Home About us Contact | |||
Epidermal Junction (epidermal + junction)
Selected AbstractsLOXL as a target to increase the elastin content in adult skin: a dill extract induces the LOXL gene expressionEXPERIMENTAL DERMATOLOGY, Issue 8 2006Valérie Cenizo Abstract:, The lysyl oxidases lysyl oxidase (LOX) and lysyl oxidase-like (LOXL) are responsible for elastin cross-linking. It was shown recently that LOXL is essential for the elastic fibres homeostasis and for their maintenance at adult age. We first determined whether or not elastin, LOX and LOXL are less expressed during adulthood. The LOX and LOXL mRNA level, quantified by real-time reverse transcriptase-polymerase chain reaction decreased in adult skin fibroblasts compared with fibroblasts from children. In contrast, the elastin mRNA level remains stable at all ages. The goal of this study was to induce elastogenesis at the adult age. Therefore, both enzymes, and in particular LOXL, of which expression is the most affected by age, could be targeted to induce elastogenesis in adult skin. We screened a library of about 1000 active ingredients to find activators capable to stimulate specifically the LOXL gene expression in adult dermal fibroblasts. The positive effect of selected active ingredients was confirmed on fibroblasts grown on monolayers and on dermal and skin equivalent cultures. One extract, obtained from dill (LYS'LASTINE V, Engelhard, Lyon, France), stimulates the LOXL gene expression in dermal equivalents (+64% increase in the LOXL mRNA level when compared with control). At the same time, the elastin detection is increased in dermal equivalents and under the dermal,epidermal junction of skin equivalents, without increase of the elastin mRNA. In conclusion, LOXL can be considered as a new target to reinduce elastogenesis. Its stimulation by a dill extract is correlated with increased elastin detection, suggesting an increase in elastogenesis efficiency. [source] Bone morphogenetic protein-mediated type II collagen expression in pilomatricoma and cutaneous mixed tumorJOURNAL OF CUTANEOUS PATHOLOGY, Issue 3 2005Hideki Mieno Background:, We have previously reported that type II collagen deposition in overlying dermo,epidermal junction (DEJ) of pilomatricoma is mediated by bone morphogenetic protein 2/4 (BMP 2/4) expressed by shadow cells (SCs) of pilomatricoma. Objective:, This time, we studied the expression of type II collagen and BMP in a large number of cases of pilomatricoma and extended our study to cutaneous mixed tumor (CMT). Results:, We found type II collagen deposition in the overlying DEJ (16 of 50 cases) and in the SCs (19/50) of pilomatricoma. The number of case of type II collagen deposition in DEJ (DEJ+) and in SCs (SC+) of pilomatricoma correlated to the chronological stage of pilomatricoma. We also found type II collagen deposition in overlying DEJ (two of 11) and in the stromal chondroid tissue (four of 11) of CMT. BMP 2 was expressed in most cases of pilomatricoma (37/50) and CMT (seven of 11). Conclusions:, The expression of type II collagen in pilomatricoma is dependent upon the chronological stage of pilomatricoma. Type II collagen expression in the overlying DEJ and chondroid matrix in CMT may be induced by BMP via the same mechanism as in pilomatricoma. [source] Balloon Cell Melanoma: Case ReportJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005Anna Yemelyanova Balloon cell melanoma (BCM) is a rare histological variant of amelanotic melanoma. The differential diagnosis of clear cell lesion includes BCM, renal cell carcinoma, clear cell sarcoma as well as a number of histiocytic and infectious processes. We report a case of BCM in a 33 year-old Indonesian man who presented with a non-tender, freely movable, non-pigmented left thigh nodule, which had been present for a year. On microscopic examination tumor consisted of a nodular infiltrate present within the dermis with superficial invasion of subcutaneous fat. Tumor cells formed nested aggregates were relatively bland in appearance and had abundant, clear cytoplasm, enlarged nuclei and prominent eosinophilic nucleoli. Rare mitotic figures were present within the deep portion of the neoplasm. No definitive nests were seen at the dermal epidermal junction or within the epidermis. Histochemical stains AFB, PAS/D, and GMS were negative. Immunoperoxidase studies were positive with antibodies to vimentin, S100, HMB45, CD68, and negative with cytokeratin, Factor XIIIA, and lysozyme. The diagnosis of BCMM was favored based on histological features, and immunoperoxidase staining pattern. We believe this case can provide additional information to help establish diagnostic criteria of this rare variant of melanoma. [source] A full-UV spectrum absorbing daily use cream protects human skin against biological changes occurring in photoagingPHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 4 2000S. Seité Background: There is overwhelming evidence that exposure of human skin to ultraviolet radiations (UVR) leads to the development of cutaneous photoaging and eventually to neoplasia. This study was designed to evaluate in humans the protection afforded by a daily use cream containing a photostable combination of UVB and UVA absorbers (Uvinul® N539, Parsol® 1789 and Mexoryl® SX) providing a continuous absorption through the entire UV spectrum, against damages induced by repeated daily exposure to solar simulated radiation (SSR). Methods: Buttock skin of 12 healthy volunteers was exposed 5 days per week for 6 weeks to one minimal erythema dose of solar simulated radiation per exposure. The following parameters in treated and untreated skin were evaluated: erythema, pigmentation, skin hydration, skin microtopography, histology and immunochemistry, and collagen and metalloproteinase (MMP) mRNA levels. Results: In SSR exposed unprotected skin sites, we observed melanization and changes in the skin hydration and microtopography. The epidermis revealed a significant increase in stratum corneum and stratum granulosum thickness. In the dermis, an enhanced expression of tenascin and a reduced expression of type I pro-collagen were evidenced just below the dermal epidermal junction. Although we were unable to visualize any change in elastic fibers in exposed buttock skin, a slightly increased deposition of lysozyme and alpha 1 antitrypsin on these fibers was observed using immunofluorescence techniques. Furthermore, types I and III collagen mRNA were slightly increased and a significant enhancement (up to 2.8-fold) of MMP-2 mRNA level was observed. The daily use cream was shown to prevent all these biological changes. Conclusion: Our results show in vivo that an appropriate full-UV spectrum product significantly reduces the solar-UV-induced skin damage, demonstrating the benefit of daily photoprotection. [source] Anti-p200 pemphigoid: A novel autoimmune subepidermal blistering diseaseTHE JOURNAL OF DERMATOLOGY, Issue 1 2007Amrei DILLING ABSTRACT Anti-p200 pemphigoid is a recently defined autoimmune subepidermal blistering disease characterized by circulating and tissue-bound autoantibodies to a 200-kDa protein (p200) of the dermal,epidermal junction (DEJ). This DEJ constituent is thought to be important for adhesion of basal keratinocytes to the underlying dermis. While the exact identity of p200 remains unknown, it has been demonstrated to be immunologically and biochemically distinct from all major autoantigens of the DEJ, including bullous pemphigoid antigens 180 and 230, laminin 1, 5 and 6, ,6,4 integrin, and type VII collagen. Clinically, most reported cases present with tense blisters as well as urticarial papules and plaques, closely resembling bullous pemphigoid. Histopathological examination of lesional skin biopsies shows subepidermal split formation and superficial inflammatory infiltrate typically dominated by neutrophils. Immunopathologically, linear deposits of immunoglobulin (Ig)G and C3 are detected along the DEJ by direct immunofluorescence microscopy of perilesional skin. Indirect immunofluorescence microscopy of patients' sera on NaCl-split human skin demonstrates circulating IgG autoantibodies labeling the dermal side of the split. By immunoblotting, these autoantibodies recognize a 200-kDa protein of human dermis. Biochemical characterization of the p200 molecule revealed a noncollagenous N-glycosylated acidic protein with an isoelectric point of approximately 5.5. We present an overview of the pathogenesis, clinical features, diagnosis and treatment of this new disease entity. [source] Partial deletion of the LAMA3 gene is responsible for hereditary junctional epidermolysis bullosa in the American Saddlebred HorseANIMAL GENETICS, Issue 1 2009K. T. Graves Summary Laminin 5 is a heterotrimeric basement membrane protein integral to the structure and function of the dermal,epidermal junction. It consists of three glycoprotein subunits: the ,3, ,3 and ,2 chains, which are encoded by the LAMA3, LAMB3 and LAMC2 genes respectively. A mutation in any of these genes results in the condition known as hereditary junctional epidermolysis bullosa (JEB). A 6589-bp deletion spanning exons 24,27 was found in the LAMA3 gene in American Saddlebred foals born with the skin-blistering condition epitheliogenesis imperfecta. The deletion confirms that this autosomal recessive condition in the American Saddlebred Horse can indeed be classified as JEB and corresponds to Herlitz JEB in humans. A diagnostic test was developed and nine of 175 randomly selected American Saddlebred foals from the 2007 foal crop were found to be carriers of the mutation (frequency of 0.026). [source] Childhood epidermolysis bullosa acquisita with autoantibodies against the noncollagenous 1 and 2 domains of type VII collagen: case report and review of the literatureBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2006M. Mayuzumi Summary Epidermolysis bullosa acquisita (EBA) is an acquired subepidermal bullous disease characterized by IgG autoantibodies to type VII collagen, a major component of anchoring fibrils. Most patients with EBA are adult and develop autoantibodies to the noncollagenous (NC) 1 domain of type VII collagen. We describe a 4-year-old Japanese boy presenting pruritic vesicles and tense blisters over his whole body. Immunofluorescence studies revealed linear IgG/C3 deposits along the dermal,epidermal junction of the patient's skin, and circulating IgG autoantibodies mapping to the dermal side of 1 M NaCl-split skin. By immunoblotting analysis using dermal extracts as a substrate, the patient's IgG antibodies labelled a 290-kDa protein corresponding to type VII collagen. Immunoblotting studies using recombinant proteins demonstrated that the patient's circulating autoantibodies recognized not only the NC1 but also the NC2 domain of type VII procollagen. Review of the previously reported cases and the present case suggested that patients with EBA with autoantibodies to regions other than the NC1 domain are all children younger than 10 years of age with clinical features of an inflammatory phenotype. [source] The alpha-3 polypeptide chain of laminin 5: insight into wound healing responses from the study of genodermatosesCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 4 2005K. J. Hamill Summary Laminin 5 (kalinin/epiligrin/nicein) is an essential structural component of the dermal,epidermal junction, composed of three polypeptide subunits: laminin ,3, ,3 and ,2. Studies of the inherited skin fragility disorder junctional epidermolysis bullosa (JEB) have suggested that the major role of this heterotrimeric protein is to act as an adhesive ligand essential for binding the epidermis to the underlying dermis and thus maintaining the integrity of the skin. Protein interaction studies have shown that the C terminus of the ,3 subunit binds to a range of integrin complexes depending on the motility status of keratinocytes. This allows laminin 5 to interact with either hemidesmosomes or the actin cytoskeleton. Recently we have reported that the absence of the N-terminal region of laminin ,3a in laryngo-onchyo-cutaneous syndrome causes excessive granulation tissue production at wound sites. As granulation tissue production is also a problem in JEB, this implicates laminin 5 in control of this wound healing response. [source] |