Culture insert device with perfusable microchannels enhancesskin model development and barrier function assessment.

The ever-stricter regulations on animal experiments in the field of cosmetic testing have prompted a surge in skin-related research with a special focus on recapitulation of theskin structurehuman skin models are seen as an important tool for skin research, which in recent years attracted a lot of attention and effort, with researchers moving from the simplest 2-layered models (dermis with epidermis) to models that incorporate other vital skin structures such as hypodermis, vascular structures, and skin appendages. In this study, we designed a microfluidic device with a reverse flange-shaped anchor that allows culturing of anskin model in a conventional 6-well plate and assessing its barrier function without transferring the skin model to another device or using additional contraptions. Perfusion of the skin model through vascular-like channels improved the morphogenesis of the epidermis compared with skin models cultured under static conditions.

Chemical- and Drug-Induced Allergic, Inflammatory, and Autoimmune Diseases Via Haptenation.

Haptens are small molecules that only elicit an immune response when bound to proteins. Haptens initially bind to self-proteins and activate innate immune responses by complex mechanisms via inflammatory cytokines and damage-associated molecular patterns and the subsequent upregulation of costimulatory signals such as cluster of differentiation 86 (CD86) on dendritic cells. Subsequent interactions between CD86 and CD28 on T cells are critically important for properly activating naive T cells and inducing interleukin 2 production, leading to the establishment of adaptive immunity via effector and memory T cells.

Upregulation of CD86 and IL-12 by rhododendrol in THP-1 cells cocultured with melanocytes through ROS and ATP.

Background: The tyrosinase inhibitor rhododendrol (RD), used as a skin whitening agent, reportedly has the potential to induce leukoderma.

Objective: Although an immune response toward melanocytes was demonstrated to be involved in leukoderma, the molecular mechanism is not fully understood.

Methods: We hypothesized that if RD is a pro-hapten and tyrosinase-oxidized RD metabolites are melanocyte-specific sensitizers, the sensitizing process could be reproduced by the human cell line activation test (h-CLAT) cocultured with melanocytes (h-CLATw/M) composed of human DC THP-1 cells and melanoma SK-MEL-37 cells.

The long non-coding RNA FLJ46906 binds to the transcription factors NF-κB and AP-1 and regulates expression of aging-associated genes.

Several features differentiate aged cells from young cells, many of which are due to changes in gene expression during the aging process. The mechanisms of altered gene expression in aging cells remain incompletely understood, and we hypothesized that long non-coding (lnc) RNAs mediate at least some of these changes. We screened for alterations in lncRNA expression with aging in skin fibroblasts and identified the lncRNA FLJ46906 to be consistently upregulated with aging in-vivo and in-vitro.

Age-related disruption of autophagy in dermal fibroblasts modulates extracellular matrix components.

Autophagy is an intracellular degradative system that is believed to be involved in the aging process. The contribution of autophagy to age-related changes in the human skin is unclear. In this study, we examined the relationship between autophagy and skin aging.

The Rpd3/HDAC complex is present at the URS1 cis-element with hyperacetylated histone H3.

In eukaryotes, the hypoacetylated state of histone N-terminal lysines at many gene-promoters, which is created by histone deacetylases (HDACs), is changed to the hyperacetylated state by the function of histone acetyltransferases (HATs) upon transcription activation. Although much insight has been obtained to date as to how modification of the histone tail regulates gene expression, little is known about how the transition between the unmodified and modified states takes place. In Saccharomyces cerevisiae, the HDAC complex containing Rpd3 (Rpd3L) represses the transcription of several sets of genes through the URS1 cis-element.