EGFR‐mediated Akt and MAPKs signal pathways play a crucial role in patulin‐induced cell proliferation in primary murine keratinocytes via modulation of Cyclin D1 and COX‐2 expression

2013 ◽  
Vol 53 (12) ◽  
pp. 988-998 ◽  
Author(s):  
Shamshad Alam ◽  
Anu Pal ◽  
Rahul Kumar ◽  
Premendra D. Dwivedi ◽  
Mukul Das ◽  
...  
2007 ◽  
Vol 101 (4) ◽  
pp. 969-978 ◽  
Author(s):  
Weiming Ouyang ◽  
Jingxia Li ◽  
Dongyun Zhang ◽  
Bing-Hua Jiang ◽  
Dr Chuanshu Huang

2010 ◽  
Vol 111 (6) ◽  
pp. 1546-1555 ◽  
Author(s):  
Youhong Liu ◽  
Janet M. Hock ◽  
Con Sullivan ◽  
Geying Fang ◽  
Allison J. Cox ◽  
...  

2015 ◽  
Vol 4 (5) ◽  
pp. 1400-1408 ◽  
Author(s):  
Wang Fei ◽  
Wang Chen ◽  
Liu Shengnan ◽  
Wang Huihui ◽  
Xi Shuhua ◽  
...  

Inorganic arsenic promotes SV-HUC-1 cells proliferation.


2019 ◽  
Vol 18 (7) ◽  
pp. 459-474 ◽  
Author(s):  
Paramita Ghosh ◽  
Debarpan Mitra ◽  
Sreyashi Mitra ◽  
Sudipta Ray ◽  
Samir Banerjee ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Que Zhang ◽  
Rui Cai ◽  
Guorong Tang ◽  
Wanrong Zhang ◽  
Weijun Pang

Abstract Background Intramuscular fat (IMF) content is a vital parameter for assessing pork quality. Increasing evidence has shown that microRNAs (miRNAs) play an important role in regulating porcine IMF deposition. Here, a novel miRNA implicated in porcine IMF adipogenesis was found, and its effect and regulatory mechanism were further explored with respect to intramuscular preadipocyte proliferation and differentiation. Results By porcine adipose tissue miRNA sequencing analysis, we found that miR-146a-5p is a potential regulator of porcine IMF adipogenesis. Further studies showed that miR-146a-5p mimics inhibited porcine intramuscular preadipocyte proliferation and differentiation, while the miR-146a-5p inhibitor promoted cell proliferation and adipogenic differentiation. Mechanistically, miR-146a-5p suppressed cell proliferation by directly targeting SMAD family member 4 (SMAD4) to attenuate TGF-β signaling. Moreover, miR-146a-5p inhibited the differentiation of intramuscular preadipocytes by targeting TNF receptor-associated factor 6 (TRAF6) to weaken the AKT/mTORC1 signaling downstream of the TRAF6 pathway. Conclusions MiR-146a-5p targets SMAD4 and TRAF6 to inhibit porcine intramuscular adipogenesis by attenuating TGF-β and AKT/mTORC1 signaling, respectively. These findings provide a novel miRNA biomarker for regulating intramuscular adipogenesis to promote pork quality.


1999 ◽  
Vol 188 (3) ◽  
pp. 289-293 ◽  
Author(s):  
Satu-Leena Sallinen ◽  
Pauli K. Sallinen ◽  
Juha T. Kononen ◽  
Kirsi M. Syrj�koski ◽  
Nina N. Nupponen ◽  
...  

2002 ◽  
Vol 81 (10) ◽  
pp. 688-694 ◽  
Author(s):  
K. Kohama ◽  
K. Nonaka ◽  
R. Hosokawa ◽  
L. Shum ◽  
M. Ohishi

TGF-β3 mediates epithelial-mesenchymal transformation during normal fusion of lip and palate, but how TGF-β3 functions during cleft lip repair remains unexplored. We hypothesize that TGF-β3 promotes fetal cleft lip repair and fusion by increasing the availability of mesenchymal cells. In this investigation, we demonstrated that cleft lips in mouse fetuses were repaired by fetal surgery, producing scarless fusion. At the site of the operation, we first observed an infusion of platelets expressing TGF-β3, followed by increased expression of cyclin D1 and tenascin-C, and coupled with increased mesenchymal cell proliferation. In an ex vivo serumless culture system, cleft lip explants fused in the presence of exogenous TGF-β3. Cultured lips also showed up-regulation in cyclin D1 and tenascin-C expression. These findings suggest that microsurgical repair of cleft lip in the fetus that produced scarless fusion is mediated by TGF-β3 regulation of mesenchymal cell proliferation and migration at the site of repair.


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