scholarly journals Cell-penetrating superoxide dismutase attenuates oxidative stress-induced senescence by regulating the p53-p21Cip1 pathway and restores osteoblastic differentiation in human dental pulp stem cells

2012 ◽  
pp. 5091 ◽  
Author(s):  
Yoon Jeong Park
Redox Biology ◽  
2017 ◽  
Vol 12 ◽  
pp. 690-698 ◽  
Author(s):  
Cristina Mas-Bargues ◽  
José Viña-Almunia ◽  
Marta Inglés ◽  
Jorge Sanz-Ros ◽  
Juan Gambini ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Lina M. Escobar ◽  
Zita Bendahan ◽  
Andrea Bayona ◽  
Jaime E. Castellanos ◽  
María-Clara González

Introduction. The aim of the present study was to determine the effects of vitamins D and E on the proliferation, morphology, and differentiation of human dental pulp stem cells (hDPSCs). Methods. In this in vitro experimental study, hDPSCs were isolated, characterized, and treated with vitamins D and E, individually and in combination, utilizing different doses and treatment periods. Changes in morphology and cell proliferation were evaluated using light microscopy and the resazurin assay, respectively. Osteoblast differentiation was evaluated with alizarin red S staining and expression of RUNX2, Osterix, and Osteocalcin genes using real-time RT-PCR. Results. Compared with untreated cells, the number of cells significantly reduced following treatment with vitamin D (49%), vitamin E (35%), and vitamins D + E (61%) after 144 h. Compared with cell cultures treated with individual vitamins, cells treated with vitamins D + E demonstrated decreased cell confluence, with more extensive and flatter cytoplasm that initiated the formation of a significantly large number of calcified nodules after 7 days of treatment. After 14 days, treatment with vitamins D, E, and D + E increased the transcription of RUNX2, Osterix, and Osteocalcin genes. Conclusions. Vitamins D and E induced osteoblastic differentiation of hDPSCs, as evidenced by the decrease in cell proliferation, morphological changes, and the formation of calcified nodules, increasing the expression of differentiation genes. Concurrent treatment with vitamins D + E induces a synergistic effect in differentiation toward an osteoblastic lineage.


2012 ◽  
Vol 53 ◽  
pp. S41
Author(s):  
M. El Alami⁎ ◽  
J.A. Viña ◽  
K.M. Abdelaziz ◽  
V. Bonet-Costa ◽  
R. López Grueso ◽  
...  

2019 ◽  
Vol 26 (25) ◽  
pp. 26170-26183 ◽  
Author(s):  
Samira Mahmoudinia ◽  
Ali Niapour ◽  
Hatef Ghasemi Hamidabadi ◽  
Mohammad Mazani

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Alejandro Victoria-Escandell ◽  
José Santiago Ibañez-Cabellos ◽  
Sergio Bañuls-Sánchez de Cutanda ◽  
Ester Berenguer-Pascual ◽  
Jesús Beltrán-García ◽  
...  

Human dental pulp stem cells (HDPSCs) are of special relevance in future regenerative dental therapies. Characterizing cytotoxicity and genotoxicity produced by endodontic materials is required to evaluate the potential for regeneration of injured tissues in future strategies combining regenerative and root canal therapies. This study explores the cytotoxicity and genotoxicity mediated by oxidative stress of three endodontic materials that are widely used on HDPSCs: a mineral trioxide aggregate (MTA-Angelus white), an epoxy resin sealant (AH-Plus cement), and an MTA-based cement sealer (MTA-Fillapex). Cell viability and cell death rate were assessed by flow cytometry. Oxidative stress was measured by OxyBlot. Levels of antioxidant enzymes were evaluated by Western blot. Genotoxicity was studied by quantifying the expression levels of DNA damage sensors such as ATM and RAD53 genes and DNA damage repair sensors such as RAD51 and PARP-1. Results indicate that AH-Plus increased apoptosis, oxidative stress, and genotoxicity markers in HDPSCs. MTA-Fillapex was the most cytotoxic oxidative stress inductor and genotoxic material for HDPSCs at longer times in preincubated cell culture medium, and MTA-Angelus was less cytotoxic and genotoxic than AH-Plus and MTA-Fillapex at all times assayed.


2021 ◽  
Vol 400 (2) ◽  
pp. 112466
Author(s):  
J.F. Huo ◽  
M.L. Zhang ◽  
X.X. Wang ◽  
D.H. Zou

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