Gold Nanoparticles Promote Osteogenic Differentiation of Mesenchymal Stem Cells through p38 MAPK Pathway

ACS Nano ◽  
2010 ◽  
Vol 4 (11) ◽  
pp. 6439-6448 ◽  
Author(s):  
Changqing Yi ◽  
Dandan Liu ◽  
Chi-Chun Fong ◽  
Jinchao Zhang ◽  
Mengsu Yang
Keyword(s):  
Stem Cells ◽  
Gold Nanoparticles ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
P38 Mapk Pathway

scholarly journals Gold Nanoparticles Combined Human β-Defensin 3 Gene-Modified Human Periodontal Ligament Cells Alleviate Periodontal Destruction via the p38 MAPK Pathway

2021 ◽  
Vol 9 ◽  
Author(s):  
Lingjun Li ◽  
Yangheng Zhang ◽  
Min Wang ◽  
Jing Zhou ◽  
Qian Zhang ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Osteogenic Differentiation ◽  
P38 Mapk ◽  
Periodontal Ligament ◽  
Mapk Pathway ◽  
Periodontal Regeneration ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
P38 Mapk Pathway

Periodontitis is a chronic inflammatory disease with plaques as the initiating factor, which will induce the destruction of periodontal tissues. Numerous studies focused on how to obtain periodontal tissue regeneration in inflammatory environments. Previous studies have reported adenovirus-mediated human β-defensin 3 (hBD3) gene transfer could potentially enhance the osteogenic differentiation of human periodontal ligament cells (hPDLCs) and bone repair in periodontitis. Gold nanoparticles (AuNPs), the ideal inorganic nanomaterials in biomedicine applications, were proved to have synergetic effects with gene transfection. To further observe the potential promoting effects, AuNPs were added to the transfected cells. The results showed the positive effects of osteogenic differentiation while applying AuNPs into hPDLCs transfected by adenovirus encoding hBD3 gene. In vivo, after rat periodontal ligament cell (rPDLC) transplantation into SD rats with periodontitis, AuNPs combined hBD3 gene modification could also promote periodontal regeneration. The p38 mitogen-activated protein kinase (MAPK) pathway was demonstrated to potentially regulate both the in vitro and in vivo processes. In conclusion, AuNPs can promote the osteogenic differentiation of hBD3 gene-modified hPDLCs and periodontal regeneration via the p38 MAPK pathway.

scholarly journals Inhibition of actin polymerization decreases osteogeneic differentiation of mesenchymal stem cells through p38 MAPK pathway

2013 ◽  
Vol 20 (1) ◽  
pp. 71 ◽  
Author(s):  
Himangshu Sonowal ◽  
Atul Kumar ◽  
Jina Bhattacharyya ◽  
Pabitra Gogoi ◽  
Bithiah Jaganathan
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
P38 Mapk ◽  
Actin Polymerization ◽  
Mapk Pathway ◽  
P38 Mapk Pathway

scholarly journals MicroRNA-16, via FGF2 Regulation of the ERK/MAPK Pathway, Is Involved in the Magnesium-Promoted Osteogenic Differentiation of Mesenchymal Stem Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Hong Qi ◽  
Yang Liu ◽  
Lu Wu ◽  
Su Ni ◽  
Jing Sun ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Mapk Pathway ◽  
Luciferase Reporter ◽  
Erk Mapk ◽  
Marrow Mesenchymal Stem Cells ◽  
Elevated Expression ◽  
Reporter Assays ◽  
Induced Changes

microRNAs (miRNAs) participate in the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). However, few reports have discussed the effect of miRNAs on the magnesium chloride (MgCl2)-induced promotion of osteogenic differentiation of BMSCs, a process involved in the healing of bone tissue. As determined in the present investigation, MgCl2 decreased miR-16 levels; increased levels of fibroblast growth factor 2 (FGF2), p-p38, and p-ERK; and promoted the osteogenic differentiation of BMSCs. Enhancement of miR-16 levels by an miR-16 mimic blocked these MgCl2-induced changes. Moreover, luciferase reporter assays confirmed that miR-16 binds to the 3′UTR region of FGF2 mRNA. Down-regulation of FGF2 blocked the MgCl2-induced increases of p-p38 and p-ERK and the promotion of the osteogenic differentiation of BMSCs. Furthermore, over-expression of miR-16 attenuated the MgCl2-induced overproduction of p-p38 and p-ERK1/2 and the high levels of osteogenic differentiation, effects that were reversed by elevated expression of FGF2. In summary, the present findings provide a mechanism by which miR-16 regulates MgCl2-induced promotion of osteogenic differentiation by targeting FGF2-mediated activation of the ERK/MAPK pathway.

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