Id1 Expression Level Determines the Differentiation of Human Dental Pulp Stem Cells.
TWIST1 plays a crucial role in dentinogenesis, and its activity depends on both a dimerization partner selection and phosphorylation. Other factors, like Id proteins, can affect the availability of dimerization partners for TWIST1, subsequently leading to diverse biological outcomes. The purpose of this study was to evaluate an impact of Id1 expression on differentiation of dental pulp stem cells (DPSCs). The altered expression of Id1 was achieved by transfection of human DPSCs with lentiviral vectors either driving an entire sequence of Id1, hence leading to Id1 overexpression, or carrying the Id1 silencing sequence. We observed that both overexpression and silencing of Id1 modulated human DPSC differentiation. Id1 overexpression resulted in a prevailing formation of TWIST1 homodimer and increased expression of genes encoding dentin sialophosphoprotein and dentin matrix protein 1, which confirm an enhanced odontogenic differentiation of DPSCs. Concurrently, Id1 silencing produced an opposite effect, slowing DPSC differentiation. These results highlight Id1 as an important modulator of molecular events during DPSC commitment and differentiation, which should be considered in dental research on tissue engineering. Moreover, we assume that the balance between TWIST1 dimerization forms in DPSCs might function in a cell-type-specific manner.
Department of Dental Prosthodontics, Medical University of Gdansk, 80-210 Gdansk, Poland izabelam@gumed.edu.pl.
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Maciejewska
Department of Molecular Medicine, Medical University of Gdansk, 80-210 Gdansk, Poland.
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Sakowicz-Burkiewicz
Department of Molecular Medicine, Medical University of Gdansk, 80-210 Gdansk, Poland.
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Pawelczyk
D000293:Adolescent; D000469:Alkaline Phosphatase / Q000032:analysis; D002113:Calcification, Physiologic / Q000502:physiology; D002118:Calcium / Q000032:analysis; D018929:Cell Culture Techniques; D002454:Cell Differentiation / Q000235:genetics / Q000502:physiology; D002478:Cells, Cultured; D003782:Dental Pulp / Q000166:cytology*; D003810:Dentinogenesis / Q000235:genetics; D016326:Extracellular Matrix Proteins / Q000235:genetics; D005786:Gene Expression Regulation / Q000235:genetics; D020868:Gene Silencing; D005822:Genetic Vectors / Q000235:genetics; D006801:Humans; D051798:Inhibitor of Differentiation Protein 1 / Q000235:genetics / Q000502:physiology*; D016086:Lentivirus / Q000235:genetics; D009687:Nuclear Proteins / Q000235:genetics; D009805:Odontogenesis / Q000235:genetics; D010750:Phosphoproteins / Q000235:genetics; D055503:Protein Multimerization / Q000235:genetics; D012795:Sialoglycoproteins / Q000235:genetics; D013234:Stem Cells / Q000502:physiology*; D014162:Transfection; D051879:Twist-Related Protein 1 / Q000235:genetics; D055815:Young Adult; D000099311:Dentin Sialophosphoprotein
D000469:Alkaline Phosphatase; D002118:Calcium; D016326:Extracellular Matrix Proteins; D051798:Inhibitor of Differentiation Protein 1; D009687:Nuclear Proteins; D010750:Phosphoproteins; D012795:Sialoglycoproteins; D051879:Twist-Related Protein 1; D000099311:Dentin Sialophosphoprotein; C513309:DMP1 protein, human; C497453:ID1 protein, human; C103173:TWIST1 protein, human
basic-helix-loop helix proteins; cell differentiation; dentin; dentin sialophosphoprotein; odontoblast; protein dimmerization