scholarly journals Local Regeneration of Dentin-Pulp Complex Using Controlled Release of FGF-2 and Naturally Derived Sponge-Like Scaffolds

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Chiaki Kitamura ◽  
Tatsuji Nishihara ◽  
Masamichi Terashita ◽  
Yasuhiko Tabata ◽  
Ayako Washio

Restorative and endodontic procedures have been recently developed in an attempt to preserve the vitality of dental pulp after exposure to external stimuli, such as caries infection or traumatic injury. When damage to dental pulp is reversible, pulp wound healing can proceed, whereas irreversible damage induces pathological changes in dental pulp, eventually requiring its removal. Nonvital teeth lose their defensive abilities and become severely damaged, resulting in extraction. Development of regeneration therapy for the dentin-pulp complex is important to overcome limitations with presently available therapies. Three strategies to regenerate the dentin-pulp complex have been proposed; regeneration of the entire tooth, local regeneration of the dentin-pulp complex from amputated dental pulp, and regeneration of dental pulp from apical dental pulp or periapical tissues. In this paper, we focus on the local regeneration of the dentin-pulp complex by application of exogenous growth factors and scaffolds to amputated dental pulp.

2020 ◽  
pp. mbc.E19-08-0474
Author(s):  
Eric N. Bunker ◽  
Graycen E. Wheeler ◽  
Douglas A. Chapnick ◽  
Xuedong Liu

Sustained cell migration is essential for wound healing and cancer metastasis. The epidermal growth factor receptor (EGFR) signaling cascade is known to drive cell migration and proliferation. While the signal transduction downstream of EGFR has been extensively investigated, our knowledge of the initiation and maintenance of EGFR signaling during cell migration remains limited. The metalloprotease TACE is responsible for producing active EGFR family ligands in the via ligand shedding. Sustained TACE activity may perpetuate EGFR signaling and reduce a cell's reliance on exogenous growth factors. Using a cultured keratinocyte model system, we show that depletion of α-catenin perturbs adherens junctions, enhances cell proliferation and motility, and decreases dependence on exogenous growth factors. We show that the underlying mechanism for these observed phenotypical changes depends on enhanced autocrine/paracrine release of the EGFR ligand TGF-α in a TACE-dependent manner. We demonstrate that proliferating keratinocyte epithelial cell clusters display waves of oscillatory extracellular signal-regulated kinase (ERK) activity, which can be eliminated by TACE knockout, suggesting that these waves of oscillatory ERK activity depend on autocrine/paracrine signals produced by TACE. These results provide new insights into the regulatory role of adherens junctions in initiating and maintaining autocrine/paracrine signaling with relevance to wound healing and cellular transformation.


2018 ◽  
Vol 44 (11) ◽  
pp. 1671-1676 ◽  
Author(s):  
Cibele Pelissari ◽  
Adriana F.C. Paris ◽  
Andrea Mantesso ◽  
Marília Trierveiler

2016 ◽  
Vol 4 (12) ◽  
pp. 1761-1772 ◽  
Author(s):  
Yeji Kim ◽  
Julie C. Liu

Protein-based microenvironments are promising tools to obtain endothelial cells since they promote hMSC differentiation without exogenous VEGF.


1986 ◽  
Vol 6 (3) ◽  
pp. 870-877 ◽  
Author(s):  
D F Stern ◽  
A B Roberts ◽  
N S Roche ◽  
M B Sporn ◽  
R A Weinberg

To identify functional relationships between oncogenes and growth factors, we compared the effects of transfected myc and ras oncogenes on the responsiveness of Fischer rat 3T3 cells to three growth factors: epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and transforming growth factor-beta (TGF-beta). Control cells did not grow in soft agar under any conditions. ras-Transfected cells grew in soft agar under all conditions tested and were insensitive to the stimulatory effects of exogenous growth factors. These cells secreted elevated levels of both EGF-like factors and TGF-beta, suggesting that the lack of responsiveness of these cells to exogenous growth factors arose from autocrine stimulation. myc-Transfected cells displayed conditional anchorage-independent growth: they formed numerous colonies in soft agar in the presence of EGF but relatively few colonies in the presence of PDGF or TGF-beta. Secretion of EGF-like factors and TGF-beta by these cells was not elevated above that of control cells. These results suggest a model for the mechanism of cooperation between myc and ras oncogenes in which ras-like genes induce growth factor production, while myc-like genes increase the responsiveness of cells to these factors.


Biomaterials ◽  
2012 ◽  
Vol 33 (16) ◽  
pp. 4078-4088 ◽  
Author(s):  
Christine Y. Chuang ◽  
Kifah Shahin ◽  
Megan S. Lord ◽  
James Melrose ◽  
Pauline M. Doran ◽  
...  

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