No abstract

The nature and distribution of cell contacts have been examined in thin sections and freeze-fracture replicas of mammary gland samples from female C3H/Crgl mice at stages from birth through pregnancy, lactation, and postweaning involution. Epithelial cells of major mammary ducts at all stages examined are linked at their luminal borders by junctional complexes consisting of tight junctions, variable intermediate junctions, occasional small gap junctions, and one or more series of desmosomes. Scattered desmosomes and gap junctions link ductal epithelial and myoepithelial cells in all combinations; hemidesmosomes attach myoepithelial cells to the basal lamina. Freeze-fracture replicas confirm the erratic distribution of gap junctions and reveal a loose, irregular network of ridges comprising the continuous tight-junctional belts. Alveoli develop early in gestation and initially resemble ducts. Later, as alveoli and small ducts become actively secretory, they lose all desmosomes and most intermediate junctions, whereas tight and gap junctions persist, The tight-junctional network becomes compact and orderly, its undulating ridges oriented predominantly parallel to the luminal surface. It is suggested that these changes in junctional morphology, occurring in secretory cells around parturition, may be related to the greatly enhanced rate of movement of milk precursors and products through the lactating epithelium, or to the profound and recurrent changes in shape of secretory cells that occur in relation to myoepithelial cell contraction, or to both.

Primary cultures of neonatal human foreskin keratinocytes converted 25-hydroxyvitamin D in high yield to a metabolite with the chromatographic behavior of 1,25-dihydroxyvitamin D3. The identity of this metabolite as 1,25-dihydroxyvitamin D3 was confirmed both by its potency in displacing 1,25-dihydroxyvitamin D3 in the chick cytosol receptor assay and by mass spectral analysis. These results suggest that 1,25-dihydroxyvitamin D3 may be formed in the epidermis to regulate vitamin D production by the epidermis and to provide an alternative to 1,25-dihydroxyvitamin D3 production by the kidneys.

Differentiation in keratinizing epithelia involves the orderly transformation of basal germinal cells into an exterior cornified layer. We have employed rhodamine-conjugated lectins to visualize distinctive changes in the localization of keratinocyte membrane glycoconjugates during epidermal differentiation. The dermis, basement membrane, and epidermal cell membranes stained positively for mannose, alpha- and beta-galactose, N-acetyl-glucosamine, and sialic acid. In contrast, only the viable epidermis demonstrated N-acetyl-galactosamine, while alpha-L-fucose staining was limited to the upper stratum spinosum and stratum granulosum. Neuraminidase treatment extended the binding of certain lectins, e.g., peanut agglutinin, to regions of the skin that otherwise did not label. Whereas the granular cell membranes displayed the largest number of carbohydrates, these sugars could no longer be visualized after granular cells differentiated into the stratum corneum. Loss of lectin staining may be attributable to the presence of a family of sugar-specific glycosidases that we obtained from granular and cornified cell cytosol fractions. Finally, as further support for sugar deletion during cornification, we found that glycosphingolipids are hydrolyzed to ceramides coincident with both loss of lectin staining and the emergence of glycosidase activity. These results suggest: 1) that carbohydrates on keratinocyte cell membranes can be used as markers of epidermal differentiation, and 2) that removal of cell surface sugars during cornification may be due to the action of specific glycosidases in the outer epidermis.

with osmium alone or with rapidly penetrating agents (e.g., n-hexanol) that are nonreactive with osmium. UItrathin sections of tissues perfused with n-butanol, but not with n-hexanol, demonstrated expanded stratum corneum Literature Cited