differentiation. In addition, metabolic processes, such as fatty acid biosynthesis, oxidative phosphorylation, or glycolysis, are essential for the osteogenic differentiation of DFCs. This review article attempts not only to bring the various factors into a coherent picture of osteogenic differentiation in DFCs, but also to relate them to recent developments in other types of osteogenic progenitor cells.

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“…The induction of the mitochondrial melatonergic pathway is therefore intimately linked to mitochondrial metabolism, as is insulin production. As well as providing direct antioxidant effects, melatonin will have a plethora of intracrine, autocrine, and paracrine effects, including providing a ‘film’ that coats the mitochondrial outer membrane, regulating membrane fluidity, and regulating the expression of mitochondrial membrane channels, receptors, and transporters [ 115 ] as well as inducing endogenous antioxidants and enzymes, such as catalase and glutathione (GSH) [ 116 ]. The capacity of a cell’s mitochondria to induce the melatonergic pathway is therefore a significant determinant of their capacity to resist challenge.…”

Section: Melatonergic Pathway and T1dmmentioning

confidence: 99%

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

Anderson¹

2023

IJMS

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Type 1 diabetes mellitus (T1DM) arises from the failure of pancreatic β-cells to produce adequate insulin, usually as a consequence of extensive pancreatic β-cell destruction. T1DM is classed as an immune-mediated condition. However, the processes that drive pancreatic β-cell apoptosis remain to be determined, resulting in a failure to prevent ongoing cellular destruction. Alteration in mitochondrial function is clearly the major pathophysiological process underpinning pancreatic β-cell loss in T1DM. As with many medical conditions, there is a growing interest in T1DM as to the role of the gut microbiome, including the interactions of gut bacteria with Candida albicans fungal infection. Gut dysbiosis and gut permeability are intimately associated with raised levels of circulating lipopolysaccharide and suppressed butyrate levels, which can act to dysregulate immune responses and systemic mitochondrial function. This manuscript reviews broad bodies of data on T1DM pathophysiology, highlighting the importance of alterations in the mitochondrial melatonergic pathway of pancreatic β-cells in driving mitochondrial dysfunction. The suppression of mitochondrial melatonin makes pancreatic β-cells susceptible to oxidative stress and dysfunctional mitophagy, partly mediated by the loss of melatonin’s induction of PTEN-induced kinase 1 (PINK1), thereby suppressing mitophagy and increasing autoimmune associated major histocompatibility complex (MHC)-1. The immediate precursor to melatonin, N-acetylserotonin (NAS), is a brain-derived neurotrophic factor (BDNF) mimic, via the activation of the BDNF receptor, TrkB. As both the full-length and truncated TrkB play powerful roles in pancreatic β-cell function and survival, NAS is another important aspect of the melatonergic pathway relevant to pancreatic β-cell destruction in T1DM. The incorporation of the mitochondrial melatonergic pathway in T1DM pathophysiology integrates wide bodies of previously disparate data on pancreatic intercellular processes. The suppression of Akkermansia muciniphila, Lactobacillus johnsonii, butyrate, and the shikimate pathway—including by bacteriophages—contributes to not only pancreatic β-cell apoptosis, but also to the bystander activation of CD8+ T cells, which increases their effector function and prevents their deselection in the thymus. The gut microbiome is therefore a significant determinant of the mitochondrial dysfunction driving pancreatic β-cell loss as well as ‘autoimmune’ effects derived from cytotoxic CD8+ T cells. This has significant future research and treatment implications.

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Melatonin promoted osteogenesis of human periodontal ligament cells by regulating mitochondrial functions through the translocase of the outer mitochondrial membrane 20

Cited by 10 publications

References 81 publications

Improving Pure Titanium’s Biological and Mechanical Characteristics through ECAP and Micro-Arc Oxidation Processes

Improving Pure Titanium’s Biological and Mechanical Characteristics through ECAP and Micro-Arc Oxidation Processes

Evaluation of Current Studies to Elucidate Processes in Dental Follicle Cells Driving Osteogenic Differentiation

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

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