Journal
IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
Volume 52, Issue 10, Pages 1001-1011Publisher
SPRINGER
DOI: 10.1007/s11626-016-0070-9
Keywords
DPSCs; Osteogenic differentiation; SIRT1; Wnt/beta-catenin
Categories
Funding
- Natural Science Foundation of China [31500647, 81500809, 81501076]
- National Basic Research Program of China (973 Program) [2012CB822104]
- Top Six Types of Talents Financial Assistance of Jiangsu Province [2015-YY-009, 2013-WSW-048]
- Jiangsu Provincial Natural Science Foundation [BK2011385, BK20150408]
- Natural Science Foundation of the Jiangsu Higher Education Institutions of China [15KJA310003]
- Graduate Student Innovation of Science and Technology Projects in Jiangsu Province [SJLX0588]
- Nantong University [YKS14015]
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Dental pulp stem cells (DPSCs), as one type of mesenchymal stem cells (MSCs), have the capability of self-renewal and differentiating along the various directions, including osteogenic, chondrogenic, neurogenic, and adipogenic. We previously study and found that tumor necrosis factor-alpha (TNF-alpha) promoted osteogenic differentiation of human DPSCs via the Wnt/beta-catenin signaling pathway in low concentration while inhibited that in high concentration. In the abovementioned process, we found that sirtuin-1 (SIRT1) had the same change compared with the characteristic protein of bone formation, such as bone morphogenetic protein 2 (BMP2), runt-related transcription factor 2 (Runx2), and collagen I (COL1). We asked whether SIRT1 could regulate osteogenesis of DPSCs. In inflammation microenvironment constructed by TNF-alpha, we tested the expression changing of SIRT1 and analyzed the function of SIRT1 on osteogenic differentiation of DPSCs. SIRT1 deacetylated beta-catenin, and then promote its accumulation in the nucleus. Accumulated beta-catenin can lead to transcription of osteogenic characteristic genes. Using the activator of SIRT1, resveratrol, could promote the above-mentioned process of osteogenic differentiation. SIRT1 could regulate osteogenesis of DPSCs through Wnt/beta-catenin signal. SIRT1, as a regulator of differentiation of DPSCs, may be a new target for cell-based therapy in oral diseases and other regenerative medicine.
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