scholarly journals Promotion of Keratinocyte Proliferation by Tracheloside through ERK1/2 Stimulation

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
JaeGoo Kim ◽  
Yu-Kyong Shin ◽  
Ki-Young Kim

Cell migration and proliferation are important for proper wound healing after skin injury. Recent studies have shown that compounds from plants could promote cell migration and proliferation. Tracheloside, which is a plant lignan, has been found to promote the growth of HaCaT cells over 40% compared to other compounds tested based on a cell proliferation assay. An in vitro scratch assay confirmed the healing activity of tracheloside (more than 2-fold increased healing activity after 24 hours of treatment compared with the control) and revealed that this activity is better than that of allantoin (1.2-fold increased after 24 hours of treatment compared with the control), a positive control. With western blot results, wound healing with tracheloside occurred through the phosphorylation of ERK1/2. Therefore, tracheloside is a good candidate to promote wound healing and could be developed as a therapeutic agent for wound treatment or used as a leading compound with higher activity.

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Robert Zajicek ◽  
Vaclav Mandys ◽  
Ondrej Mestak ◽  
Jan Sevcik ◽  
Radana Königova ◽  
...  

A number of implantable biomaterials derived from animal tissues are now used in modern surgery. Xe-Derma is a dry, sterile, acellular porcine dermis. It has a remarkable healing effect on burns and other wounds. Our hypothesis was that the natural biological structure of Xe-Derma plays an important role in keratinocyte proliferation and formation of epidermal architecturein vitroas well asin vivo. The bioactivity of Xe-Derma was studied by a cell culture assay. We analyzed growth and differentiation of human keratinocytes culturedin vitroon Xe-Derma, and we compared the results with formation of neoepidermis in the deep dermal wounds treated with Xe-Derma. Keratinocytes cultured on Xe-Derma submerged in the culture medium achieved confluence in 7–10 days. After lifting the cultures to the air-liquid interface, the keratinocytes were stratified and differentiated within one week, forming an epidermis with basal, spinous, granular, and stratum corneum layers. Immunohistochemical detection of high-molecular weight cytokeratins (HMW CKs), CD29, p63, and involucrin confirmed the similarity of organization and differentiation of the cultured epidermal cells to the normal epidermis. The results suggest that the firm natural structure of Xe-Derma stimulates proliferation and differentiation of human primary keratinocytes and by this way improves wound healing.


2021 ◽  
Vol 41 (1) ◽  
Author(s):  
Azela Glady ◽  
Arno Vandebroek ◽  
Masato Yasui

Abstract Background Wound healing is a complex biological process and complete skin regeneration is still a critical challenge. Extracellular vesicles (EVs) play essential roles in cell communication and cell regeneration, and recent studies have suggested that EVs may contribute to wound healing, though the molecular mechanisms behind this contribution remain unclear. For these reasons, we decided to use EVs isolated from human keratinocytes (HaCaT) in vitro to determine the potential mechanism of action of EV-derived wound healing. Method Scratch assays were used to determine cell migration and proliferation. Scratched cells were exposed to EVs in multiple conditions to determine how they affect wound healing. Statistical analysis between groups was carried out to using Student’s two-sided t test. A p value of <  0.05 was considered statistically significant. Result We found that proteomic analysis of purified EVs shows enrichment of proteins associated with cell communication and signal transduction, such as MAPK pathways, and keratinocyte and fibroblast cultures exposed to EVs had higher levels of proliferation, migration, and ERK1/2 and P38 activation. Moreover, we found that treatment with specific ERK1/2 and P38 signaling inhibitors PD98059 and SB239063 impaired EV-mediated cell migration, which suggests that ERK1/2 and P38 signaling is essential for EV-induced wound healing. Conclusion HaCaT cell-derived EVs accelerate the migration and proliferation of human keratinocytes and fibroblasts and may promote wound healing via the activation of MAPKinase pathways. These findings may be key in developing new methods to treat wounds and accelerate wound healing in the future.


Author(s):  
Gary A. Monteiro ◽  
Harini G. Sundararaghavan ◽  
Anthony V. Fernandes ◽  
David I. Shreiber

The organized movement of cells is critical during tissue morphogenesis and wound healing. While different tissue cells use distinct mechanisms for migration, the underlying biophysical balance of adhesive and tractional forces for effective migration is similar. The extracellular matrix provides the structural framework through which a cell can migrate. In particular, collagen is an abundant and ubiquitous ECM protein that supports cell migration. The excellent biocompatibility and physiological relevance of collagen have made it a primary material for tissue engineered regenerative therapies and in vitro studies with tissue equivalents.


1999 ◽  
Vol 35 (9) ◽  
pp. 510-514 ◽  
Author(s):  
Hari H. P. Cohly ◽  
James W. Stephens ◽  
Michael F. Angel ◽  
James C. Johnson ◽  
Angel K. Markov

1998 ◽  
Vol 91 (Supplement) ◽  
pp. S14
Author(s):  
James W. Stephens ◽  
Had H. P. Cohly ◽  
Michael F. Angel ◽  
Angel K. Markov

2020 ◽  
Author(s):  
Lauren Pruett ◽  
Christian Jenkins ◽  
Neharika Singh ◽  
Katarina Catallo ◽  
Donald Griffin

AbstractA powerful tool to improve tissue integration with biomaterial scaffolds for the regeneration of damaged tissues is to promote cell migration using chemotactic gradients of growth factors. This approach has been realized by the exogenous delivery of growth factors, which unfortunately also limits the scaffold’s ability to meet each wound’s unique spatial and temporal regenerative needs. To address this limitation, we present a new approach to gradient generation by incorporating heparin microislands, which are spatially isolated heparin-containing microparticles that create chemotactic microgradients through reorganization of endogenous local growth factors. We incorporated heparin microislands within microporous annealed particle (MAP) scaffolds, which allows us to tune their incorporation ratiometrically to create a heterogenous microenvironment. In this manuscript, we demonstrate the ability of heparin microislands to organize uniform growth factors into spontaneous microgradients and control downstream cell migration in vitro. Further, we present their ability to significantly improve wound healing outcomes (epidermal regeneration and vascularization) in a diabetic wound model relative to two clinically relevant controls.


2019 ◽  
Vol 20 (15) ◽  
pp. 3679 ◽  
Author(s):  
Lin Chen ◽  
Alyne Simões ◽  
Zujian Chen ◽  
Yan Zhao ◽  
Xinming Wu ◽  
...  

Wounds within the oral mucosa are known to heal more rapidly than skin wounds. Recent studies suggest that differences in the microRNAome profiles may underlie the exceptional healing that occurs in oral mucosa. Here, we test whether skin wound-healing can be accelerating by increasing the levels of oral mucosa-specific microRNAs. A panel of 57 differentially expressed high expresser microRNAs were identified based on our previously published miR-seq dataset of paired skin and oral mucosal wound-healing [Sci. Rep. (2019) 9:7160]. These microRNAs were further grouped into 5 clusters based on their expression patterns, and their differential expression was confirmed by TaqMan-based quantification of LCM-captured epithelial cells from the wound edges. Of these 5 clusters, Cluster IV (consisting of 8 microRNAs, including miR-31) is most intriguing due to its tissue-specific expression pattern and temporal changes during wound-healing. The in vitro functional assays show that ectopic transfection of miR-31 consistently enhanced keratinocyte proliferation and migration. In vivo, miR-31 mimic treatment led to a statistically significant acceleration of wound closure. Our results demonstrate that wound-healing can be enhanced in skin through the overexpression of microRNAs that are highly expressed in the privileged healing response of the oral mucosa.


2014 ◽  
Vol 125 ◽  
pp. 183-192 ◽  
Author(s):  
Isabel Arranz-Valsero ◽  
Laura Soriano-Romaní ◽  
Laura García-Posadas ◽  
Antonio López-García ◽  
Yolanda Diebold

2013 ◽  
Vol 203 (4) ◽  
pp. 673-689 ◽  
Author(s):  
Ah-Lai Law ◽  
Anne Vehlow ◽  
Maria Kotini ◽  
Lauren Dodgson ◽  
Daniel Soong ◽  
...  

Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism. Here, we report that Lpd directly binds active Rac, which regulates a direct interaction between Lpd and the Scar/WAVE complex via Abi. Consequently, Lpd controls lamellipodium size, cell migration speed, and persistence via Scar/WAVE in vitro. Moreover, Lpd knockout mice display defective pigmentation because fewer migrating neural crest-derived melanoblasts reach their target during development. Consistently, Lpd regulates mesenchymal neural crest cell migration cell autonomously in Xenopus laevis via the Scar/WAVE complex. Further, Lpd’s Drosophila melanogaster orthologue Pico binds Scar, and both regulate collective epithelial border cell migration. Pico also controls directed cell protrusions of border cell clusters in a Scar-dependent manner. Taken together, Lpd is an essential, evolutionary conserved regulator of the Scar/WAVE complex during cell migration in vivo.


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