Declaraciones

¿Ha recibido algún tipo de financiamiento para realizar su investigación sobre esta temática?
No

¿Ha recibido algún pago, honorario u otra compensación por su trabajo acerca de esta investigación?
No

¿Tiene vínculos financieros con alguna entidad que podría llegar a competir estrechamente con los medicamentos, materiales o instrumentos tratados en su investigación?
No

¿Posee o ha solicitado una patente relacionada a los materiales, productos o instrumentos utilizados en su investigación?
No

Este trabajo no cuenta con el apoyo de ningún financiamiento directo o indirecto. El autor asume plena responsabilidad sobre el mismo.

Objectives: To ascertain the link between cell senescence and skin ageing.

Introduction: As cells get older, they accumulate damage which, once it disrupts normal cell function, leads to cellular senescence. In this state, cells are unable to divide, become larger and release lots of secretory factors, such as inflammatory cytokines, which can damage surrounding cells and tissue. A number of compounds that selectively kill senescent cells (termed senolytics) have been identified, and human trials testing the efficacy of such compounds have now begun. However, the degree of presence of senescent cells in skin is relatively unknown.

Materials / method: A skin biopsy was taken from 200 people of European ancestry, ranging from 20-80 years of age. Photographs of individuals were used to estimate perceived age and the extent of skin wrinkling, and the biopsies used to count the number of cells positive for the senescence marker p16 and measure elastin content. In the laboratory, we used Ultraviolet radiation (UVR) to drive melanocytes into a senescent state and employed them in melanoderms (laboratory grown skin equivalents) to study their impact on epidermal physiology.

Results: Senescent melanocytes were the main senescent cell in the epidermis, with 10% of melanocytes senescent in 60 year olds (<1% in 20-30 year olds). Those with high numbers of senescent melanocytes looked old for their age, had increased wrinkles, and aged elastin in the upper dermis. There was increased DNA damage in keratinocytes surrounding senescent melanocytes V normal melanocytes. UVR driven senescent melanocytes damaged and disrupted normal keratinocyte functioning in melanoderms which was negated by killing the senescent melanocytes.

Conclusion: Senescent melanocytes are a key feature of aged skin, cause DNA damage to surrounding cells, disrupt normal keratinocyte functioning and associate with aged elastin and looking older. This work strongly implicates cell senescence as a key driver of ageing in skin and tantalising highlights the use of senolytics as a major new route to slowing and treating skin ageing.

Declaraciones

¿Ha recibido algún tipo de financiamiento para realizar su investigación sobre esta temática?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): Unilever

¿Ha recibido algún pago, honorario u otra compensación por su trabajo acerca de esta investigación?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): Unilever

¿Tiene vínculos financieros con alguna entidad que podría llegar a competir estrechamente con los medicamentos, materiales o instrumentos tratados en su investigación?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): Unilever

¿Posee o ha solicitado una patente relacionada a los materiales, productos o instrumentos utilizados en su investigación?
No

Este trabajo es presentado gracias al apoyo de: Unilever

Objectives: In the present work, the ability of O3 to induce inflammasome activation was determined in different skin models, ranging from 2D (human keratinocytes) to 3D models in vitro and ex vivo.

Introduction: Several pollutants have been shown to affect skin physiology, among which ozone (O3) is one of the most toxic. Prolonged exposure to O3 leads to increased oxidative damage and cutaneous inflammation. The correlation between O3 exposure and inflammatory cutaneous conditions (atopic dermatitis, psoriasis, acne and eczema) has been already suggested, although the mechanism involved is still unclear. In the last few decades, a new multiprotein complex, the inflammasome, has been discovered and linked to tissue inflammation, including inflammatory skin conditions.

Materials / method: 2D, 3D and skin explants were exposed to ozone.

Results: Results clearly showed that O3 exposure increased both transcript and protein levels of the main inflammasome complex, such as ASC and caspase-1. Furthermore, by using both immunofluorescence and an ASC oligomerization assay the formation of the complex was determined together with increased secreted levels of both IL-18 and IL-1β. Of note is that H2O2 and to a less extent 4HNE (both considered the main mediators of O3 interaction with cellular membranes) were also able to activate skin inflammasome while the use of catalase prevents the activation.

Conclusion: This study demonstrated that O3 can activate cutaneous inflammasome in a redox dependent manner suggesting a possible role of this new pathway in pollution induced inflammatory skin conditions.

Declaraciones

¿Ha recibido algún tipo de financiamiento para realizar su investigación sobre esta temática?
No

¿Ha recibido algún pago, honorario u otra compensación por su trabajo acerca de esta investigación?
No

¿Tiene vínculos financieros con alguna entidad que podría llegar a competir estrechamente con los medicamentos, materiales o instrumentos tratados en su investigación?
No

¿Posee o ha solicitado una patente relacionada a los materiales, productos o instrumentos utilizados en su investigación?
No

Este trabajo no cuenta con el apoyo de ningún financiamiento directo o indirecto. El autor asume plena responsabilidad sobre el mismo.

Objectives: The objectives of these studies was to investigate and model the formation of senescence cells in skin after to environmental insult and to determine if this has a correlation to skin aging.

Introduction: The proliferative cells of the body have been shown to have a limited cell division capacity and eventually stop dividing in a process called cellular senescence. Senescence is characterized by several changes such as enlargement, beta-galactosidase staining and expression of several protein markers such as p16INK4a and the loss of cell division. Senescence has also been shown to be initiated by cellular stresses such as oxidative stress, Grow Factor and DNA damage. The in vivo accumulation of senescent cells has been suggested to be a major causal mechanism of the aging phenotype.

Materials / method: We investigated the effects of pollution and IR on the formation of senescence cells in skin models. Senescence was measured by histological markers such as beta Gal, p16, p21 and Ki67 staining. In addition, SASP markers were assessed by measuring the levels of IL-1, IL-6, IL-8 released into the media.

Results: We have observed increase senescence with the exposure to hydrogen peroxide, UV, pm 2.5 and IR. A significant enhancement of expression in proteins associated with the senescence secretome, IL-1, IL-6, IL-8, VEGF-A, MMP-1, was observed with all of these environmental triggers. These damaging agents trigger the expression of SASP and can be inhibited by use of several agents.

Conclusion: Taken together, this research suggests that preventing the accumulation of senescent cells, or clearing them once formed, is a promising strategy to delay, prevent, or potentially reverse some signs and symptoms of aging.

Declaraciones

¿Ha recibido algún tipo de financiamiento para realizar su investigación sobre esta temática?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): Estee Lauder Companies

¿Ha recibido algún pago, honorario u otra compensación por su trabajo acerca de esta investigación?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): Estee Lauder Companies

¿Tiene vínculos financieros con alguna entidad que podría llegar a competir estrechamente con los medicamentos, materiales o instrumentos tratados en su investigación?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): Estee Lauder Companies

¿Posee o ha solicitado una patente relacionada a los materiales, productos o instrumentos utilizados en su investigación?
No

Este trabajo es presentado gracias al apoyo de: Estee Lauder Companies

Objectives: Optimizing post-laser recovery and improving treatment results: Evaluation of the antiaging and regenerative effects of a cosmeceutical treatment based on the secretion of Cryptomphalus aspersa 40%.

The main objective of this study was to demonstrated that Cryptomphalus aspersa secretion (SCA) improveS the antiaging results, improves the skin healing and reduces the down time after laser procedure.

Introduction: Some procedures like ablative fractional lasers induces a controlled damage in the skin that results in the improvement of the aging cutaneous signs.
The treatment with the Secretion of Cryptomphalus aspersa (SCA), a technology produced by a mollusk and rich in glycosaminoglycans, antioxidants and growth factors demonstrated regenerating, antioxidant and dermo-repair activities. The results of different studies with SCA shown that its use induces the improvement of clinical signs of photoaging.

Materials / method: Regarding to determine whether the application of SCA improves the clinical results, tolerance and skin regeneration after different treatments, we will show recent studies performed with SCA 40% applied immediately after different kind of lasers.

Results: The studies demonstrated that SCA 40%, applied immediately after laser and sustained on the following days is able to accelerate the recovery of the damage produced by the laser and significantly reduce the adverse effects associated. In addition, SCA treatment during the time between laser sessions could improve the tolerance to the laser treatment.

Conclusion: The immediate and sustained use of SCA during one week after performed laser treatment, improves the clinical results, tolerance and skin regeneration.

Declaraciones

¿Ha recibido algún tipo de financiamiento para realizar su investigación sobre esta temática?
No

¿Ha recibido algún pago, honorario u otra compensación por su trabajo acerca de esta investigación?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): Medical Director Dermatology at Cantabria Labs

¿Tiene vínculos financieros con alguna entidad que podría llegar a competir estrechamente con los medicamentos, materiales o instrumentos tratados en su investigación?
Si
Por favor especifique las entidades (individuo, empresa, sociedad): MEDICAL DIRECTOR AT CANTABRIA LABS

¿Posee o ha solicitado una patente relacionada a los materiales, productos o instrumentos utilizados en su investigación?
No

Este trabajo es presentado gracias al apoyo de: CANTABRIA LABS