scholarly journals Withdrawn: Geraniin inhibits TNF-α-induced impairments of osteogenesis through NF-κB and p38 MAPK signalling pathways in bone marrow stem cells

2017 ◽  
Vol 2 (2) ◽  
pp. 47-52 ◽  
Author(s):  
Chao Lu ◽  
Shichang Gao ◽  
Ge Xu
2006 ◽  
Vol 203 (3) ◽  
pp. S92
Author(s):  
Meijing Wang ◽  
Paul Crisostomo ◽  
Keith Lillemoe ◽  
Daniel Meldrum

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ran Ran ◽  
Haoqing Yang ◽  
Yangyang Cao ◽  
Wanhao Yan ◽  
Luyuan Jin ◽  
...  

Abstract Background Epiregulin (EREG) is an important component of EGF and was demonstrated to promote the osteo/dentinogenic differentiation of stem cells from dental apical papilla (SCAPs). Whether EREG can stimulate the osteo/dentinogenic differentiation of dental pulp stem cells (DPSCs) in inflammatory environment is not clear. The purpose of the present study is to investigate the role of EREG on the osteo/dentinogenic differentiation ability of DPSCs in inflammatory environment. Methods DPSCs were isolated from human third molars. Short hairpin RNAs (shRNAs) were used to knock down EREG expression in DPSCs. Recombinant human EREG (rhEREG) protein was used in the rescue experiment. TNF-α was employed to mimic the inflammatory environment in vitro. Alkaline phosphatase (ALP) staining, Alizarin red staining, quantitative calcium analysis, and real-time RT-PCR were performed to detect osteo/dentinogenic differentiation markers and related signalling pathways under normal and inflammatory conditions. Results EREG depletion promoted the ALP activity and mineralization ability of DPSCs. The expression of BSP, DMP-1, and DSPP was also enhanced. Moreover, 50 ng/mL rhEREG treatment decreased the osteo/dentinogenic differentiation potential of DPSCs, while treatment with 10 ng/mL TNF-α for 4 h increased the expression of EREG in DPSCs. Conversely, EREG knockdown rescued the impaired osteo/dentinogenic differentiation ability caused by TNF-α treatment. Further mechanistic studies showed that EREG depletion activated the p38 MAPK and Erk signalling pathways in DPSCs under normal and inflammatory conditions. Conclusions Our results demonstrated that EREG could inhibit the osteo/dentinogenic differentiation potential of DPSCs via the p38 MAPK and Erk signalling pathways. Under inflammatory environment, EREG depletion enhanced osteo/dentinogenic differentiation potential of DPSCs by improving the expression of p-p38 MAPK and p-Erk.


2001 ◽  
Vol 120 (5) ◽  
pp. A62-A62
Author(s):  
S FORBES ◽  
M ALISON ◽  
K HODIVALADILKE ◽  
R JEFFERY ◽  
R POULSOM ◽  
...  

2008 ◽  
Vol 7 ◽  
pp. 114-115
Author(s):  
R AKCHURIN ◽  
T RAKHMATZADE ◽  
E SKRIDLEVSKAYA ◽  
L SAMOYLENKO ◽  
V SERGIENKO ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Wen-Ching Tzaan ◽  
Hsien-Chih Chen

Intervertebral disc (IVD) degeneration is a multifactorial process that is influenced by contributions from genetic predisposition, the aging phenomenon, lifestyle conditions, biomechanical loading and activities, and other health factors (such as diabetes). Attempts to decelerate disc degeneration using various techniques have been reported. However, to date, there has been no proven technique effective for broad clinical application. Granulocyte colony-stimulating factor (GCSF) is a growth factor cytokine that has been shown to enhance the availability of circulating hematopoietic stem cells to the brain and heart as well as their capacity for mobilization of mesenchymal bone marrow stem cells. GCSF also exerts significant increases in circulating neutrophils as well as potent anti-inflammatory effects. In our study, we hypothesize that GCSF can induce bone marrow stem cells differentiation and mobilization to regenerate the degenerated IVD. We found that GCSF had no contribution in disc regeneration or maintenance; however, there were cell proliferation within end plates. The effects of GCSF treatment on end plates might deserve further investigation.


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