scholarly journals Role of carbonic anhydrases in skin wound healing

2017 ◽  
Vol 49 (5) ◽  
pp. e334-e334 ◽  
Author(s):  
Harlan Barker ◽  
Marleena Aaltonen ◽  
Peiwen Pan ◽  
Maria Vähätupa ◽  
Pirkka Kaipiainen ◽  
...  
2019 ◽  
Vol 7 ◽  
Author(s):  
Peng Hu ◽  
Qinxin Yang ◽  
Qi Wang ◽  
Chenshuo Shi ◽  
Dali Wang ◽  
...  

Abstact Cutaneous regeneration at the wound site involves several intricate and dynamic processes which require a series of coordinated interactions implicating various cell types, growth factors, extracellular matrix (ECM), nerves, and blood vessels. Mesenchymal stromal cells (MSCs) take part in all the skin wound healing stages playing active and beneficial roles in animal models and humans. Exosomes, which are among the key products MSCs release, mimic the effects of parental MSCs. They can shuttle various effector proteins, messenger RNA (mRNA) and microRNAs (miRNAs) to modulate the activity of recipient cells, playing important roles in wound healing. Moreover, using exosomes avoids many risks associated with cell transplantation. Therefore, as a novel type of cell-free therapy, MSC-exosome -mediated administration may be safer and more efficient than whole cell. In this review, we provide a comprehensive understanding of the latest studies and observations on the role of MSC-exosome therapy in wound healing and cutaneous regeneration. In addition, we address the hypothesis of MSCs microenvironment extracellular vesicles (MSCs-MEVs) or MSCs microenvironment exosomes (MSCs-MExos) that need to take stock of and solved urgently in the related research about MSC-exosomes therapeutic applications. This review can inspire investigators to explore new research directions of MSC-exosome therapy in cutaneous repair and regeneration.


2014 ◽  
Vol 3 (4) ◽  
pp. 304-314 ◽  
Author(s):  
Michael Sung-Min Hu ◽  
Robert C. Rennert ◽  
Adrian McArdle ◽  
Michael T. Chung ◽  
Graham G. Walmsley ◽  
...  

2020 ◽  
Vol 21 (14) ◽  
pp. 5092
Author(s):  
Toini Pemmari ◽  
Jaakko Laakso ◽  
Maarit S. Patrikainen ◽  
Seppo Parkkila ◽  
Tero A. H. Järvinen

Carbonic anhydrases (CAs) contribute to tumor cell migration by generating an acidic environment through the conversion of carbon dioxide to bicarbonate and a proton. CA VI is secreted to milk and saliva, and it could contribute to wound closure, as a potential trophic factor, in animals that typically lick their wounds. Our aim was to investigate whether human CA VI improves skin-wound healing in full-thickness skin-wound models. The effect was studied in Car6 −/− knockout mice and wild type littermates. Half of both mice strains were given topically administered, milk-derived CA VI after wounding and eight hours later. The amount of topically given CA VI exceeded the predicted amount of natural saliva-delivered CA VI. The healing was followed for seven days and studied from photographs and histological sections. Our results showed no significant differences between the treatment groups in wound closure, re-epithelization, or granulation tissue formation, nor did the Car6 genotype affect the healing. Our results demonstrate that CA VI does not play a major role in skin-wound healing and also suggest that saliva-derived CA VI is not responsible for the licking-associated improved wound healing in animals.


2020 ◽  
Vol 133 (18) ◽  
pp. 2236-2238
Author(s):  
Shi-Lu Yin ◽  
Ze-Lian Qin ◽  
Xin Yang

Antibiotics ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1377
Author(s):  
Oriana Simonetti ◽  
Giulio Rizzetto ◽  
Giulia Radi ◽  
Elisa Molinelli ◽  
Oscar Cirioni ◽  
...  

Among the most common complications of both chronic wound and surgical sites are staphylococcal skin infections, which slow down the wound healing process due to various virulence factors, including the ability to produce biofilms. Furthermore, staphylococcal skin infections are often caused by methicillin-resistant Staphylococcus aureus (MRSA) and become a therapeutic challenge. The aim of this narrative review is to collect the latest evidence on old and new anti-staphylococcal therapies, assessing their anti-biofilm properties and their effect on skin wound healing. We considered antibiotics, quorum sensing inhibitors, antimicrobial peptides, topical dressings, and antimicrobial photo-dynamic therapy. According to our review of the literature, targeting of biofilm is an important therapeutic choice in acute and chronic infected skin wounds both to overcome antibiotic resistance and to achieve better wound healing.


2019 ◽  
Vol 16 (1) ◽  
pp. 18-26
Author(s):  
Mardin O. Mohammed ◽  
Osman J. Ali ◽  
Sozan A. Muhamad ◽  
Salam H. Ibrahim ◽  
Goran M. Raouf ◽  
...  

2010 ◽  
Vol 207 (9) ◽  
pp. 1825-1833 ◽  
Author(s):  
Laura Campbell ◽  
Elaine Emmerson ◽  
Faith Davies ◽  
Stephen C. Gilliver ◽  
Andre Krust ◽  
...  

Post-menopausal women have an increased risk of developing a number of degenerative pathological conditions, linked by the common theme of excessive inflammation. Systemic estrogen replacement (in the form of hormone replacement therapy) is able to accelerate healing of acute cutaneous wounds in elderly females, linked to its potent antiinflammatory activity. However, in contrast to many other age-associated pathologies, the detailed mechanisms through which estrogen modulates skin repair, particularly the cell type–specific role of the two estrogen receptors, ERα and ERβ, has yet to be determined. Here, we use pharmacological activation and genetic deletion to investigate the role of both ERα and ERβ in cutaneous tissue repair. Unexpectedly, we report that exogenous estrogen replacement to ovariectomised mice in the absence of ERβ actually delayed wound healing. Moreover, healing in epidermal-specific ERβ null mice (K14-cre/ERβL2/L2) largely resembled that in global ERβ null mice. Thus, the beneficial effects of estrogen on skin wound healing are mediated by epidermal ERβ, in marked contrast to most other tissues in the body where ERα is predominant. Surprisingly, agonists to both ERα and ERβ are potently antiinflammatory during skin repair, indicating clear uncoupling of inflammation and overall efficiency of repair. Thus, estrogen-mediated antiinflammatory activity is not the principal factor in accelerated wound healing.


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