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Rac1 Regulates the Proliferation, Adhesion, Migration, and Differentiation of MDPC‐23 Cells

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Introduction Stem cells are responsible for replacing damaged pulp tissue; therefore, promoting their survival and inducing their adhesion to dentin are vital. As a member of the Rho family of… Click to show full abstract

Introduction Stem cells are responsible for replacing damaged pulp tissue; therefore, promoting their survival and inducing their adhesion to dentin are vital. As a member of the Rho family of guanosine triphosphatases, Rac1 is an important regulator of osteoblast functions. However, little is known about its role in regenerative endodontic procedures. The current study examined the role of Rac1 in the proliferation, migration, and odontoblastic differentiation of MDPC‐23 cells. Methods MDPC‐23 cells were transfected with small interfering RNA to knock down Rac1 expression, and then their proliferation, migration, adhesion, and odontoblastic differentiation were examined in vitro. Results MDPC‐23 cells transfected with si‐Rac1 exhibited the increased expression of several key odontogenic protein markers, including Dmp1, Dspp, Runx2, and alkaline phosphatase, as well as decreased proliferation and migration in vitro. The results suggest that Rac1 might regulate nuclear factor kappa B signaling in MDPC‐23 cells. Conclusion Rac1 may have vital roles in the proliferation, migration, adhesion, and odontoblastic differentiation of MDPC‐23 cells. HighlightsThe inhibition of Rac1 expression resulted in decreased MDPC‐23 cell proliferation.The inhibition of Rac1 might regulate nuclear factor kappa B signaling in MDPC‐23 cells.The depletion of Rac1 reduced MDPC‐23 cell adhesion and migration.Rac1 silencing promoted the odontoblastic differentiation of MDPC‐23 cells.

Keywords: mdpc cells; adhesion; proliferation; migration; rac1; mdpc

Journal Title: Journal of Endodontics
Year Published: 2017

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