Cobalt chloride supplementation induces stem-cell marker expression and inhibits osteoblastic differentiation in human periodontal ligament cells

Osathanon, Thanaphum; Vivatbutsiri, Philaiporn; Sukarawan, Waleerat; Sriarj, Wannakorn; Pavasant, Prasit; Sooampon, Sireerat

doi:10.1016/j.archoralbio.2014.08.018

Cited by 45 publications

(43 citation statements)

References 38 publications

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“…Similar passage of cells from healthy individuals was used as the controls. Cell isolation protocol was performed according to previous publications (Nowwarote, Osathanon, Jitjaturunt, Manopattanasoontorn, & Pavasant, ; Osathanon et al, ). Teeth were rinsed with phosphate‐buffered saline, and periodontal tissues at the middle third of the root length were gently scraped.…”

Section: Methodsmentioning

confidence: 99%

Amelogenesis imperfecta: A novel FAM83H mutation and characteristics of periodontal ligament cells

et al. 2018

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Section: Methodsmentioning

confidence: 99%

Amelogenesis imperfecta: A novel FAM83H mutation and characteristics of periodontal ligament cells

et al. 2018

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“…hPDL cells were cultured and characterized as reported in our previous study [Osathanon et al, ]. Third molars from healthy young individuals, age 18–25‐year‐old, were extracted as recommended by their dentist and with informed consent of the patient.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Histone Deacetylases Enhances the Osteogenic Differentiation of Human Periodontal Ligament Cells

Huynh

Everts

Pavasant

et al. 2015

J of Cellular Biochemistry

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One of the characteristics of periodontal ligament (PDL) cells is their plasticity. Yet, the underlying mechanisms responsible for this phenomenon are unknown. One possible mechanism might be related to epigenetics, since histone deacetylases (HDACs) have been shown to play a role in osteoblast differentiation. This study was aimed to investigate the role of HDACs in osteogenic differentiation of human PDL (hPDL) cells. HDAC inhibitor trichostatin A (TSA) had no effect on cell viability as was assessed by MTT assay. Osteogenic and adipogenic differentiation was analyzed by gene expression, ALP activity and mineral deposition. Western blotting was used to investigate the effect of TSA on histone acetylation and protein expression. In the presence of the HDAC inhibitor osteogenic differentiation was induced; osteoblast-related gene expression was increased significantly. ALP activity and mineral nodule formation were also enhanced. Inhibition of HDACs did not induce differentiation into the adipocyte lineage. hPDL highly expressed HDACs of both class I (HDAC 1, 2, 3) and class II (HDAC 4, 6). During osteogenic differentiation HDAC 3 expression gradually decreased. This was apparent in the absence and presence of the inhibitor. The level of acetylated Histone H3 was increased during osteogenic differentiation. Inhibition of HDAC activity induced hyperacetylation of Histone H3, therefore, demonstrating Histone H3 as a candidate target molecule for HDAC inhibition. In conclusion, hPDL cells express a distinguished series of HDACs and these enzymes appear to be involved in osteogenic differentiation. This finding suggests a potential application of TSA for bone regeneration therapy by hPDL cells.

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“…A hypoxia state can be achieved and maintained by utilizing hypoxic chambers; however, changes of gas media (95% N 2 and 5% CO 2 ) for long-term cell culture are cost-and time-consuming. Therefore, hypoxia-mimicking agents such as cobalt chloride (CoCl 2 ) and deferoxamine (DFO) have been tried in the expansion of stem cells [12]; however, the cytotoxicity of this agent is still an issue [8]. In a hypoxic state, cell metabolism shifts from oxidative phosphorylation (OxPhos) to glycolysis for generation of adenosine triphosphate (ATP) and metabolic intermediates [13].…”

Section: Introductionmentioning

confidence: 99%

“…* p < 0:05, relative to control; * * p < 0:01, relative to control. 12 Stem Cells International suggesting that hypoxia-induced proliferation was dependent on GPR91. Succinate moves freely between the mitochondria and the cytosol via the dicarboxylic acid translocator in the mitochondrial inner membrane and the voltage-dependent anion channel (VDAC/porin) in the mitochondrial outer membrane [19].…”

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Succinate Supplement Elicited “Pseudohypoxia” Condition to Promote Proliferation, Migration, and Osteogenesis of Periodontal Ligament Cells

Mao

Yang

Zhao

et al. 2020

Stem Cells International

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Most mesenchymal stem cells reside in a niche of low oxygen tension. Iron-chelating agents such as CoCl2 and deferoxamine have been utilized to mimic hypoxia and promote cell growth. The purpose of the present study was to explore whether a supplement of succinate, a natural metabolite of the tricarboxylic acid (TCA) cycle, can mimic hypoxia condition to promote human periodontal ligament cells (hPDLCs). Culturing hPDLCs in hypoxia condition promoted cell proliferation, migration, and osteogenic differentiation; moreover, hypoxia shifted cell metabolism from oxidative phosphorylation to glycolysis with accumulation of succinate in the cytosol and its release into culture supernatants. The succinate supplement enhanced hPDLC proliferation, migration, and osteogenesis with decreased succinate dehydrogenase (SDH) expression and activity, as well as increased hexokinase 2 (HK2) and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), suggesting metabolic reprogramming from oxidative phosphorylation to glycolysis in a normal oxygen condition. The succinate supplement in cell cultures promoted intracellular succinate accumulation while stabilizing hypoxia inducible factor-1α (HIF-1α), leading to a state of pseudohypoxia. Moreover, we demonstrate that hypoxia-induced proliferation was G-protein-coupled receptor 91- (GPR91-) dependent, while exogenous succinate-elicited proliferation involved the GPR91-dependent and GPR91-independent pathway. In conclusion, the succinate supplement altered cell metabolism in hPDLCs, induced a pseudohypoxia condition, and enhanced proliferation, migration, and osteogenesis of mesenchymal stem cells in vitro.

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Cobalt chloride supplementation induces stem-cell marker expression and inhibits osteoblastic differentiation in human periodontal ligament cells

Cited by 45 publications

References 38 publications

Amelogenesis imperfecta: A novel FAM83H mutation and characteristics of periodontal ligament cells

Amelogenesis imperfecta: A novel FAM83H mutation and characteristics of periodontal ligament cells

Inhibition of Histone Deacetylases Enhances the Osteogenic Differentiation of Human Periodontal Ligament Cells

Succinate Supplement Elicited “Pseudohypoxia” Condition to Promote Proliferation, Migration, and Osteogenesis of Periodontal Ligament Cells

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