Wound Healing

and, J. A. McGrath; Breathnach, S.M.

doi:10.1002/9780470750520.ch11

Cited by 6 publications

(12 citation statements)

References 236 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, newer dressings have emerged that have specific, clinically relevant qualities. These include: collagens, hydrofibres, antimicrobial dressings, debriding agents, odour‐absorbing dressings, biosynthetic dressings and hyaluronic acid dressings (17). Among them, a slow‐release iodine preparation, cadexomer iodine, has been demonstrated to be useful for chronic venous ulcers (18–22), diabetic foot ulcers (23), decubitus ulcers (24) and infected wounds (25,26).…”

Section: Discussionmentioning

confidence: 99%

Cadexomer as well as cadexomer iodine induces the production of proinflammatory cytokines and vascular endothelial growth factor by human macrophages

Ohtani

Mizuashi

Ito

et al. 2007

Experimental Dermatology

View full text Add to dashboard Cite

Although cadexomer iodine is widely used for the treatment of skin ulcers such as decubitus ulcers, the mechanism by which it enhances wound healing is not clear. Recently, it has been demonstrated that macrophages play an important role in wound healing by inducing inflammation and angiogenesis. We examined the effects of cadexomer and cadexomer iodine on tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6, IL-8, IL-10, IL-12 p 40, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) production by macrophages. Human macrophages were obtained by culturing CD14+ monocytes with macrophage colony stimulating factor (M-CSF) in the presence or absence of cadexomer or cadexomer iodine. The production of cytokines and the expression of mRNA were evaluated by enzyme linked immunosorbent assay (ELISA) of the culture supernatants and by reverse transcriptase polymerase chain reaction (RT-PCR) analysis, respectively. In addition, we examined the tissue concentration of VEGF in the wounds treated with or without cadexomer iodine. Cadexomer and cadexomer iodine significantly increased the expression of IL-1 beta, IL-8, TNF-alpha and VEGF mRNA, while they did not affect that of IL-6, IL-10, IL-12 p 40 or bFGF mRNA. In addition, they significantly increased the production of IL-1 beta and TNF-alpha. Although we could not detect increased production of VEGF in the culture supernatants, the western blot analysis of macrophages demonstrated the increased production of VEGF by the treatment with either cadexomer or cadexomer iodine. The treatment with cadexomer iodine increased the tissue concentration of VEGF in the skin wounds. These data suggest that cadexomer and cadexomer iodine have beneficial effects on wound healing in addition to those related to their antibacterial activity.

show abstract

Section: Discussionmentioning

confidence: 99%

Cadexomer as well as cadexomer iodine induces the production of proinflammatory cytokines and vascular endothelial growth factor by human macrophages

Ohtani

Mizuashi

Ito

et al. 2007

Experimental Dermatology

View full text Add to dashboard Cite

show abstract

“… 9 , 51 The membrane is formed mainly by networks of laminin 332 and collagen IV, which overlap and connect by the action of other molecules. 9 , 52 , 53 Several proteins of the cell surface of the keratinocytes and the extracellular matrix are inserted in this network and interact in a specific way with each other, ensuring the adhesion of the skin layers. 9 , 52 , 54 …”

Section: Junctional Epidermolysis Bullosamentioning

confidence: 99%

“…Pathogenic variants in the genes that encode the components of the dermoepidermal junction result in the absence or disturbance of their functions and the consequent decrease in adhesion of the skin layers, which leads to the characteristic JEB phenotypes. 9 , 52 …”

Section: Junctional Epidermolysis Bullosamentioning

confidence: 99%

“…It is through these protein-protein interactions that laminin 332 acts as a support for dermoepidermal adhesion. 9 , 41 , 52

Figure 6 Schematic representation of the main structures involved in the adhesion of the skin layers. The main proteins associated with junctional epidermolysis bullosa ( to the right of the figure) interact in order to allow the connection of the keratin intermediate filaments to the anchoring fibrils (formed by type VII collagen) in the dermis.…”

Section: Junctional Epidermolysis Bullosamentioning

confidence: 99%

“…Consequently, the epidermis and dermis separate at the level of the lamina lucida, resulting in typical JEB phenotypes. 52 The phenotypic severity and, therefore, the clinical subtype of JEB are related to the expression of laminin 332. The most severe form, severe JEB, is usually caused by loss of function variants (null variants), such as the substitutions that generate a premature stop codon (nonsense variants) and those that alter the reading phase (frameshift variants), thus resulting in the complete absence of laminin 332.…”

Section: Junctional Epidermolysis Bullosamentioning

confidence: 99%

See 2 more Smart Citations

Inherited epidermolysis bullosa: update on the clinical and genetic aspects

Mariath

Santin

Schüler‐Faccini

et al. 2020

Anais Brasileiros de Dermatologia

View full text Add to dashboard Cite

Inherited epidermolysis bullosa is a group of genetic diseases characterized by skin fragility and blistering on the skin and mucous membranes in response to minimal trauma. Epidermolysis bullosa is clinically and genetically very heterogeneous, being classified into four main types according to the layer of skin in which blistering occurs: epidermolysis bullosa simplex (intraepidermal), junctional epidermolysis bullosa (within the lamina lucida of the basement membrane), dystrophic epidermolysis bullosa (below the basement membrane), and Kindler epidermolysis bullosa (mixed skin cleavage pattern). Furthermore, epidermolysis bullosa is stratified into several subtypes, which consider the clinical characteristics, the distribution of the blisters, and the severity of cutaneous and extracutaneous signs. Pathogenic variants in at least 16 genes that encode proteins essential for the integrity and adhesion of skin layers have already been associated with different subtypes of epidermolysis bullosa. The marked heterogeneity of the disease, which includes phenotypes with a broad spectrum of severity and many causal genes, hinders its classification and diagnosis. For this reason, dermatologists and geneticists regularly review and update the classification criteria. This review aimed to update the state of the art on inherited epidermolysis bullosa, with a special focus on the associated clinical and genetic aspects, presenting data from the most recent reclassification consensus, published in 2020.

show abstract

Biologie der Wundheilung

Auböck

2007

Manual Der Wundheilung

View full text Add to dashboard Cite

Wound Healing

Cited by 6 publications

References 236 publications

Cadexomer as well as cadexomer iodine induces the production of proinflammatory cytokines and vascular endothelial growth factor by human macrophages

Cadexomer as well as cadexomer iodine induces the production of proinflammatory cytokines and vascular endothelial growth factor by human macrophages

Inherited epidermolysis bullosa: update on the clinical and genetic aspects

Biologie der Wundheilung

Contact Info

Product

Resources

About