Gene expression advances skin reconstruction and wound repair better on silk fibroin-based materials than on collagen-based materials

Materialia ◽  
2020 ◽  
Vol 9 ◽  
pp. 100519 ◽  
Author(s):  
Tomoko Hashimoto ◽  
Katsura Kojima ◽  
Yasushi Tamada
Keyword(s):  
Gene Expression ◽  
Silk Fibroin ◽  
Wound Repair ◽  
Skin Reconstruction

scholarly journals Loss of keratin 6 (K6) proteins reveals a function for intermediate filaments during wound repair

2003 ◽  
Vol 163 (2) ◽  
pp. 327-337 ◽  
Author(s):  
Pauline Wong ◽  
Pierre A. Coulombe
Keyword(s):  
Gene Expression ◽  
Wound Repair ◽  
Tissue Injury ◽  
Blood Clot ◽  
Explant Culture ◽  
Null Mouse ◽  
Actin Organization ◽  
Mammalian Tissues

The ability to heal wounds is vital to all organisms. In mammalian tissues, alterations in intermediate filament (IF) gene expression represent an early reaction of cells surviving injury. We investigated the role of keratin IFs during the epithelialization of skin wounds using a keratin 6α and 6β (K6α/K6β)-null mouse model. In skin explant culture, null keratinocytes exhibit an enhanced epithelialization potential due to increased migration. The extent of the phenotype is strain dependent, and is accompanied by alterations in keratin IF and F-actin organization. However, in wounded skin in vivo, null keratinocytes rupture as they attempt to migrate under the blood clot. Fragility of the K6α/K6β-null epidermis is confirmed when applying trauma to chemically treated skin. We propose that the alterations in IF gene expression after tissue injury foster a compromise between the need to display the cellular pliability necessary for timely migration and the requirement for resilience sufficient to withstand the rigors of a wound site.

Adult Stem Cells Seeded on Electrospinning Silk Fibroin Nanofiberous Scaffold Enhance Wound Repair and Regeneration

2016 ◽  
Vol 16 (6) ◽  
pp. 5498-5505 ◽  
Author(s):  
Sheng-Yang Xie ◽  
Li-Hua Peng ◽  
Ying-Hui Shan ◽  
Jie Niu ◽  
Jie Xiong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Silk Fibroin ◽  
Wound Repair ◽  
Adult Stem Cells

Analysis of gene expression in the wound repair/regeneration process

2001 ◽  
Vol 12 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Xinmin Li ◽  
Subburaman Mohan ◽  
Weikuan Gu ◽  
David J. Baylink
Keyword(s):  
Gene Expression ◽  
Wound Repair ◽  
Regeneration Process

scholarly journals Nrf Transcription Factors in Keratinocytes Are Essential for Skin Tumor Prevention but Not for Wound Healing

2006 ◽  
Vol 26 (10) ◽  
pp. 3773-3784 ◽  
Author(s):  
Ulrich auf dem Keller ◽  
Marcel Huber ◽  
Tobias A. Beyer ◽  
Angelika Kümin ◽  
Christina Siemes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transgenic Mice ◽  
Wound Repair ◽  
Target Genes ◽  
Dominant Negative ◽  
Skin Tumor ◽  
Cellular Stress Response ◽  
Skin Development

ABSTRACT The Nrf2 transcription factor is a key player in the cellular stress response through its regulation of cytoprotective genes. In this study we determined the role of Nrf2-mediated gene expression in keratinocytes for skin development, wound repair, and skin carcinogenesis. To overcome compensation by the related Nrf1 and Nrf3 proteins, we expressed a dominant-negative Nrf2 mutant (dnNrf2) in the epidermis of transgenic mice. The functionality of the transgene product was verified in vivo using mice doubly transgenic for dnNrf2 and an Nrf2-responsive reporter gene. Surprisingly, no abnormalities of the epidermis were observed in dnNrf2-transgenic mice, and even full-thickness skin wounds healed normally. However, the onset, incidence, and multiplicity of chemically induced skin papillomas were strikingly enhanced, whereas the progression to squamous cell carcinomas was unaltered. We provide evidence that the enhanced tumorigenesis results from reduced basal expression of cytoprotective Nrf target genes, leading to accumulation of oxidative damage and reduced carcinogen detoxification. Our results reveal a crucial role of Nrf-mediated gene expression in keratinocytes in the prevention of skin tumors and suggest that activation of Nrf2 in keratinocytes is a promising strategy to prevent carcinogenesis of this highly exposed organ.

scholarly journals Wound repair capacity in type 2 diabetes elder patients: assessment by gene expression profiling (GEP) analysis

2010 ◽  
Vol 10 (S1) ◽  
Author(s):  
M Cuzzola ◽  
A Dattola ◽  
A Meliadò ◽  
P Scaramozzino ◽  
I Callea ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type 2 Diabetes ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Wound Repair ◽  
Repair Capacity ◽  
Elder Patients

scholarly journals Wound-induced polyploidization is driven by Myc and supports tissue repair in the presence of DNA damage

2018 ◽  
Author(s):  
Janelle Grendler ◽  
Sara Lowgren ◽  
Monique Mills ◽  
Vicki P. Losick
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Cell Division ◽  
Tissue Repair ◽  
Wound Repair ◽  
Mitotic Cell ◽  
S Phase ◽  
Polyploid Cell ◽  
Mitotic Cell Cycle ◽  
Viable Option

AbstractTissue repair requires either polyploid cell growth or cell division, but the molecular mechanism promoting polyploidy and limiting proliferation remains poorly understood. Here we find that injury to the adult Drosophila epithelium causes cells to enter the endocycle through the activation of Yorkie dependent genes (myc, e2f1, or cycE). Myc is even sufficient to induce the endocycle in the post-mitotic epithelium. As result, epithelial cells enter S phase but mitosis is blocked by inhibition of mitotic gene expression. The mitotic cell cycle program can be activated by simultaneously expressing the mitotic activator, Stg, while genetically depleting fzr. However, forcing cells to undergo mitosis is detrimental to wound repair as the adult fly epithelium accumulates DNA damage and mitotic errors ensue when cells are forced to proliferate. In conclusion, we find that wound-induced polyploidization enables tissue repair when cell division is not a viable option.

Glucocorticoid-regulated gene expression during cutaneous wound repair

2000 ◽  
pp. 217-239 ◽  
Author(s):  
Hans-Dietmar BEER ◽  
Reinhard Fässler ◽  
Sabine Werner
Keyword(s):  
Gene Expression ◽  
Wound Repair ◽  
Cutaneous Wound ◽  
Regulated Gene Expression

scholarly journals Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Beata Narożna ◽  
Wojciech Langwiński ◽  
Claire Jackson ◽  
Peter M. Lackie ◽  
John W. Holloway ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profile ◽  
Wound Repair ◽  
Mirna Gene ◽  
Bronchial Epithelium ◽  
Airway Epithelial ◽  
Epithelial Repair ◽  
Mirna Genes ◽  
Normal Human Bronchial Epithelium ◽  
Normal Human

Purpose. Airway epithelium acts as a protective barrier against the particles from the inhaled air. Damage to the epithelium may result in loss of the barrier function. Epithelial repair in response to injury requires complex mechanisms, such as microRNA, small noncoding molecules, to regulate the processes involved in wound repair. We aimed to establish if the microRNA gene expression profile is altered during the airway epithelial repair in differentiated cells. Methods. miRNA gene expression profile during the wound closure of differentiated normal human bronchial epithelium (NHBE) from one donor was analysed using quantitative real-time PCR. We have analysed the expression of 754 genes at five time points during a 48-hour period of epithelium repair using TaqMan Low Density Array. Results. We found out that 233 miRNA genes were expressed in normal human bronchial epithelium. Twenty miRNAs were differentially expressed during the wound repair process, but only one (miR-455-3p) showed significance after FDR adjustment (p=0.02). Using STEM, we have identified two clusters of several miRNA genes with similar expression profile. Pathway enrichment analysis showed several significant signaling pathways altered during repair, mainly involved in cell cycle regulation, proliferation, migration, adhesion, and transcription regulation. Conclusions. miRNA expression profile is altered during airway epithelial repair of differentiated cells from one donor in response to mechanical injury in vitro, suggesting their potential role in wound repair.

scholarly journals Progression of Repair and Injury in Human Liver Slices

2018 ◽  
Vol 19 (12) ◽  
pp. 4130
Author(s):  
Alison E.M. Vickers ◽  
Anatoly V. Ulyanov ◽  
Robyn L. Fisher
Keyword(s):  
Gene Expression ◽  
Human Liver ◽  
Wound Repair ◽  
Specific Gene ◽  
Drug Induced ◽  
Kidney Slices ◽  
Liver Slices ◽  
Liver And Kidney ◽  
Injury And Repair ◽  
Human Liver Slices

Human liver slice function was stressed by daily dosing of acetaminophen (APAP) or diclofenac (DCF) to investigate injury and repair. Initially, untreated human liver and kidney slices were evaluated with the global human U133A array to assess the extended culture conditions. Then, drug induced injury and signals of repair in human liver slices exposed to APAP or DCF (1 mM) were evaluated via specific gene expression arrays. In culture, the untreated human liver and kidney slices remained differentiated and gene expression indicated that repair pathways were activated in both tissues. Morphologically the human liver slices exhibited evidence of repair and regeneration, while kidney slices did not. APAP and DCF exposure caused a direct multi-factorial response. APAP and DCF induced gene expression changes in transporters, oxidative stress and mitochondria energy. DCF caused a greater effect on heat shock and endoplasmic reticulum (ER) stress gene expression. Concerning wound repair, APAP caused a mild repression of gene expression; DCF suppressed the expression of matrix collagen genes, the remodeling metalloproteases, cell adhesion integrins, indicating a greater hinderance to wound repair than APAP. Thus, human liver slices are a relevant model to investigate the mechanisms of drug-induced injury and repair.

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