Differentiation-associated localization of small prolne-rich rotein in normal and diseased human skin

Abstract

The expression of SPRR (small proline-rich protein) was investigated in normal human skin and in diseased skin from patients with psoriasis, squamous cell carcinoma, basal cell epithelioma, naevus pigmentosus, ichthyosis vulgaris and several inflammatory skin diseases, by immunohistochemical staining. A polyclonal antibody was raised against a synthetic peptide for a C-terminal common region for SPRR1 and SPRR3. In immunoblot analysis, a positive band of 18 kDa was detected, which showed the presence of SPRR1 in human epidermal keratinocytes. In normal epidermis, positive staining for SPRR was observed in keratinocytes in the granular layer and the uppermost or two spinous cell layers, with no staining of the other spinous or basal layers. The staining was obvious at the cell periphery, weak at the cytoplasm, and absent in the nucleus. Staining was observed in several outer layers of the follicular infundibulum to the isthmus. No staining was detected in the inner root sheath of the hair follicles, hair matrix, sebaceous gland, eccrine gland, eccrine duct, melanocytes, Langerhans cells or fibroblasts. The arrectores pilorum, striated muscles, muscle layers of vessels, and myoepithelia of eccrine gland, were weakly stained. In psoriatic skin, stained keratinocytes were distributed in the spinous cell layers except for the basal layer. In ichthyosis vulgaris, SPRR was barely expressed in the uppermost living cell layers of the epidermis. In epidermolytic hyperkeratosis, degenerated squamous cells widely expressed SPRR. In Darier's disease, dyskeratotic cells were clearly stained. In squamous cell carcinoma, staining was observed in keratotic cells around horny pearls. In basal cell epithelioma, naevus pigmentosus, and malignant melanoma, the tumour cells or naevus cells were not stained. The distribution of SPRR was similar to that of involucrin in normal and several diseased skin, except for ichthyosis vulgaris. We conclude that SPRR is expressed in close association with epidermal differentiation in normal skin and skin diseases. The alteration of the expression of the proteins correlated to terminal differentiation, and differs from disease to disease.

Suppressive Effect of IL-4 on IL-13-Induced Genes in Mouse Lung

“…Selective effects on this cell type are particularly intriguing because IL-13 induces STAT6-dependent AHR and goblet cell hyperplasia in transgenic mice in which only epithelial cells can activate STAT6 (17). Although the SPRR gene family has previously been associated with epithelial cells, this association has been restricted primarily to squamous epithelial cells (63). The products of these genes contribute to the cellular envelope of squamous epithelial cells, which decreases epithelial permeability and perhaps increases epithelial rigidity (64,65).…”

Transcript Signatures in Experimental Asthma: Identification of STAT6-Dependent and -Independent Pathways

“…In addition, the late asthma gene set contained numerous protease inhibitors implicated in tissue repair such as the cathepsin genes. Additionally, a series of small proline-rich (SPRR) proteins involved in squamous cell differentiation and remodeling (43,44) were induced. Table I provides an extensive summary of dynamically regulated genes and verification of representative early and late genes by Northern blot analysis is shown in Fig.…”

Molecular Cloning and Expression of Keratinocyte Proline-rich Protein, a Novel Squamous Epithelial Marker Isolated During Skin Development

“…The precursor proteins of CE are crosslinked via isopeptide bonds formed by the action of transglutaminases (10). A growing number of proteins are now known to be components of the epidermal CE, including cystatin ␣, desmoplakin, elafin, loricrin, involucrin, plasminogen activator inhibitor-2, and the SPRs (4,5,11,12). Interestingly, the components of the CE vary in different epithelia and body sites.…”