2015
DOI: 10.18632/aging.100728 View full text |Buy / Rent full text
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Abstract: Osteoporosis is an age-related progressive bone disease. Trp53 (p53) is not only a famous senescence marker but also a transcription regulator which played a critical role in osteogenesis. However, how p53 contributes to the bone mass loss in age-related osteoporosis is still unclear. Here, we found that bone mass and osteogenic differentiation capacity of mesenchymal stem cells (MSCs) is significantly reduced with advancing age. Serum levels of TNF-α and INF-γ and senescence-associated ß-galactosidase, p16, p… Show more

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“…Similarly, we found that modulating Bre expression affected the expression of the transcription factors Runx2, Osx, and Pparg, suggesting a mechanism through which Bre affects the lineage commitment of stem cells. Furthermore, several studies have demonstrated that mbMSCs from osteoporotic OVX mice or older mice have significantly enhanced adipogenic potential, but greatly reduced osteogenic potential [27,44]. Our data suggest that the downregulation of Bre following OVX could be responsible such alterations to the differentiation potential of MSCs.…”
Section: Discussionmentioning
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rupbmjkragerfmgwileyiopcupepmcmbcthiemesagefrontiersapsiucrarxivemeralduhksmucshluniversity-of-gavle
“…Similarly, we found that modulating Bre expression affected the expression of the transcription factors Runx2, Osx, and Pparg, suggesting a mechanism through which Bre affects the lineage commitment of stem cells. Furthermore, several studies have demonstrated that mbMSCs from osteoporotic OVX mice or older mice have significantly enhanced adipogenic potential, but greatly reduced osteogenic potential [27,44]. Our data suggest that the downregulation of Bre following OVX could be responsible such alterations to the differentiation potential of MSCs.…”
Section: Discussionmentioning
“…p53 signaling pathways are known to be involved in the lineage commitment of MSCs, with their negative regulation of bone formation being well described both in vivo and in vitro [20][21][22][23][24][25][26][27]. Knocking out Mdm2 in osteoblasts significantly impaired murine bone formation, indicating that Mdm2 modulates p53 during in vivo bone development [22].…”
Section: Discussionmentioning
“…Furthermore, miR-17-5p overexpression promotes osteogenic differentiation of MSCs (mesenchymal stem cells) [35]. However, during aging and in pro-inflammatory diseases, miR-17-5p expression was observed low in MSCs, concomitant with compromised osteogenic differentiation [36]. miR-17 overexpression partially rescued this defect by repressing Smurf1 (Smad ubiquitin regulatory factor one) [37] and SMAD7.…”
Section: Aging the Mir-17-92 Cluster And Mir-17-5pmentioning
“…These findings underlined the crucial role of BMSCs in regulation of angiogenesis and will be helpful in understanding the cellular basis of osteoporosis. Accumulating evidence suggests that the function of BMSCs is extensively impaired during aging and estrogen deficiency, leading to the progression of osteoporosis (11)(12)(13)(14)(15)(16). In this study, we found that, along with the decline of osteogenic differentiation capacity, osteoporotic BMSCs secreted less angiogenic factors to induce angiogenesis.…”
Section: Discussionmentioning
“…The decline of BMSC function in maintaining bone homeostasis is a seminal mechanism of bone loss in osteoporosis. Our recent studies have confirmed that decreased BMSC osteogenic differentiation leads to bone formation defects during osteoporosis (11)(12)(13)(14)(15)(16), but whether the decline in angiogenesis is related to BMSC dysfunction remains unknown.…”
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