scholarly journals Effect of Luteolin and Apigenin on the Expression of Oct-4, Sox2, and c-Myc in Dental Pulp Cells withIn VitroCulture

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Lu Liu ◽  
Zhengjun Peng ◽  
Zezhen Xu ◽  
Xi Wei

Introduction. Dental pulp cells (DPCs) are promising cell source for dental tissue regeneration. Recently, small molecules which optimize microenvironment or activate the reprogramming network provide a new way to enhance the pluripotency. Two promising bioflavonoids luteolin and apigenin were reported to enhance reprogramming efficiency in mouse embryonic fibroblast (MEF). However, their effect and underlying mechanism in cell fate determination of human DPCs remain unclear.Methods. To elucidate the effect of luteolin and apigenin on the cell fate determination of DPCs, we explored the cell proliferation, cell cycle, senescence, apoptosis, expression of pluripotency markers Oct-4, Sox2, and c-Myc, and multilineage differentiation capability of DPCs with luteolin or apigenin treatment.Results. We demonstrated that luteolin and apigenin inhibited cell proliferation, arrested DPCs in G2/M and S phase, and upregulated PI value and apoptosis. Moreover, luteolin and apigenin increased telomerase activity, maintained DPCs in a presenescent state, and activated the expression of Oct-4, Sox2, and c-Myc at a dose- and time-dependent pattern in DPCs even at late passages, albeit repressed lineage-specific differentiation.Conclusions. Addition of luteolin and apigenin in the culture medium might provide an effective way to maintain DPCs in an undifferentiated stage and inhibit lineage-specific differentiation.

2014 ◽  
Vol 19 (3) ◽  
pp. 239-253 ◽  
Author(s):  
Shohei Murakami ◽  
Ritsuko Shimizu ◽  
Paul-Henri Romeo ◽  
Masayuki Yamamoto ◽  
Hozumi Motohashi

2016 ◽  
Vol 104 (3) ◽  
pp. 324-329 ◽  
Author(s):  
Shin’ichiro Yasunaga ◽  
Yoshinori Ohno ◽  
Naoto Shirasu ◽  
Bo Zhang ◽  
Kyoko Suzuki-Takedachi ◽  
...  

Oral Diseases ◽  
2013 ◽  
Vol 21 (1) ◽  
pp. 97-105 ◽  
Author(s):  
N Ozeki ◽  
H Yamaguchi ◽  
T Hiyama ◽  
R Kawai ◽  
K Nakata ◽  
...  

10.1038/ni793 ◽  
2002 ◽  
Vol 3 (5) ◽  
pp. 443-450 ◽  
Author(s):  
Kenji Tanigaki ◽  
Hua Han ◽  
Norio Yamamoto ◽  
Kei Tashiro ◽  
Masaya Ikegawa ◽  
...  

RSC Advances ◽  
2019 ◽  
Vol 9 (64) ◽  
pp. 37300-37311 ◽  
Author(s):  
Zixiang Wu ◽  
Shujing Liang ◽  
Wenyu Kuai ◽  
Lifang Hu ◽  
Airong Qian

The recent advances of miRNAs and lncRNAs in determining the cell fate of MSCs.


2005 ◽  
Vol 25 (21) ◽  
pp. 9460-9468 ◽  
Author(s):  
Anita Borton Hjelmeland ◽  
Stephen H. Schilling ◽  
Xing Guo ◽  
Darryl Quarles ◽  
Xiao-Fan Wang

ABSTRACT Runx2 is required for osteoblast differentiation but is expressed in certain nonosteoblastic cells without activating the differentiation process, suggesting that its activity is suppressed through a lineage-specific mechanism. Here we report that primary mouse dermal fibroblasts lacking Smad3 can acquire an osteoblast-like phenotype, including activation of Runx2 activity, expression of osteoblast-specific genes, and calcium deposition. We further show that negative regulation of Runx2 activity by Smad3 in dermal fibroblasts is likely mediated by controlling the expression of Msx2, an antagonist of Runx2 in this cellular context. These data support the presence of a novel mechanism for controlling cell fate determination of mesenchymal lineages by preventing differentiation toward the osteoblastic lineage via negative regulation of Runx2 activity.


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