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Wound healing is an essential but complex physiological process that involves the collaboration of various cell types and factors. The kinetic of wound healing is divided into 3 phases which overlap: inflammatory phase, repair phase consisting of cell proliferation and migration, and remodeling phase. We have developed a patented active ingredient from passion fruit, maracuja oil concentrate, rich in unsaponifiable fraction, obtained from one of our sustainable supply chains. Evaluated on 2D in vitro models, the extract induced the proliferation and migration of keratinocytes and fibroblasts, and increased hyaluronic acid.
Mesenchymal Stem Cells (MSC) are endowed with the capacity to sense environmental cues and to generate an integrated adaptive responses. So far it is, however, largely unexplored how MSC sense their environment and how they mount an adaptive response to shape the function and activation state of distinct immune cells during tissue injury. Here, we wished to investigate how MSC adaptively regulate neutrophils function under conditions of wound infection, where MSCs suppression of neutrophil functions would be detrimental.
Besides exhibiting direct microbicidal properties, antimicrobial peptides also display various immunomodulatory functions, including keratinocyte production of cytokines and chemokines, proliferation, migration and wound healing. Recently, a novel antimicrobial peptide named AMP- IBP5 (antimicrobial peptide derived from insulin-like growth factor-binding protein 5) was shown to exhibit antimicrobial activity against numerous pathogens, even at concentrations comparable to those of well-known antimicrobial peptides, such as human β-defensins and LL-37.
Background: Recessive dystrophic epidermolysis bullosa (RDEB) is one of the more severe forms of epidermolysis bulosa, which is a group of genetic skin fragility disorders characterized by blisters and skin erosions in response to minor injury. The pathogenesis of RDEB involves mutations in COL7A1 that encodes type VII collagen (Col7), the main constituent of the anchoring fibrils that anchor the epidermal basement membrane to the papillary dermis. Mesenchymal stem cells promote wound healing, can differentiate into multiple cell lineages, and also have the immunomodulately properties.
Wound induced hair follicle neogensis (WIHN) is a model of tissue regeneration in adults where hair follicles develop de novo following deep wounding. dsRNA generated after wounding activates TLR3 to induce WIHN in mice but mechanisms involved and the translatability to humans is unclear. By transcriptome and proteomic analysis, we unexpectedly found a highly significant (p<3.6x10ˆ-15 and p<8.2x10ˆ-80, respectively) overlap of upregulated genes in keratinocytes following treatment with dsRNA or retinoic acid (RA).
Fibrosis is a process of abnormal accumulation of extracellular matrix (ECM) substrates, which have been a key driver of progressive organ dysfunction. Keloids are representative fibro-proliferative disease of skin with abnormal fibroblast activity. However, the treatment options are limited and current drug development platforms cannot fully reflect mechanosensitive property of the disease. Strain devices with an expandable silicone such as polydimethylsiloxane (PDMS) culture membranes can mimic mechanically dynamic tissue environments.
In contrast to fetal scarless healing, adult skin tends to repair with fibrosis when injured, leading to scar formation. Whether and how scarless healing in adults can be achieved is unclear. We found that, in contrast to extensive scarring induced by macrothermal damage, adult mice could heal scarlessly when the thermal injury was divided into zones microthermal damage. Though the microthermal injury also induced epidermal necrosis with dermal collagen denaturation, there was no myofibroblast activation.
Mesenchymal stem cells have been increasingly utilized in cell-based therapies due to their versatile regenerative properties. However, while the senescent decline of stem cell function has been broadly implicated in the functional deterioration of organs and tissues, the molecular basis for this observation remains largely uncharacterized despite its critical physiologic relevance. In this investigation, we compared the regenerative efficacy of bone marrow-derived mesenchymal stem cells (BM-MSCs) harvested from young (μ = 24 years, = 8.3 years) and aged (μ = 73 years, = 3.7 years) human donors in a previously validated xenograft wound healing model.
Fractional carbon dioxide laser resurfacing (FxCR) is a routine treatment of Dermatology while many patients suffered the damage of skin barrier function after FxCR. The purpose of this study is to evaluate the effectiveness and benefits of AMPs and HA compound mask on wound healing after FxCR on human and mouse skin. Twenty-four subjects were treated with FxCR on the bilateral cheeks. AMPs and HA compound mask was applied on the FxCR-treated area of left cheek. The erythema index (EI), melanin index (MI), transepidermal water loss (TEWL) of FxCR-treated areas on both cheeks were measured.
Skin aging is associated with phenotypic changes in cutaneous structures, and with various features such low resistance to oxidative stress and DNA damage, decreased extracellular matrix protein synthesis, and the appearance of markers of aging. Cellular senescence is an irreversible state of cell cycle arrest that is induced during cellular aging. It is considered as one of the nine hallmarks of aging. Thee accumulation of senescent cells with age and the expression of factors impacting the surrounding environment (inflammatory cytokines, proteases) contribute in turn to tissue aging.
Skin wound healing is severely compromised in patients with diabetes and can lead to ulcer formation requiring lower limb amputation. It has been shown that diabetic skin fibroblasts have a differential expression of growth factors, which could impair wound healing by reducing reepithelialisation by keratinocytes and angiogenesis. Current research on human diabetic fibroblasts and keratinocytes are mostly conducted in two-dimensional monolayer cultures, which do not mimic the structure of the skin and are not representative of in vivo tissues.
Macrophages play important roles during wound healing, and the delayed wound healing in diabetic mice were associated with sustained inflammation and M1 macrophage infiltration. We hypothesized that macrophage polarization is different between diabetic and normal rats near the wound area and contributes to sustained inflammation, and this difference has direct impacts on epidermal keratinocyte function in the context of reepithelialization. In this study, the STZ-induced diabetic rats were injected with anti-TNF-α molecule (Etanercept) to reduce inflammation and evaluate its impact on diabetic wound healing.
Wound healing, a process of repair after skin injury can be divided into three phases: inflammatory phase, proliferative phase, and tissue remodeling. These steps are precisely regulated by a variety of mediators, such as cytokines and chemokines. Inflammatory phase, the first stage of wound healing, especially features an inflammatory reaction via these mediators. Recent reports demonstrated that cytoplasmic DNA-sensor cyclic GMP-AMP synthase (cGAS) activates the stimulator of interferon genes (STING) via production of cyclic GMP-AMP (cGAMP) and subsequently induces inflammatory cytokines including type interferon.
Multiple innate immune pathways are activated upon skin injury to reestablish the antimicrobial barrier and prevent infection. Damage to the skin often elicits acute pain and activation of the nervous system which communicates intimately with the immune system. Here, we show that pharmacological or genetic ablation of TRPV1-mediated nociception impairs innate antiviral responses to skin injury. We previously reported that IL-27 plays a role in skin wound repair and is released by CD301b+ dendritic cells.
Autophagy, a major cellular degradative and recycling pathway, is now considered to be essential for cell health and longevity, as well as a critical player in the cellular aging process. As a highly conserved mechanism, it is responsible for the continuous recycling and renewal of intracellular organelles, lipids, and proteins and is also a vital source of energy for cells. Autophagy can be considered to be a very efficient quality control mechanism that maintains cell efficiency and health. Decrease of autophagic activity has recently been associated with age.
Since entering the industrialized age, we have introduced artificial lights in our life, this is called Light Pollution. Artificial light has been created in order to lengthen the days either for work or for our modern life. This causes a loss of the normal evening/night reduction in light that used to give clues to our body to be ready for sleep and other functions, impacting our natural circadian rhythm. Our biological functions rhythm has been found to be dependent on us being exposed to daylight and darkness and the disruption of this rhythm by light pollution has been now shown to have profound health effects.
Ozone pollution at ground level is a growing worldwide environmental problem. Increased air pollution, UV exposure, and elevated temperatures all contribute to the formation of ozone (O3). Many studies, including those by the U.S. Environmental Protection Agency, have shown that average levels in places such as Los Angeles can reach concentrations greater than 0.4 ppm (The standard set level by the US-EPA is currently at 0.075 ppm averaged over 8 hours). It has been proven that it creates oxidative damages on lipids from the epidermis but we also wanted to evaluate the impact on main repair mechanisms such as circadian rhythm and autophagy.
In skin, capillaries are densely networked in the upper dermis and play critical roles in the supply of oxygen and nutrients as well as the maintenance of body temperature. However, the capillaries relevance on the skins physical features like dermal elasticity remain totally unknown. First, we have succeeded in visualizing blood vessels non-invasively using OCT (Optical Coherence Tomography) (Hara et al., JDS in press) revealing that skin elasticity was strongly correlated with the capillaries density as well as their size, suggesting that capillaries could play an indispensable role in skin elasticity and its aging.
Aquaporin-3, a water/glycerol-transporting protein, has been shown to play a role in regulating proliferation and differentiation in keratinocytes. Abnormalities in the levels and/or localization of AQP3 have been found in many skin diseases, for instance, an aberrant localization of AQP3 in psoriasis. A previous study demonstrated that a streptozotocin-induced diabetic rat model exhibited impaired re-epithelialization and altered AQP3 expression during the wound healing process. Advanced glycation end products (AGEs) accumulate in a chronic hyperglycemic state, and AGEs have been shown to impair wound healing, a major diabetic complication, via microvasculopathy and impaired macrophage function.
While oral wound healing has been considered an ideal system of wound resolution, the specific molecular events that differentiate oral wound healing are poorly understood in humans. Our objective was to define the mechanisms that drive healing in both oral and skin compartments, and how the results could be translated to improve wound healing. A human clinical study showed oral wound resolved faster compared to skin wound. RNA-sequencing, Gene Ontology, IPA and histological analysis using paired human oral and skin samples revealed significantly different patterns in gene expression, molecular functions and biological processes, especially keratinization, epidermal cell differentiation, responses to biotic stimulus and inflammation.