Modulation of Gene Expression in a Sterile Atopic Dermatitis Model and Inhibition of Adhesion by Fucoidan.

Atopic dermatitis is a multifactorial pathology that includes perturbations of gene expression and increased adhesion of Fucoidans are seaweed-derived sulfated fucose-rich polysaccharides that are known to be anti-inflammatory and may inhibit adhesion of pathogens. Fucoidan was assessed for effects on gene expression of an in vitro 3D model of atopic dermatitis. It was also assessed for inhibitory effects on the adhesion of bacteria onto 3D reconstructed skin.

The activation of cultured keratinocytes by cholesterol depletion during reconstruction of a human epidermis is reminiscent of monolayer cultures.

Transient cholesterol depletion from plasma membranes of human keratinocytes has been shown to reversibly activate signalling pathways in monolayer cultures. Consecutive changes in gene expression have been characterized in such conditions and were interestingly found to be similar to transcriptional changes observed in keratinocytes of atopic dermatitis (AD) patients. As an inflammatory skin disease, AD notably results in altered histology of the epidermis associated with a defective epidermal barrier.

Increased abundance of cytoplasmic and nuclear caveolin 1 in human diploid fibroblasts in H(2)O(2)-induced premature senescence and interplay with p38alpha(MAPK).

Treatment of IMR-90 human diploid fibroblasts with a sublethal concentration of H(2)O(2) induces premature senescence. We investigated the protein abundance, subcellular localization and involvement of caveolin 1 in premature senescence. Caveolin 1 is a scaffolding protein able to concentrate and organize signaling molecules within the caveolae membrane domains.

Role of TGF-beta1-independent changes in protein neosynthesis, p38alphaMAPK, and cdc42 in hydrogen peroxide-induced senescence-like morphogenesis.

The role of TGF-beta1 in hydrogen peroxide-induced senescence-like morphogenesis has been described. The aim of this work was to investigate whether TGF-beta1-independent changes in protein synthesis are involved in this morphogenesis and to study possible mechanisms occurring earlier than TGF-beta1 overexpression. Among the multiple TGF-beta1-independent changes in protein neosynthesis, followed or not by posttranslational modifications, identified by proteomic analysis herein, those of ezrin, L-caldesmon, and HSP27 were particularly studied.

Upregulation of annexin A2 in H(2)O(2)-induced premature senescence as evidenced by 2D-DIGE proteome analysis.

Human diploid fibroblasts undergo premature senescence after treatment with sublethal concentration of H(2)O(2). We report the first proteomic study of microsomal proteins in the context of H(2)O(2)-induced premature senescence by using 2D-DIGE approach. Twelve different proteins with altered abundance at day 3 after treatment with H(2)O(2) were identified.

Transient increased extracellular release of H2O2 during establishment of UVB-induced premature senescence.

In this work, we found that extracellular release of H(2)O(2) is 1.5- to 6-fold higher in skin human diploid fibroblasts exposed to UVB in conditions inducing premature senescence when compared to control cells without exposure to UVB. The apparent decrease in H(2)O(2) production from 0 to 72 h after the last exposure to UVB was not due to increased enzymatic activity of catalase or glutathione peroxidase.

Comparison of replicative senescence and stress-induced premature senescence combining differential display and low-density DNA arrays.

Human diploid fibroblasts (HDFs) exposed to subcytotoxic stress display many features of senescence. Using differential display RT-PCR, gene expression of HDFs in premature senescence induced by tert-butylhydroperoxide or ethanol and in replicative senescence was compared to gene expression of HDFs at early cumulative population doublings. Thirty genes of known function were identified from the 265 differentially displayed cDNA fragments.