scholarly journals Arecoline suppresses epithelial cell viability by upregulating tropomyosin-1 through the transforming growth factor-β/Smad pathway

2020 ◽  
Vol 58 (1) ◽  
pp. 1244-1251
Author(s):  
Long Li ◽  
Liqun Gu ◽  
Zhigang Yao ◽  
Yuehong Wang ◽  
Zhangui Tang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Cell Viability ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Smad Pathway

scholarly journals Changes in cardiac resident fibroblast physiology and phenotype in aging

2018 ◽  
Vol 315 (4) ◽  
pp. H745-H755 ◽  
Author(s):  
JoAnn Trial ◽  
Katarzyna A. Cieslik
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Cardiac Fibroblasts ◽  
Transforming Growth Factor Β ◽  
Tissue Homeostasis ◽  
Apparent Paradox ◽  
Smad Pathway ◽  
Activated Fibroblasts ◽  
Resident Fibroblast

The cardiac fibroblast plays a central role in tissue homeostasis and in repair after injury. With aging, dysregulated cardiac fibroblasts have a reduced capacity to activate a canonical transforming growth factor-β-Smad pathway and differentiate poorly into contractile myofibroblasts. That results in the formation of an insufficient scar after myocardial infarction. In contrast, in the uninjured aged heart, fibroblasts are activated and acquire a profibrotic phenotype that leads to interstitial fibrosis, ventricular stiffness, and diastolic dysfunction, all conditions that may lead to heart failure. There is an apparent paradox in aging, wherein reparative fibrosis is impaired but interstitial, adverse fibrosis is augmented. This could be explained by analyzing the effectiveness of signaling pathways in resident fibroblasts from young versus aged hearts. Whereas defective signaling by transforming growth factor-β leads to insufficient scar formation by myofibroblasts, enhanced activation of the ERK1/2 pathway may be responsible for interstitial fibrosis mediated by activated fibroblasts. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/fibroblast-phenotypic-changes-in-the-aging-heart/ .

Effects of Titanium Ions on Osteogenesis of MC3T3-E1 Cells Through Transforming Growth Factor-β/Smad Signaling Pathway

2019 ◽  
Vol 9 (6) ◽  
pp. 852-859
Author(s):  
Anqian Wu ◽  
Xue Li ◽  
Hongqiang Yu ◽  
Xirui Xin ◽  
Xinxin Ding ◽  
...  
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Osteogenic Potential ◽  
High Concentration ◽  
Smad Pathway ◽  
Low Concentration ◽  
Smad Signaling Pathway ◽  
Cells Cultured

Titanium (Ti) and its alloys have been now widely used in the denture implantation. However, due to corrosion, the surface of the implants may release titanium (IV) (Ti(IV)) ions affecting the periimplant environment. Studies have found that Ti ions at high concentration may improve the activity of osteoclasts and increase the inflammation, the mechanism of which is still unclear. Our study aimed to explore the effects of the Ti ions at low concentration (10 μmol/L) on the MC3T3-E1 cells which were of great osteogenic potential and whether the TGF-β/Smad pathway played an important role during the process. We confirmed that 10 μmol/L Ti ions could improve the proliferation of MC3T3-E1 cells in a time-independent way. The expressions of Smad2/3, p-Smad2/3 and osteogenesis related genes were upregulated when the MC3T3-E1 cells cultured in the medium with 10 mol/L Ti ions. In summary, low concentration of Ti ions (10 μmol/L) could promote the differentiation of MC3T3-E1 cells through the TGF-β/Smad pathway.

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