LOCALIZATION OF 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-II IN HUMANEPITHELIAL TISSUES

The enzyme 11 beta-hydroxysteroid dehydrogenase type II (11 beta HSD2) confers specificity on the renal mineralocorticoid receptor by inacti vating glucocorticoids. Mutations in this gene give rise to the syndro me of apparent mineralocorticoid excess, a congenital condition charac terized by sodium retention, severe hypertension, and often by growth retardation. It is not known whether 11 beta HSD2 or another enzyme co nfers specificity in nonrenal sodium transporting epithelia, such as t hose in the sweat gland, salivary gland, and gastrointestinal tract. W e previously have used the HUH23 antibody to localize 11 beta HSD2 in the human kidney, vascular smooth muscle cells, and placenta. In the p resent study, we have examined a range of human epithelia for the pres ence of 11 beta HSD2. In the skin, staining was seen in eccrine sweat glands and arterioles, whereas weak HUH23 immunostaining was observed in the epidermis. Staining was absent from sebaceous glands and hair f ollicles. In the parotid gland, the 11 beta HSD2 enzyme was present in striated and excretory ducts, whereas in the submandibular gland, it was found in striated and interlobular ducts. Acini, adipocytes, and a ssociated tumor tissue did not stain with the HUH23 antibody. In the g astrointestinal tract, HUH23 stained ileal enterocytes, colonic absorp tive cells, and epithelial goblet cells, whereas the rectum contained areas of staining and nonstaining absorptive cells. Gastrointestinal s tructures, such as the lamina propria, Peyer's patch, and goblet cells within the crypts of Lieberkuhn did not stain with the antibody. This study demonstrates the presence of 11<betaHSD2 in nonrenal sodium-tra nsporting epithelia and describes a range of tissues affected in the s yndrome of apparent mineralocorticoid excess.