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Plos One : Loss of the Osteogenic Differentiation Potential During Senescence is Limited to Bone Progenitor Cells and is Dependent on P53, Volume 8

By Gallouzi, Imed Eddine

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Book Id: WPLBN0003951533
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Loss of the Osteogenic Differentiation Potential During Senescence is Limited to Bone Progenitor Cells and is Dependent on P53, Volume 8  
Author: Gallouzi, Imed Eddine
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
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Publisher: Plos

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Gallouzi, I. E. (n.d.). Plos One : Loss of the Osteogenic Differentiation Potential During Senescence is Limited to Bone Progenitor Cells and is Dependent on P53, Volume 8. Retrieved from http://netlibrary.net/


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Description : DNA damage can lead to the induction of cellular senescence. In particular, we showed that exposure to ionizing radiation (IR) leads to the senescence of bone marrow-derived multipotent stromal cells (MSC) and osteoblast-like stromal cells (OB–SC), a phenotype associated with bone loss. The mechanism by which IR leads to bone dysfunction is not fully understood. One possibility involves that DNA damage-induced senescence limits the regeneration of bone progenitor cells. Another possibility entails that bone dysfunction arises from the inability of accumulating senescent cells to fulfill their physiological function. Indeed, we show here that exposure to IR prevented the differentiation and mineralization functions of MSC, an effect we found was limited to this population as more differentiated OB–SC could still form mineralize nodules. This is in contrast to adipogenesis, which was inhibited in both IR-induced senescent MSC and 3T3-L1 pre-adipocytes. Furthermore, we demonstrate that IRinduced loss of osteogenic potential in MSC was p53-dependent, a phenotype that correlates with the inability to upregulate key osteogenic transcription factors. These results are the first to demonstrate that senescence impacts osteogenesis in a cell type dependent manner and suggest that the accumulation of senescent osteoblasts is unlikely to significantly contribute to bone dysfunction in a cell autonomous manner.

 

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