Search results for "Oct4"

showing 3 items of 3 documents

Heterogeneity of Stem Cells in the Thyroid

2019

Identification of thyroid stem cells in the past few years has made important contributions to our understanding of the cellular and molecular mechanisms that induce tissue regeneration and repair. Embryonic stem (ES) cells and induced-pluripotent stem cells have been used to establish reliable protocols to obtain mature thyrocytes and functional follicles for the treatment of thyroid diseases in mice. In addition, the discovery of resident thyroid progenitor cells, along with other sources of stem cells, has defined in detail the mechanisms responsible for tissue repair upon moderate or severe organ injury.In this chapter, we highlight in detail the current state of research on thyroid ste…

Parafollicular cellThyroid regenerationendocrine systemendocrine system diseasesCellular differentiationThyroid GlandOct4BiologySettore MED/13 - EndocrinologiaSca103 medical and health sciencesMice0302 clinical medicineThyroid resident stem cellIn vivoEmbryonic stem cells (ES cells)Embryonic Stem CellSolid cell nest (SCN)medicineActivin-A030212 general & internal medicineProgenitor cellTSHAnimalRegeneration (biology)ResearchThyroidThyroid follicleThyrosphereCell DifferentiationEmbryonic stem cellIn vitroOrgan repairCell biologymedicine.anatomical_structureStem cellSide population (SP)Thyroperoxidase (TPO)Thyroglobulin (Tg)Human
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Role of p16INK4a and BMI-1 in oxidative stress-induced premature senescence in human dental pulp stem cells

2017

Human dental pulp stem cells (hDPSCs) are a source for cell therapy. Before implantation, an in vitro expansion step is necessary, with the inconvenience that hDPSCs undergo senescence following a certain number of passages, loosing their stemness properties. Long-term in vitro culture of hDPSCs at 21% (ambient oxygen tension) compared with 3–6% oxygen tension (physiological oxygen tension) caused an oxidative stress-related premature senescence, as evidenced by increased β-galactosidase activity and increased lysil oxidase expression, which is mediated by p16INK4a pathway. Furthermore, hDPSCs cultured at 21% oxygen tension underwent a downregulation of OCT4, SOX2, KLF4 and c-MYC factors, w…

AdultMale0301 basic medicineSenescenceAginghDPSCs human dental pulp stem cellsMSC mesenchymal stem cellsAdolescentCellular differentiationClinical BiochemistryCell Culture TechniquesOSKM OCT4 SOX2 KLF4 and c-MYCBiologymedicine.disease_causeBiochemistryCell therapyKruppel-Like Factor 4Young Adult03 medical and health sciencesDental pulp stem cellsmedicineHumansOxygen tensionlcsh:QH301-705.5SIPS stress-induced premature senescenceCells CulturedCellular SenescenceCyclin-Dependent Kinase Inhibitor p16Dental PulpMDA malondialdehydePolycomb Repressive Complex 1lcsh:R5-920Stem CellsOrganic ChemistryCell DifferentiationOxygen tensionCell biologyOxygenOxidative Stress030104 developmental biologylcsh:Biology (General)Cell cultureRegenerative medicineImmunologyFemaleStem celllcsh:Medicine (General)Oxidative stressResearch PaperRedox Biology
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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