Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the basement membrane (BM) in atrophic tubules in human kidney biopsies were studied by electron microscopy and by immunohistochemistry on cryostat sections with antibodies against collagen type I, type III, type IV, laminin, EMA, keratin and vimentin. The BM showed different degrees of thickening with formation of reduplications which contained fibrocytes. Remnants of cytoplasm of epithelial cells and fibrocytes were incorporated in the thickened BM. This showed signs of lysis and disintegration, indicating that the redundant BM formed by the epithelial cells is removed, although imperfectly, by interstitial cells. Thinning of the BM was another frequent finding. Immunohistochemistry showed a clear reactivity for collagen type IV and laminin in all BM material. The epithelial cells showed multilayering and a peculiar type of dark cells extending underneath adjacent cells and separating them from their BM attachment.
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PMID:Basement membrane changes in atrophic tubules in the human kidney. 210 47

The disappearance of palatal medial edge epithelium (MEE) after fusion of secondary palatal shelves is often cited as a classical example of embryonic remodeling by programmed cell death. We reinvestigated this phenomenon in 16-day rat embryos, using light and electron microscopy. We confirm reports that the periderm of the two-layered MEE begins to slough after shelves assume horizontal positions. In vitro, peridermal cells are not able to slough and are trapped during the adhesion process. In vivo, however, surface cells shed before the shelves in the anterior palate adhere, allowing junctions to form between opposing basal epithelial cells. Midline seams so formed consist of two layers of basal cells, all of which appear healthy. Even though its cells are dividing, growth of the seam fails to keep pace with palatal growth and it thins to one layer of cells, and then breaks up into small islands. The basal lamina disappears and elongating MEE cells extend filopodia into adjacent connective tissue. Electron micrographs reveal transitional steps in loss of epithelial characteristics and gain of fibroblast-like features by transforming MEE cells. One such feature, observed with the aid of immunofluorescence, is the turn of the mesenchymal cytoskeletal protein, vimentin. No cell death or macrophages are observed after adhesion and thinning over most of the palate. These data indicate that MEE is an ectoderm that retains the ability to transform into mesenchymal cells. Epithelial-mesenchymal transformation may be expressed in other embryonic remodelings (R.L. Trelstad, A. Hayashi, K. Hayashi, and P.K. Donahue, 1982, Dev. Biol. 92, 27), resulting in heretofore unsuspected conservation of embryonic cell populations.
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PMID:Medial edge epithelium transforms to mesenchyme after embryonic palatal shelves fuse. 246 46

To investigate the pathogenesis of congenital hydrocephalus the brains of HTX rats aged between 16 days and 4 weeks and the brains of normal Wistar rats of the same ages were examined. In the fetal HTX rat brains, the lateral ventricles were symmetrically dilated from 20 days of gestation. The neuroepithelium bordering the ventricles showed thinning with cellular disarrangement and deformity. Similar neuroepithelial abnormalities were also found in the lateral ventricles of the HTX rat brain with no macroscopic signs of hydrocephalus at 20 days of gestation. The neuroepithelium showed flattening of the cells, widening of the intercellular spaces, formation of microvilli on the detached lateral cell surfaces, and frequent macrophage infiltration. On the other hand, the neuroepithelial cells of the third ventricle and the aqueduct were affected less severely or showed no significant abnormalities. Immunohistochemically, most of the neuroepithelium and ependyma of the lateral ventricles were positive for vimentin in both prenatal and postnatal hydrocephalic HTX rats, while a small number or none of those in normal control rats were positive. These morphological changes suggested that preferential involvement of the lateral ventricular neuroepithelium might be closely associated with the pathogenesis of congenital hydrocephalus in HTX rats.
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PMID:Neuroepithelial and ependymal changes in HTX rats with congenital hydrocephalus: an ultrastructural and immunohistochemical study. 958 75

In the rat lung, primary saccules are transformed into alveoli from postnatal Days 4 to 13, after which time there is a 20% reduction in the number of lung fibroblasts as the interstitial volume of the alveolar walls decreases. Our objective was to determine whether apoptosis is a factor in the observed decrease in the number of interstitial lung fibroblasts beyond Day 13. We used both histologic and flow cytometric assays to detect in lung fibroblasts the DNA fragmentation and condensation that are characteristic of apoptosis. In addition, we evaluated levels of bcl-2 and BAX messenger RNAs (mRNAs) using a reverse transcriptase-polymerase chain reaction (RT-PCR) assay. Apoptotic cells were quantitated in glycol methacrylate-embedded sections of neonatal rat lungs using the terminal transferase dUTP-digoxygenin nick end-labeling (TUNEL) method. Although TUNEL-positive interstitial cells were observed in the lungs of rats ranging in age from 10 to 16 d, a dramatic increase in apoptotic cells was seen on Day 17. Although diminished in number, TUNEL-positive cells were still present on Day 28. Hoechst-stained apoptotic bodies were observed in isolated lung cells that were vimentin-positive and factor VIII-negative, which identified the apoptotic cells as fibroblasts as opposed to endothelial cells. Flow cytometric analysis of freshly isolated lung fibroblasts stained with Hoechst 33342 indicated a 24% increase in chromatin condensation in cells from 17-d versus 16-d rats. DNA fragmentation was also quantitated by flow cytometry in freshly isolated fibroblasts labeled with BODIPY-conjugated dUTP in the presence of terminal deoxynucleotidyl transferase. The percentage of lung fibroblasts containing fragmented DNA was 51.4 +/- 13.4 in 17-d, 36.9 +/- 8.6 in 18-d, and 13.8 +/- 5.4 in 19-d rat pups. Finally, evaluation by RT-PCR indicated that on postnatal Day 17, mRNA for bcl-2, which inhibits apoptosis, was decreased to 73.5 +/- 11.4% (P < 0.001) of Day 5 controls; whereas mRNA for BAX, which enhances apoptosis, was increased to 243.0 +/- 102.0% (P < 0.001) of Day 5 values. These results demonstrate that rat lung fibroblasts undergo apoptosis after the completion of alveolarization, and suggest that this decrease in fibroblast number plays an important role in the thinning and remodeling of the alveolar walls of the lung.
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PMID:Lung fibroblasts undergo apoptosis following alveolarization. 992 13

The matrix metalloproteinases (MMPs) and endothelin-1, a potent vasoconstrictor and mitogen for smooth muscle cells, have been shown to be involved in the pathogenesis of various vascular disorders. However, the expression of endothelin-1 and the activation of MMPs have not been fully evaluated in plexogenic pulmonary arteriopathy (PPA). Immunohistochemical and confocal microscopic studies were conducted to evaluate the reactivity of lung tissue from six patients with pulmonary hypertension for alpha-smooth muscle actin (alpha-SMA), desmin, vimentin, factor VIII, endothelin-1, various types of MMPs (MMP-1, MMP-2, MMP-3, MMP-7 and MMP-9), membrane type-MMPs (MT-MMPs), tissue inhibitors of MMPs (TIMPs), and type IV collagen. Four major arterial morphological abnormalities were recognized in PPA: muscularization of pulmonary arterioles, onion-skin lesions, cellular and mature plexiform lesions, and atheromas in elastic pulmonary arteries. Reactivity for MMP-2 and MT-1-MMP was found in endothelial cells and, to a lesser extent, in myofibroblasts proliferating in various lesions of PPA. Increased expression of endothelin-1 was observed in the latter cells and in endothelial cells. Some myofibroblasts were positive for MMP-3 and MMP-7 in the vascular lesions except for mature plexiform lesions. MMP-1, MMP-9 and TIMP-2 tended to be positive only in the atheromatous lesions. Staining for type IV collagen showed focal thinning and discontinuities of the endothelial basement membrane in plexiform lesions. This study demonstrates colocalization of MMP-2 with MT-1-MMP and increased expression of endothelin-1 in various arterial lesions of PPA. These changes may play important roles in the remodeling of arterial structures, particularly of basement membranes, in this disorder.
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PMID:Immunohistochemical study of endothelin-1 and matrix metalloproteinases in plexogenic pulmonary arteriopathy. 1216 97

In late gestation, morphological maturation of fetal lung includes septal thinning of potential airspaces, a process accelerated by exogenous glucocorticoids. Apoptosis occurs in normal fetal lung. Glucocorticoids increase apoptosis in several tissues. The authors hypothesized that exogenous glucocorticoids would increase apoptosis in fetal lung, primarily in the interstitium. They administered dexamethasone (DEX), 1 mg/kg, or vehicle (Control) to pregnant rats at 19 days of gestation. Fetuses were delivered at 3, 7, 12, or 24 hours post injection. DEX decreased fetal body weight and lung weight, DNA, and protein 12 hours post injection. Using the terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) reaction to label apoptotic cells in lung, they calculated an apoptotic index (AI, apoptotic cells/1000 total cells) for each fetus. Average DEX AI (3.6+/-2.6, mean+/-SD) was greater than Control (1.7+/-0.5) (P<.02). All DEX AIs were greater than Control AIs at 3, 7, and 12 hours, but were similar to Controls at 24 hours post injection. Apoptotic cells appeared to be interstitial, based on colocalization with vimentin staining. Presence of apoptotic cells was confirmed by electron microscopy and detection of the nucleosomal ladder pattern on DNA electrophoresis. The authors conclude that maternal administration of dexamethasone increases apoptosis in fetal lung, primarily in the interstitium. They speculate that apoptosis may contribute to morphological fetal lung maturation induced by endogenous glucocorticoids.
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PMID:Maternally administered dexamethasone transiently increases apoptosis in lungs of fetal rats. 1274 47

We describe the results from genetic dissection of a QTL region on chicken chromosome 2, shown to affect egg weight and quality in an earlier genome scan of an F2 intercross between two divergent egg layer lines. As the 90% confidence intervals for the detected QTL covered tens of centiMorgans, new analyses were needed. The datasets were re-analysed with denser marker intervals to characterise the QTL region. Analysis of a candidate gene from the original QTL region, vimentin, did not support its role in controlling egg white thinning. Even after reanalysis with additional seven markers in the QTL area, the 90% confidence intervals remained large or even increased, suggesting the presence of multiple linked QTL for the traits. A grid search fitting two QTL on chromosome 2 for each trait suggested that there are two distinct QTL areas affecting egg white thinning in both production periods and egg weight in the late production period. The results indicate possible pleiotropic effects of some of the QTL on egg quality and egg weight. However, it was not possible to make a distinction between close linkage versus pleiotropic effects.
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PMID:A region on chicken chromosome 2 affects both egg white thinning and egg weight. 1609 15

We used a neonatal mouse model to examine the histogenesis of uterine adenomyosis, and to test whether adenomyosis is due to an abnormality in myometrial differentiation, or in extracellular matrix proteins expression. We also studied the effects of tamoxifen and estradiol on uterine development, myometrial differentiation, and organization. Female CD1 pups were treated with oral tamoxifen (1 mg/kg) (n=27) or estradiol (0.1 mg/kg) (n=24) from age 1 to 5 days. Uteri from control (n=27) and treated mice were obtained on days 2, 5, 10, 15, and 42 of age. We examined the sections histologically, using image analysis and immunohistochemistry for alpha-smooth muscle actin (alpha-SMA), desmin, vimentin, laminin, fibronectin, and estrogen receptor-alpha. Following tamoxifen exposure, all uteri showed adenomyosis by 6 weeks of age (seen as early as day 10). The inner myometrium showed thinning, lack of continuity, disorganization, and bundling. alpha-SMA expression was normal. Desmin expression normally showed a wave of maturation that was absent in tamoxifen-treated mice. In the estradiol group, adenomyosis was not observed. All uterine layers were normally developed, but hypertrophied. The inner myometrium retained its circular arrangement. There was no difference in the localization of laminin or fibronectin between groups (laminin expression was reduced in the tamoxifen treated uteri). Vimentin could not be detected in all groups. Our results suggest that the development of the inner myometrium is particularly sensitive to estrogen antagonism, and can be affected by steroid receptors modulation. Disruption of the inner myometrium may play a role in the development of uterine adenomyosis.
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PMID:The effects of tamoxifen and estradiol on myometrial differentiation and organization during early uterine development in the CD1 mouse. 1945 Nov 94

A 15-year-old boy presented with an anaplastic supratentorial ependymoma causing massive intratumoral calcification, without contributory medical and family history, and manifesting as persistent headache for 2 months. Physical examination found no neurological deficit except for visual defect in the right lower quadrant, with intact visual acuity. Blood examination showed no abnormalities. Cranial computed tomography revealed a huge calcified mass in the left parietooccipital lobe, with extensive perilesional brain edema. Cranial radiography showed diffuse and symmetrical thinning of the calvarial bone. Magnetic resonance imaging confirmed the tumor as an assembly of medullated masses with extraventricular location, 7 x 6.5 x 6.5 cm in diameter, and appearing as heterogeneous intensity on both T(1)- and T(2)-weighted images with inhomogeneous enhancement except for the central cores. The patient underwent tumor resection. Intraoperative findings revealed that the cortical veins overlying the tumor were reddish and moderately engorged. The hypervascular tumor, entirely extraventricular in location, was totally resected without neurological deterioration. Histological examination revealed that the tumor was highly cellular with hyperchromatic nuclei and cell atypia. Necrosis, mitotic figures, and perivascular pseudorosette formations were frequently seen. Immunohistochemical study showed positive staining for glial fibrillary acidic protein, S-100 protein, vimentin, and epithelial membrane antigen, but negative for synaptophysin. The MIB-1 labeling index was 26.5%. The findings were compatible with anaplastic ependymoma (World Health Organization classification grade 3). Ependymoma should be included in the differential diagnosis of a supratentorially located, extraventricular mass with massive intratumoral calcification.
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PMID:Huge supratentorial extraventricular anaplastic ependymoma presenting with massive calcification--case report. 2018 83

We previously demonstrated that in the CD-1 mouse, which exhibits a high incidence of age-related adenomyosis, neonatal exposure to tamoxifen induced premature uterine adenomyosis and was associated with abnormal development particularly of the inner myometrium. In the present study, we examined the effect of neonatal tamoxifen administration upon uterine development in the C57/BL6J mouse strain that is not known to develop uterine adenomyosis. Female C57/BL6J pups (n=20) were treated with oral tamoxifen (1 mg/kg) from age 1 to 5 days. Uteri from control and treated mice were obtained on days 5, 10, 15 and 42 of age. We examined sections histologically using image analysis and immunohistochemistry for alpha-smooth muscle actin (ACTA2, alpha-SMA), desmin, vimentin, laminin, fibronectin and oestrogen receptor-alpha (ESR1). Following tamoxifen exposure, all uteri showed inner myometrium thinning, lack of continuity, disorganisation and bundling. However, adenomyosis was not seen in any uterus. ACTA2 immunostaining was less in the circular muscle layer of treated mice. The temporal pattern of desmin immunostaining found in control mice was absent in tamoxifen-treated mice. There was no difference in the localisation of laminin or fibronectin between control and tamoxifen-treated groups. However, laminin immunostaining was reduced in the circular muscle layer of treated mice. Vimentin could not be detected in either group. In conclusion, our results demonstrate that the development of the inner myometrium is particularly sensitive to oestrogen antagonism, and is affected by steroid receptor modulation. Although tamoxifen induces inner myometrial changes including that of ACTA2, desmin, ESR1 and laminin expression in C57/BL6J neonatal mice similar to those induced in CD-1 mice, C57/BL6J mice did not develop premature adenomyosis. Thus, disruption of the development and differentiation of the inner myometrium cannot alone explain the development of tamoxifen-associated adenomyosis, and this must be dependent upon its interaction with strain-dependent factors.
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PMID:Neonatal administration of tamoxifen causes disruption of myometrial development but not adenomyosis in the C57/BL6J mouse. 2036 91


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