Evaluation of epithelial maturity in hormonally related stomatitis.
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Aged↗
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Results for “epithelial maturation”
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From immature to mature epithelium: unveiling structural dynamics and transcriptional programs in rainbow trout intestinal barrier.
The intestinal epithelium is crucial for nutrient absorption, immune defense, and barrier function in farmed fish. However, the molecular mechanisms underlying its development and maturation in salmonids remain poorly characterized, hindering our ability to address pervasive gut health challenges in aquaculture. In this study, we use the RTgutGC cell line to implement an epithelial maturation model with the aim of characterizing the global transcriptional program in rainbow trout (Oncorhynchus mykiss). We evaluated in vitro culture conditions to generate a polarized epithelial barrier with high transepithelial electrical resistance (TEER = 75.8 Ω × cm2), low permeability (6.2 × 10-6 cm/s), and well-defined apical specializations, including microvilli-like structures and clusters of these structures (brush border). Comparative transcriptomic profiling between immature (7 days post-seeding, dps) and mature (28 dps) epithelia revealed 3,817 differentially expressed genes (DEGs). Functional enrichment analysis showed that maturation was characterized by the downregulation of proliferative and ribosomal pathways and the concerted upregulation of processes critical for barrier function, including transmembrane transport, proteolysis, cell adhesion, extracellular matrix organization, and tight junction assembly. We identified a core set of 60 genes indicators of epithelial maturation, encompassing solute transporters (slc26a6, slc43a2), tight junction proteins (tjp1, cldn1, cldn3, cldn5, cldn18, among others), and structural components essential for microvilli formation and polarization (cdhr5b, pard6a). By integrating ultrastructural, functional, and transcriptomic data, this study established a framework for future mechanistic investigations into gut development and maturation in vitro. This set of mature epithelium indicators has diverse applications, such as the design of nutritional and pharmacological interventions to improve gut health and resilience in farmed fish.
Animals↗
Difference between mammary epithelial cells from mature virgin and primiparous mice.
Mammary epithelial cells from mature virgin mice are similar to those from primiparous mice in several respects. However, there is one known difference. The cells from the mature virgin must traverse the cell cycle in order to become competent to make casein and enzymatically active alpha-lactalbumin in vitro; those from the primiparous animal can make these proteins without first traversing the cycle. In this regard, cells from human placental lactogen- and prolactin-treated mature virgins are, after involution, similar to those from primiparous mice. The developemental block in the cells from the mature virgin, imposed by preventing cell cycle traversal, has been partially delineated. It does not appear to reside at the levels of ultrastructural maturation or the formation of casein messenger RNA. Rather, the lesion is postranscriptional and may be at the level of translation, or posttranslational modification, or both.
Animals↗
Translocation of dimeric IgA through neoplastic colon cells in vitro.
We studied the translocation of dimeric IgA across epithelium, using neoplastic human colon cells in culture as a source of epithelial cells, and immunoelectronmicroscopy with peroxidase-labeled antigens and antibodies. The cells had some of the ultrastructural characteristics of normal, mature epithelial cells, i.e., polarity, desmosomal junctions, and secretory component on their basal and lateral plasma membranes. Horseradish peroxidase-labeled dimeric IgA, exposed to the cells at 0 degrees C, bound selectively to secretory component on the cell surfaces. At 37 degrees C, the bound dimeric IgA was taken into the cells by endocytosis and transported apically through the cytoplasm in vesicles. After 30 min, IgA was discharged across the apical surface. Neither colchicine (10(-4) M) nor cytochalasin B (10(-5) M) interfered with binding or endocytosis of dimeric IgA, but colchicine inhibited intracellular transport of the IgA-containing vesicles. These experiments demonstrated that dimeric IgA can be transported through living intestinal epithelial cells in vitro. The transport includes 1) specific binding of IgA dimers to secretory component on plasma membranes, 2) endocytosis of IgA in vesicles, 3) transcytoplasmic transport of the IgA-containing vesicles by a process involving microtubules, and 4) discharge of IgA at the apical surfaces.
Binding Sites, Antibody↗
C bodies and R bodies in the epithelial cells of normal and diseased human rectum.
Small spherical, extracellular bodies (C bodies) measuring 20 to 80 nm in diameter and enclosed by a trilaminar membrane 7 nm wide surrounded the microvilli of human rectal epithelial cells. Similar bodies were observed within membrane-bound vesicles (R bodies) in the apical cytoplasm. The C bodies associated with the mature epithelial cells of the luminal surface were more numerous than those associated with the immature cells of the crypts, where the R bodies predominated. A decreased number of C bodies was observed in ulcerative colitis. We concluded that the membrane-bound C bodies surrounding the microvilli were cellular in origin and arose from R bodies within the cytoplasm of the rectal epithelial cells.
Cell Membrane↗
Human vaginal epithelial multilayer tissue culture.
Fragments of normal human adult vagina, when explanted onto glass slides gave rise to outgrowing sheets of pure epithelium, which had microscopic morphological features in common with normal vaginal epithelium. Infrequent fibroblast contamination was observed. Proliferating epithelial cells formed multilayers of stratified squamous epithelium and demonstrated a progressive decrease in proliferative activity after 14 days. Continuous lines of epithelial cells were not obtained. Even in the absence of estrogens, transmission electron microscopy revealed evidence of keratinization of the superficial cells of the multilayer. Scanning electron microscopy of the surface of mature epithelial cells in culture revealed ultrastructural features that closely resembled those present on the surface of exfoliated cells obtained by scraping the vagina in vivo. This in vitro tissue culture model of human vaginal epithelium may provide a simple method of studying factors that influence vaginal epithelium growth, maturation and function.
Cell Differentiation↗
Distal enhancer-insulator module of GDF6 is essential for cochlear formation.
Several genes guide inner ear development, and mutations in these genes can cause malformations that result in congenital hearing loss. However, the contribution of noncoding regulatory elements remains largely unclear. This study investigates the function of distal enhancer elements in the transcriptional regulation of GDF6, a gene implicated in cochlear development. Using mouse models with targeted deletions, human inner ear organoids, and CRISPR interference (CRISPRi), we identified a downstream regulatory interval harboring a developmental enhancer required to maintain GDF6 expression during otic epithelial maturation and cochlear morphogenesis. Deletion of this regulatory region or targeting of CRISPRi-based repressors to these regions resulted in decreased GDF6 expression, failure of otic-epithelium development, and prevention of hair cell-like differentiation, reflecting cochlear aplasia observed in patients with corresponding genomic deletions. These findings highlight the contribution of long-range regulatory elements to auditory development and illustrate how their disruption contributes to human deafness.
Animals↗
Multifocal nephroblastic neoplasia.
Among 23 patients with multifocal metanephric neoplasia were 14 patients with 43 grossly visible subcapsular tumorlets, 0.3-3.5 cm in diameter, that were apparently derived from nodular renal blastema. Tumorlets are defined as circumscribed lesions that are visible on the exterior surface of the kidney, produce either a raised nodule or, in a few instances, a shallow depression, and are independent of the main tumor(s). Most tumorlets displayed homogeneous epithelial maturation. A substantial minority of tumorlets retained a blastemic character and a few were histologically malignant. Tumorlets tended to be multiple and bilateral but were absent in 9 patients with multifocal disease, including 4 of 10 with bilateral tumors. About half the lesions that achieved tumorlet status, including those that gave rise to clinical tumors, underwent malignant transformation. Contralateral tumorlets should not be mistaken for metastasis and do not adversely affect prognosis. The incidence of neoplasia among young, close relatives of patients with multifocal disease appeared to be excessive, but no clear excess of major anomalies, hemihypertrophy, or minor genitourinary tract anomalies was revealed by a retrospective survey of hospital charts.
Child↗
Hereditary mucoepithelial dysplasia: a disease apparently of desmosome and gap junction formation.
A previously unrecognized autosomal dominant syndrome affecting oral, nasal, vaginal, urethral, anal, bladder, and conjunctival mucosa with cataracts, follicular keratosis, nonscarring alopecia, and terminal lung disease is described in a four-generation kindred of German extraction. Severe photophobia, tearing, and nystagmus in infancy heralds the development of keratitis, corneal vascularization, and lens cataracts. Repeated corneal transplants have failed. Red, periorificial mucosal lesions involving the above structures are noted by 1 year of age and may persist throughout life. Chronic rhinorrhea and repeated upper respiratory infections frequently progress to bilateral pneumonia accompanied by loss of hair, diarrhea, occasional melena, enuresis, pyuria, and hematuria. Spontaneous pneumothorax is frequent, terminating in fibrocystic-type lung disease and cor pulmonale. Women have had repeated abnormal vaginal PAP smears. Histologically the mucosal epithelium shows dyshesion, thinning of the epithelial layer, and dyskeratosis. Mucosal PAP smears show lack of epithelial maturation, cytoplasmic vacuoles and inclusions, and individual cell dyskeratosis. Histochemically there is a lack of cornification and keratinization. Ultrastructural studies show lack of keratohyalin granules, a paucity of desmosomes, intercellular accumulations, cytoplasmic vacuolization, and formation of bands and aggregates of filamentous fibers and structures in the cytoplasm resembling desmosomes and gap junctions. The condition is probably a panepithelial cell defect of desmosomal and gap junction structure most prominently affecting mucosal epithelia associated with an increased susceptibility to a variety of adventitious organisms.
Adult↗
MHC restriction of murine T lymphocyte reactivity analysed by growth of bone marrow cells in vitro on thymus epithelial monolayers.
Mature mouse T lymphocytes, derived from long-term culture of bone marrow cells on thymus epithelial monolayers, were analysed with respect to their ability to co-operate with B cells (for antibody production) or T cells (in the generation of cytotoxic cells) when the bone marrow T precursor cells and the thymus epithelial cells differ at defined regions of the major histocompatibility complex. A pool of more mature bone marrow T-cell precursors gave rise to T cells interacting only with T/B lymphocytes sharing MHC determinants with the strain of origin of the bone marrow cells used. In contrast, a more immature bone marrow T-cell precursor pool produced T lymphocytes which had acquired MHC restriction (in terms of co-operativity with T/B cells) as defined by the MHC determinants of the thymus epithelium, and not those MHC determinants of the cultured bone marrow population. In addition, some evidence was obtained for Ir gene control (mapping in the MHC region) in the development of the repertoire of T cells involved in production of cytotoxic responses in vitro to TNP-modified self antigens.
Animals↗
Hypoxia-inducible factor 2 regulates alveolar regeneration after repetitive injury in three-dimensional cellular and in vivo models.
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease in which repetitive epithelial injury and incomplete alveolar repair result in accumulation of profibrotic intermediate/transitional "aberrant" epithelial cell states. The mechanisms leading to the emergence and persistence of aberrant epithelial populations in the distal lung remain incompletely understood. By interrogating single-cell RNA sequencing (scRNA-seq) data from patients with IPF and a mouse model of repeated lung epithelial injury, we identified persistent activation of hypoxia-inducible factor (HIF) signaling in these aberrant epithelial cells. Using mouse genetic lineage-tracing strategies together with scRNA-seq, we found that these disease-emergent aberrant epithelial cells predominantly arose from airway-derived (Scgb1a1-CreER-traced) progenitors and exhibited transcriptional programs of Hif2a activation. In mice treated with repetitive intratracheal bleomycin, deletion of Epas1 (Hif2a) but not Hif1a, from airway-derived progenitors, or administration of the small-molecule HIF2 inhibitor PT-2385, using both prevention and rescue approaches, attenuated experimental lung fibrosis, reduced the appearance of aberrant epithelial cells, and promoted alveolar repair. In mouse alveolar organoids, genetic or pharmacologic inhibition of Hif2 promoted alveolar differentiation of airway-derived epithelial progenitors. In addition, treatment of human distal lung organoids with PT-2385 increased colony-forming efficiency, enhanced protein and transcriptional markers of alveolar type 2 epithelial cell maturation, and prevented the emergence of aberrant epithelial cells. Together, these studies showed that HIF2 activation drives the emergence of aberrant epithelial populations after repetitive injury and that targeted HIF2 inhibition may represent an effective therapeutic strategy to promote functional alveolar repair in IPF and other interstitial lung diseases.
Animals↗
[Effect of fixed bridges on the maturation process of the epithelial cells of the alveolar ridge mucosa].
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Acrylic Resins↗
Plasma membranes from rat intestinal epithelial cells at different stages of maturation. I. Preparation and characterization of plasma membrane subfractions originating from crypt cells and from villous cells.
To determine the mechanism of the maturation of the brush border membrane in intestinal epithelial cells, purification of the plasma membrane from undifferentiated rat crypt cells and of the basal-lateral membrane from villous cells has been performed. The method is based on density perturbation of the mitochondria to selectively disrupt their association with the membrane. With both cell populations, two membrane subfractions displaying the same respective density on sucrose gradient have been obtained with an overall yield of 15--20% and a 10-fold enrichment of the plasma membrane markers 5'-nucleotidase and (Na+ + K+)-dependent, ouabain-sensitive ATPase chosen to follow their purification. The four fractions were constituted by sheets and apparently closed vesicles of various sizes. Each fraction was characterized by a distinct protein composition and different levels of enzyme activities. The cells, used for the preparation of the membranes, were isolated as a villus to crypt gradient. This separation and that of the membranes, led to the conclusion that the (Na+ + K+)-dependent ATPase is localized principally in the plasma membrane of all cells whatever their state of maturation, while 5'-nucleotidase is predominantly located in the basal-lateral membrane of the villous cells and may serve as a specific marker for the purification of this membrane. Finally it has been shown that aminopeptidase, dissacharidases and alkaline phosphatase do not appear simultaneously in the maturation process of the cells, alkaline phosphatase being absent from the crypt cells and aminopeptidase being the first to be synthesized. This enzyme seems to appear in the crypt cells membrane before being integrated into the mature brush border membrane.
Aging↗
[Benign non-epithelial tumors of the stomach].
Six cases of mature non-epithelial tumours of the stomach are described; epithelioid leiomyoma, leiomyoma, lipoma, two fibromata and angiofibrolipoma. Noteworthy is the extremely rarely occurring epithelioid leiomyoma. In one case, lipoma and chronic peptic ulcer coexisted. All the stomach tumours under study were mature benign ones, but some of them presented a clinical course with signs of malignancy probably due to the endogastric growth of the tumour, its dimensions, and its localization near the stomach outlet, as well as to the breach of integrity of the mucous membrane above the tumour.
Cell Transformation, Neoplastic↗
Bacterial adherence to epithelial cells in the nasopharynx in children.
The presence of attached bacteria to epithelial cells from the nasopharyngeal surface of the soft palate, from the adenoid surface and from the secretions covering the adenoid was studied in 10 children undergoing adenoidectomy. Large numbers of bacteria were seen to attach to mature normal squamous epithelial cells from the soft palate and in the secretions, whereas attachment to adenoid epithelial cells was rare. Using differential interference contrast microscopy, bacteria-carrying epithelial cells were seen to have their surface covered by microridges characteristic of normal mature squamous epithelial cells. Sections of adenoid tissue showed bacterial infiltration of adenoid tissue to be virtually nonexistent in the patient group.
Adenoidectomy↗
Pathogenesis of diarrhoea caused by astrovirus infections in lambs.
Experimental infection of 2-day-old gnotobiotic lambs with lamb astrovirus produced mild diarrhoea after an incubation period of about 48 hours. No other clinical symptoms developed. Infection was studied by immunofluorescent and histological examination of tissues from the lambs. Astroviruses infected only mature villus epithelial cells and subepithelial macrophages in the small intestine, where they produced partial villus atrophy. Infected enterocytes were replaced with cuboidal cells from the crypts, and the lesion gradually healed by 5 days after infection. No serological relationship was detected by immunofluorescence between lamb astrovirus antigen in gut sections and antisera to either calf or human astrovirus.
Animals↗
[Mucoepidermoid tumor of the epipharynx].
Case report about a mukoepidermoid-tumor, which was investigated by means of histology and electron microscopy. The localisation of this tumor in the epipharynx is a rarity and unknown in the literature. The variable differentiated tumor consists of epidermoid cells with different graduation of maturity, of epithelial cells from the gland ducts and primitive acini as well as in the majority of undifferentiated cell types. The tumor seems to be of a "low grade malignity".
Adenocarcinoma, Mucinous↗
Clinical, histologic, cytologic, and ultrastructural characteristics of the oral lesions from hereditary mucoepithelial dysplasia. A disease of gap junction and desmosome formation.
Hereditary mucoepithelial dysplasia is an autosomal, dominantly inherited disorder affecting all of the orificial mucosa with cataracts, follicular keratosis of skin, nonscarring alopecia, bouts of pneumonia, spontaneous pneumothorax, and terminal cor pulmonale. The oral lesion is a fiery red, flat or micropapillary-appearing mucosa most frequently involving the gingiva and hard palate. All oral and pharyngeal mucosa may be involved, however. Red scrotal mucosa of the tongue is common. Histologically, the oral mucosa shows a lack of cornified and keratinized cells, a decrease in the thickness of the epithelial cell layer, dyshesion, and dyskeratosis. Papanicolaou smears show lack of epithelial cell maturation, poikilocytosis, anisocytosis, large paranuclear cytoplasmic vacuoles, and cytoplasmic strand-shaped inclusions. Ultrastructural features include a paucity of desmosomes, intercellular accumulations of amorphous material, cytoplasmic vacuoles, and paranuclear lesions with strands of material resembling gap junctions and desmosomes. The condition most likely represents a basic defect in gap junction and desmosome formation.
Adult↗