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Scanning electron microscopic study of degeneration and regeneration in the olfactory epithelium after axotomy.

The olfactory epithelium of the adult hamster (Mesocricetus auratus) was examined with the scanning electron microscope following olfactory nerve axotomy. Axotomy results in retrograde degeneration of mature olfactory neurons. Maximum degeneration was observed around day 4. During the degeneration period the epithelium consists primarily of supporting and basal cells. Microvillar columnar supporting cells were observed to have fine cellular processes extending from their lateral border to neighbouring cells. Supporting cells extended to the basal lamina where they terminated in foot-like processes of variable shapes (club, splay and hook). Basal cells which gave rise to new replacement olfactory neurons were observed near the basal lamina. They had a rough cellular surface covered with small granules and fine cellular extensions. Bowman's gland duct cells extended unbranched through the epithelium where they formed funnel duct openings covered with microvilli. During early recovery periods (5-30 days) the number of olfactory neurons in the lower epithelium region increased. We observed olfactory neurons with developing axon and dendritic processes. Specialized growth cone structures were seen at the tips. Olfactory neuron growth cones were elongated or club-shaped and had a ruffled membrane surface. Several thin filopodia extended from the growth cone and made contact with adjacent cells. At late recovery periods (35-120 days) there was a marked increase in the number of olfactory neurons within the middle and lower epithelium regions. Numerous dendritic processes extended to the epithelial surface and terminated in knob-like ciliated structures. Olfactory axons passed basally, forming small intra-epithelial bundles that penetrated the basal lamina then fasciculated into larger bundles within the lamina propria. This study provides detailed three-dimensional observations of the olfactory epithelium following neuron injury, and describes neural degenerative changes, replacement of olfactory neurons, development and maturation. In addition, we describe the structure and basal attachment of supporting cells and their glial-like relation with olfactory neurons.

Animals↗

Apico-basal osmotic gradient induces transcytosis in cultured renal collecting duct epithelium.

The present experiments report the existence of an apico-basal plasma membrane shuttle in cultured renal collecting duct principal cell epithelium. Apical and basal perfusion under isotonic conditions, 290 mosm phosphate-buffered saline (PBS), has no effect on the shape of the epithelium. In contrast, gradient perfusion of the epithelium with 75 mosm PBS on the apical side and 290 mosm PBS on the basal side for 10 min alters the morphology of the epithelium by causing the originally columnar epithelial cells to become lower, the intercellular spaces to dilate, and the intracellular vesicles to enlarge. Perfusion of the epithelium with isotonic PBS in the presence of electron-dense cellular markers such as gold-coupled GPCDI antibody, recognizing a glycoprotein in the plasma membrane of collecting duct cells (W.W. Minuth, G. Lauer, S. Bachman and W. Kriz, Histochemistry 80:171-182, 1984), cationized ferritin (CF), horseradish peroxidase (HRP) and native ferritin (NF) for 10 min reveals their binding at the apical plasma membrane. Little endocytosis is observable. However, after labeling the luminal side by the cellular markers and following exposure to apical hypotonicity, 75 mosm PBS for 10 min, endocytosis of all markers is enhanced to a high degree. Furthermore, the gold-coupled GPCDI antibody and cationized ferritin are transported within vesicles unidirectionally through the epithelium and are exocytosed at the basolateral aspect, indicating the retrieval and possible translocation of apical plasma membrane. In contrast, volume markers such as NF and HRP are also endocytosed under osmotic gradient exposure, but are not seen to be transcytosed. Therefore, the function of this membrane pathway seems not to be related to water reabsorption, but may be part of a cellular response as protection against the osmotic gradient.

Animals↗

Is the airway epithelium responsible for histamine metabolism in the trachea of guinea pigs?

The aim of the study was to investigate whether or not the epithelium plays an active role in histamine metabolism, via the histaminase and/or methyltransferase pathways. Isolated tracheas from guinea pigs sensitized to egg albumin (EA) were used. The epithelium was either left intact or removed from the preparations. The tracheal tubes were mounted in a chamber, allowing estimation of smooth muscle tension, and perfused with buffer. In some experiments the perfusate was collected for determination of histamine and methylhistamine. Mepyramine was used to evaluate the contribution of histamine to the EA-induced contraction. Mepyramine reduced the contraction by 90% when the epithelium was removed; with intact epithelium the reduction was 47%. Aminoguanidine, a histaminase inhibitor, significantly potentiated the response to EA when the epithelium was left intact. Traces of methylhistamine were detected in tissue extracts and perfusates. We conclude that histaminase is present in the preparation and that it can contribute to the inhibitory effect of the epithelium by means of histamine degradation.

Amine Oxidase (Copper-Containing)↗

Long-term observations on morphological changes of choledochal epithelium after choledochoenterostomy in rats.

Morphological changes of the common bile duct were observed macroscopically and microscopically 20 months after choledochojejunostomy and choledochocolonostomy in rats. The common bile ducts were remarkably dilated in all rats of both experimental models. Choledochal stones consisting of fatty acid calcium and calcium bilirubinate were seen in two of six rats with choledochojejunostomy and two of five rats with choledochocolonostomy. The main pathological change observed in both the groups was remarkable hyperplasia of the choledochal epithelium. Only one rat with choledochojejunostomy revealed normal epithelium with choledochal stone formation. Intestinal metaplasia was seen in two rats with choledochojejunostomy and all with choledochocolonostomy. Squamous pseudostratification of the epithelium indicating atypism was observed in two rats with choledochojejunostomy. Sialomucin producing cells and sulfomucin producing cells were seen in the hyperplastic portion of the epithelium. No malignant alteration of the epithelium was detected. These findings indicate that long-lasting exposure to digestive enzymes and bacteria causes epithelial hyperplasia and further exposure to digestive enzymes plays a major role in appearance of the epithelial atypism. Carcinogenesis of the choledochal epithelium under such an environment will need much more time to be established.

Animals↗

Ubiquitous expression of HLA-DR antigens on human small intestinal epithelium.

To clarify the frequency of the expression of HLA-DR antigens on the human small intestinal epithelium and the variation of such expression, 43 specimens (duodenum 16, jejunum 8, ileum 19; histologically normal 33, pathologic lesions 10) were studied for HLA-DR expression by indirect immunoperoxidase staining using monoclonal antibodies against HLA-DR antigens. All specimens reacted with anti-HLA-DR antibodies with minor variations. Most specimens showed decreasing intensity from the top of the villi toward the base of the villi and no staining in the crypt. In about half of the specimens, clear peripheral and cytoplasmic staining of the epithelial cells was observed. In some cases, the staining of the apical portion of the epithelium was patchy. The expression was unrelated to the lymph follicle. This ubiquitous expression of HLA-DR antigens on the small intestinal epithelium presents a striking contrast to an absence of the antigens on the normal large intestinal epithelium. A preliminary study on the pathologic lesions demonstrated the following changes in the expression of HLA-DR antigens; appearance of HLA-DR antigens on the crypt epithelium in Crohn's disease, loss of HLA-DR antigens on the epithelium covering the area of cell infiltration in macroglobulinemia and covering adenoma in familial polyposis coli.

Antibodies, Monoclonal↗

Effects of vitamin A-deficiency and inflammation on the conducting airway epithelium of Syrian golden hamsters.

The effects of vitamin A-deficiency and inflammation were studied in the conducting airways of Syrian golden hamsters. An important goal of the study was to characterize epithelial changes that occur early in vitamin A-deficiency, that might precede yet predispose to infection, and precipitate inflammatory changes in the lungs. Age-matched vitamin A-replete control and vitamin A-deprived hamsters were killed at 33 days of age (preweight-plateau); at 41 days of age (weight plateau-early weight loss); and at 48-55 days of age (prolonged weight plateau followed by weight loss). A tablet containing bromodeoxyuridine (BrdU) was implanted subcutaneously into each hamster 7 h before it was killed. No changes were seen in the conducting airway epithelium of vitamin A-deprived hamsters in the preweight plateau. However, labelling of secretory cells for BrdU was reduced 6-7 fold in the epithelium lining the lobar bronchus (p less than 0.0002) and the bronchioles (p less than 0.0001), and the proportions of ciliated cells were decreased (p less than 0.0001) at both airway levels in vitamin A-deficient hamsters in the weight plateau-early weight loss stage. Changes in cellular morphology were minimal in the intrapulmonary airway epithelium at this time but a few small focal patches of epidermoid metaplasia were seen in the tracheal epithelium. Small foci of inflammation were closely associated with the airways in the weight plateau, and the inflammation became more widespread when the deficiency was prolonged. The results suggest that the defense of the lungs to infection was impaired initially in the vitamin A-deficient hamsters by a widespread reduction in the numbers of ciliated cells throughout the epithelium of the conducting airways (trachea, bronchi, bronchioles). At the foci of inflammation, labelling of epithelial secretory cells for BrdU was greatly increased at all airway levels. A highly stratified cornifying epidermoid metaplasia developed in the tracheal epithelium, and goblet cell metaplasia developed in the cranial portion of the lobar bronchus, in association with submucosal inflammation. Goblet cell metaplasia appeared to be the only abnormality that was not reversed when vitamin A was restored to the diet.

Age Factors↗

Basis of chloride transport in ciliary epithelium.

The aqueous humor is formed by the bilayered ciliary epithelium. The pigmented ciliary epithelium (PE) faces the stroma and the nonpigmented ciliary epithelium (NPE) contacts the aqueous humor. Cl(-) secretion likely limits the rate of aqueous humor formation. Many transport components underlying Cl(-) secretion are known. Cl(-) is taken up from the stroma into PE cells by electroneutral transporters, diffuses to the NPE cells through gap junctions and is released largely through Cl(-) channels. Recent work suggests that significant Cl(-) recycling occurs at both surfaces of the ciliary epithelium, providing the basis for modulation of net secretion. The PE-NPE cell couplet likely forms the fundamental unit of secretion; gap junctions within the PE and NPE cell layers are inadequate to maintain constancy of ionic composition throughout the epithelium under certain conditions. Although many hormones, drugs and signaling cascades are known to have effects, a persuasive model of the regulation of aqueous humor formation has not yet been developed. cAMP likely plays a central role, potentially both enhancing and reducing secretion by actions at both surfaces of the ciliary epithelium. Among other hormone receptors, A(3) adenosine receptors likely alter intraocular pressure by regulating NPE-cell Cl(-) channel activity. Recently, functional evidence for the regional variation in ciliary epithelial secretion has been demonstrated; the physiologic and pathophysiologic implications of this regional variation remain to be addressed.

Animals↗

Estradiol receptor binding to the epithelium of uterine lumen and glands: region- and time-related changes during preimplantation and periimplantation periods studied by autoradiography.

The presence and changes of estradiol nuclear binding and related functions in uterine luminal and glandular epithelium were studied before and after blastocyst implantation using receptor autoradiography with (3)H-estradiol-17beta in association with (3)H-thymidine incorporation and immunocytochemical binding of antibody to estrogen receptor ER-alpha. (3)H-estradiol nuclear binding is present but variable during days 1.5-7.5 of pregnancy. Sites of strong nuclear binding of (3)H-estradiol exhibit strong immunocytochemical staining with ER-alpha antibody. Qualitative and quantitative evaluation of autoradiograms reveal that there is a general increase of nuclear (3)H-estradiol binding during the first 3 days after fertilization in both luminal and glandular epithelium. The binding of estradiol is stronger in glandular epithelium from day 2.5 to day 7.5, paralleled by a rise in (3)H-thymidine incorporation on day 2.5. By comparison, in the epithelium of the uterine lumen (3)H-estradiol nuclear binding is low, but relatively high in epithelial cells at lateral branching of the lumen where the increase in (3)H-estradiol binding corresponds to an increased labeling index with (3)H-thymidine. A highly differentiated binding of (3)H-estradiol to luminal and glandular epithelium was demonstrated with region- and time-specific changes of related effects on cell proliferation, differentiation, and secretion, probably involving involution and remodeling. The strong (3)H-estradiol binding to glandular epithelium suggests that estradiol exerts pronounced effects on glandular activities in the periimplantation period.

Animals↗

Correlation of cyclooxygenase-2 and aromatase immunohistochemical expression in invasive ductal carcinoma, ductal carcinoma in situ, and adjacent normal epithelium.

The purpose of our study was to evaluate the correlation between cyclooxygenase-2 (COX-2) and aromatase immunohistochemical expression in ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) present in the same breast, as well as in adjacent stroma and normal epithelium, we still correlated with nuclear grade, histologic grade, presence or absence of comedonecrosis, tumor size, and age at diagnosis. Forty-seven cases were evaluated through the use of anti-aromatase and anti-COX-2 polyclonal antibodies. Making the correlation of COX-2 and aromatase expression, we observed that COX-2 expression in IDC was correlated with aromatase expression in IDC (p < 0.001), DCIS (p < 0.001), normal epithelium (p = 0.024), and stroma tumor (p < 0.001). When the correlation was made between COX-2 expression in DCIS with aromatase, we observed positive correlation in IDC (p < 0.001), DCIS (p < 0.001), normal epithelium (p = 0.013), and stroma tumor (p < 0.001). In the correlative analysis of COX-2 expression in normal epithelium with aromatase in different evaluated tissues, we observed the following statistical results: IDC (p < 0.001), DCIS (p < 0.001), normal epithelium (p = 0.005), and stroma tumor (p = 0.047). Our results demonstrate the high correlation between COX-2 and aromatase expression in IDC, DCIS and normal epithelium, showing the importance of these two enzymes in the induction, promotion and progression of breast cancer.

Adult↗

Steroid hormone effects on the proliferation of human ovarian surface epithelium in vitro.

OBJECTIVE: The histologically bland-appearing epithelium of the human ovary is responsible for approximately 90% of ovarian cancers. Capitalizing on our ability to propagate this tissue in vitro, we have begun to characterize the steroid hormone responsiveness of the human ovarian surface epithelium. STUDY DESIGN: Primary cultures of the human ovarian surface epithelium are characterized as normal epithelium on the basis of morphologic features, normal karyotype, and immunohistochemistry demonstrating AE1/AE3 cytokeratin positivity and factor VIII negativity. Estrogen and progestin receptors were quantitatively analyzed with a standard receptor-ligand binding assay. Cellular proliferation in response to 1 x 10(-7) mol/L 17 beta-estradiol, progesterone, dihydrotestosterone, and dexamethasone were assessed by means of cell counts and a tetrazolium-based colorimetric assay. RESULTS: Scatchard analyses identified 8.8 x 10(3) estrogen receptors per cell in the premenopausal human ovarian surface epithelium cells, whereas the postmenopausal cells were negative for estrogen receptors. A total of 3.2 to 13.0 x 10(3) progestin receptors per cell was identified, with variable progestin receptor expression in the postmenopausal cells. No significant effect on cell growth could be demonstrated as a result of any of the steroid hormones investigated under the study conditions. CONCLUSIONS: Expression of estrogen and progestin receptors in human ovarian surface epithelium cells may be related to menopausal status. Steroid hormones, however, did not influence cell proliferation under these experimental conditions.

Cell Division↗

Enhancement of avian mandibular chondrogenesis in vitro in the absence of epithelium.

The roles of mandibular epithelium in chondrogenesis and growth of mandibular mesenchyme were examined in organ cultures. Epithelium and mesenchyme were separated from the mandibular arches of chick embryos at stages before and after the onset of chondrogenesis in vivo (stages 18-28). Isochronic and heterochronic tissue recombinations were prepared. Removal of the mandibular epithelium resulted in reduced growth of the explants and enhanced chondrogenesis, resulting in increased levels of mRNAs for type II collagen and aggrecan. The presence of mandibular epithelium promoted cell division in loosely arranged undifferentiated tissue from the mandibular mesenchyme and resulted in increased levels of type I collagen mRNA. Enhanced chondrogenesis was also observed in the mesenchyme isolated with basement membrane and isolated mesenchyme grown within Matrigel. These findings suggest that mandibular epithelium has mitogenic and chondrogenic-inhibitory effects on the underlying mesenchyme that are stage independent. Furthermore, the chondrogenic-inhibitory effect of mandibular epithelium on the underlying mesenchymal cells is not mediated by basement membrane.

Aggrecans↗

Intracellular activities of chloride, potassium and sodium ions in rabbit corneal epithelium.

The mechanism of ion transport in the epithelium of rabbit cornea was studied by determining the intracellular ion activity of Cl-, Na+ and K+ under various conditions. Ionic activities were measured by means of microelectrodes containing liquid ion-exchangers selective for Cl-, Na+ or K+. The Cl- activity in basal cells of the epithelium in Na+ containing bathing solutions amounts to 28 +/- 2 mM (n = 11). This value is 1.9-times greater than expected on the basis of passive distribution across the tear side membrane. This finding suggests the existence of a Cl- accumulating process. Replacement of Na+ in the aqueous bathing solution by choline or tetraethylammonium results in a reversible decrease in Cl- activity to 22 +/- 1 mM (n = 11, P less than 0.025). The ratio of observed and predicted Cl- activity decreased significantly from 1.9 to 1.4 (P less than 0.05). The decrease in Cl- activity due to Na+ replacement was rather slow. In contrast, after readmittance of Na+ to the aqueous bathing solution, Cl- activity rose to a stable level within 30 min. These results indicate involvement of Na+ in Cl- accumulation into the basal cells of the epithelium. The K+ and Na+ activities of the basal cells of rabbit corneal epithelium in control bathing solutions were 75 +/- 4 mM (n = 13) and 24 +/- 3 mM (n = 12), respectively. The results can be summarized in the following model for Cl- transport across corneal epithelium. Cl- is accumulated in the basal cells across the aqueous side membrane, energized by a favourable Na+ gradient. Cl- will subsequently leak out across the tear side membranes. Na+ is extruded again across the aqueous side membrane of the epithelium by the (Na+ + K+)-ATPase.

Animals↗

Odd-and even-numbered fatty acids. Their contrasting behavior in normal and fowlpox virus-infected epithelium.

Upon infection with fowlpox virus, the amount of odd-numbered fatty acids in chick scalp epithelium shows a significant decrease compared with control values. This effect begins quite early and progresses throughout the period of infection. Individual members of the odd-numbered family (C15--C27 inclusive) were quantitatively related to the group as a whole during most of the infection. Experiments involving the administration of labeled acetate in vivo demonstrated an increase in the synthesis of even-numbered fatty acids and a decrease in the synthesis of odd-numbered fatty acids in infected epithelium. The reduced synthesis of odd-numbered fatty acids in infected epithelium could also be demonstrated with labeled propionate. The influence of the alpha-oxidation pathway was assayed in chick scalp epithelium in vivo by the administration of [1-14C,9,10-3H] stearic acid. The C17 acids formed had a 3H/14C ratio similar to that of the C16 acids, indicating that most label incorporation into C17 was due to beta-oxidation to acetate followed by resynthesis into fatty acids. C17 fatty acids from control and infected epithelium had similar 3H/14C ratios, indicating that the alpha-oxidation pathway probably does not contribute to the differences in odd-numbered fatty acid content observed. In assays for fatty acid synthetase activty, both [14C] acetyl-CoA and [14C]-propionyl-CoA were used as initial acceptors. The specific activities of preparations from infected scalp were similar to those of control preparations with both substrates. These results suggest that there is no decline in the ability to utilize propionate for fatty acid synthesis in infected epithelium.

Acetates↗

A comparison of developmental changes in surface charge in mouse blastocysts and uterine epithelium using DEAE beads and dextran sulfate in vitro.

The ability of 3.5-day mouse blastocysts and vesicles prepared from maternal uterine epithelium to adhere to surfaces by charge interactions was compared by observing their adhesion to DEAE-Sephadex beads in the presence of increasing concentrations of dextran sulfate. The adhesion frequency for both the blastocysts and epithelium declined in a manner suggesting that predominantly ionic sites were being titrated, but differences between the two tissues in characteristics of the titration curve and susceptibility to neuraminidase digestion indicated that nonionic interactions were relatively more important for blastocysts. Because the threshold concentration of dextran sulfate required to initiate displacement of uterine epithelium from the DEAE beads was at least 4X that required to initiate the displacement of blastocysts, we argue that the uterine epithelium had at least 4X more interactive charged groups on its surface than the blastocysts. These differences were even more pronounced 4.5 days after mating, a time when attachment to the uterine epithelium is normally first seen in vivo. Blastocysts isolated at this time showed a marked increase in resistance to polyanion competition, but the epithelium showed a nearly 50% decline in surface negative charge that was not compensated by nonionic mechanisms. These observations support the conclusion that the initial adhesion of blastocysts in vivo is accompanied by a reduction in negativity of the uterine epithelial surface and by the formation of new trophoblast cell surfaces that adhere by nonelectrostatic interactions.

Agglutination↗

Alpha-enolase is restricted to basal cells of stratified squamous epithelium.

We have developed a monoclonal antibody against a 50-kDa protein that binds preferentially to basal cells in the limbus of rat, rabbit, and human corneas (J. D. Zieske, G. Bukusoglu, and M. A. Yankauckas, Invest. Ophthalmol. Visual Sci. 33, 143-152, 1992). Here we report on the purification and identification of the antigen. The 50-kDa antigen was purified from rabbit limbal and corneal epithelium using HPLC methodology including anion exchange (DEAE) followed by reverse-phase (C18) chromatography. The purified 50-kDa protein was then digested with endoproteinase Lys-C, and a reproducible profile comprising approximately 20 peptides was observed by reverse-phase HPLC of the digest. Sequence analysis of five peptides ranging in length from 4 to 20 residues revealed that the 50-kDa protein was alpha-enolase, a glycolytic enzyme. Overall, 57 amino acids were identified with a 95% sequence homology. Localization of alpha-enolase in rat epithelium by immunofluorescence microscopy demonstrated that simple epithelium contained low or undetectable levels of the enzyme. Stratified squamous epithelium, however, showed high levels of alpha-enolase, which was localized specifically to cells of the basal layer. Epidermal, corneal limbal, oral mucosal, vaginal, and laryngeal epithelium all showed cytoplasmic binding specific to the basal cells. These data indicate that the glycolytic enzyme alpha-enolase is preferentially localized in the basal cell layer of stratified squamous epithelium and suggest that glycolytic activity is concentrated in these cells. The localization pattern suggests that a major change in metabolism occurs as cells leave the mitotically active basal cell layer and migrate toward terminal differentiation in the suprabasal cell layers.

Amino Acid Sequence↗

Acetylcholinesterase activity as a marker for the development of the ciliary epithelium in the chicken embryo.

Specific histochemical staining for acetylcholinesterase was first visible in the presumptive ciliary epithelium on day 4 of embryonic development. The enzyme did not appear in the neural retina until day 6. The presence or absence of this enzyme activity enabled us to differentiate the presumptive ciliary epithelium from the adjacent presumptive neural retina early in development. In the rat embryo, acetylcholinesterase was not found in the ciliary epithelium at any stage, although its appearance in the neural retina followed a temporal pattern similar to that seen in chicken embryos. Weak AChE staining was seen in the ciliary epithelium of the rat by 15 days after birth. The function of acetylcholinesterase in the developing ciliary epithelium is unknown, but from the data currently available it is unlikely to be involved in the degradation of acetylcholine. Our observations suggest that some previous studies of retinal development may have misinterpreted events occurring in the embryonic ciliary epithelium as characteristics of the peripheral retina.

Acetylcholinesterase↗

5 alpha-androstane-3 beta,17 beta-diol hydroxylating enzymes in stroma and epithelium of human benign prostatic hyperplasia (BPH).

As enzymatic hydroxylation of 5 alpha-androstane-3 beta,17 beta-diol (3 beta-diol) may be a factor in controlling the 5 alpha-dihydrotestosterone (DHT) content in the prostate, we were interested in activity and distribution of these enzymes in epithelium and stroma of human benign prostatic hyperplasia (BPH). The enzyme activities were measured after mechanical separation of BPH tissue from 15 patients of various ages into stroma and epithelium, and optimization of the in vitro transformation of 3 beta-diol to hydroxylated products, which were analyzed by HPLC. The main results were: (1) 3 beta-diol was hydroxylated at C-7 alpha, C-7 beta, C-6 alpha, and C-6 beta. (2) The mean Michaelis constant Km (nM +/- SEM) for hydroxylation at C-7 alpha(beta) (168 +/- 21) was significantly lower than at C-6 alpha(beta) (601 +/- 43) without differences between stroma and epithelium. (3) Hydroxylation at alpha position dominated significantly over that at beta. (4) The mean maximal metabolic rate Vmax (pmol . mg protein-1 . h-1) of hydroxylation at C-6 alpha was about 7-fold lower in stroma (3.4 +/- 0.2) than in epithelium (23.8 +/- 4.1), concerning the other hydroxylations, Vmax was about 1.6-fold lower in stroma. (5) With increasing age of the patients there was a significant decrease of the 3 beta-diol hydroxylation in stroma and epithelium. It is discussed that the significantly lower activity of 3 beta-diol hydroxylation in stroma compared to epithelium and the decrease of activity with increasing age might potentiate the DHT accumulation in stroma of BPH.

Aged↗

Epithelium modulates the reactivity of ovalbumin-sensitized guinea-pig airway smooth muscle.

Mechanical removal of the airway epithelium alters the in vitro reactivity of airway smooth muscle. The modulation of reactivity may involve the release of inhibitory and excitatory factors from epithelial cells. Guinea pigs sensitized with ovalbumin have been used as an animal model of airway hyperreactivity. We evaluated the influence of the epithelium on the reactivity of in vitro tracheal smooth muscle from control and ovalbumin-sensitized guinea pigs, and the extent to which the presence of the epithelium affects the contractile response to in vitro challenge with ovalbumin. In both control and ovalbumin-sensitized tissues, epithelium removal increased the sensitivity of the preparations to histamine, methacholine and isoproterenol to a similar extent, i.e., 2- to 2.5-fold. Epithelium removal resulted in an 8.1-fold increase in sensitivity to ovalbumin in sensitized tissues. The epithelium appears not only to modulate the reactivity of the tissues to bronchoactive agents, but it also influences the magnitude of the contractile response following antigen challenge.

Animals↗