Histology and histopathology Vol.24, nº3 (2009)

Ir a Estadísticas

Permanent URI for this collection

http://hdl.handle.net/10201/177597

Browse

Recent Submissions

Now showing 1 - 5 of 13
  • Thumbnail Image
    Publication
    Open Access
    Chondrocyte-like apoptosis in temporomandibular joint disc internal derangement as a repair-limiting mechanism. An in vivo study
    (Murcia : F. Hernández, 2009) Loreto, C.; Musumeci, G.; Leonardi, R.
    Temporomandibular joint internal derangement (TMJ ID) is characterised by disc displacement and degenerative tissue changes involving an active cellular response, with cell phenotype transformation from fibroblast-like to fibrochondrocyte and, eventually, to chondrocyte-like, possibly as a response to abnormal loading. However, only small patches of chondral tissue are detected in TMJ discs with ID. We decided to explore the reasons for such incomplete tissue change, postulating an involvement of the apoptosis process. Twenty-one discs removed from 19 patients with TMJ ID were processed for TRAIL and DR5 immunohistochemical localisation, and subjected to the TUNEL assay. Overexpression of DR5 receptor and its ligand (TRAIL) in chondrocyte-like cells suggested activation of programmed cell death, as also demonstrated by TUNEL-positive cells. The data suggest a failed adaptive response to disc displacement through chondroid metaplasia. The apoptotic death of chondrocyte-like cells, which is at least partly regulated by TRAIL and its death receptor, appears to underpin the failed disc repair, eventually leading to its perforation.
  • Thumbnail Image
    Publication
    Open Access
    Expression of enzymes involved in synthesis and metabolism of estradiol in human breast as studied by immunocytochemistry and in situ hybridization
    (Murcia : F. Hernández, 2009) Li, Zhuo; Luu-The, Van; Poisson-Paré, David; Ouellet, Johanne; Li, Songyun; Labrie, Fernand; Pelletier, Georges
    It is well documented that human breast is actively involved in the local formation of estrogens. To determine the site(s) of action of enzymes involved in synthesis and metabolism of the most potent estrogen estradiol (E2), we have studied the expression of the following enzymes: 3ß-hydroxysteroid dehydrogenase (3-HSD), 17ß-HSD types 1, 2, 5, 7 and 12, aromatase, steroid sulfatase (STS) and estrogen sulfotransferase (EST) 1E1 at the cellular level in breast. Both in situ hybridization and immunocytochemistry were used for enzyme localization in normal breast tissues. For immunocytochemistry, we used rabbit antibodies, while in situ hybridization studies were performed using (35S)- labeled cRNA probes. Similar results were obtained with both approaches. All the enzymes (3ß-HSD; 17ß-HSD types 1, 5, 7 and 12; aromatase) involved in the conversion of circulating dehydroepiandrosterone (DHEA) to E2 as well as STS which converts estradiol sulfate (E2-S) to E2 have been found to be expressed in epithelial cells of acini and/or ducts as well as the stromal cells. Moreover, 17ß-HSD type 2 and EST1E1, two enzymes which inactivate E2, have been also localized in the same cell types. The present results indicate the enzymes which play a role in the synthesis and metabolism of E2 are expressed in both epithelial and stromal cells in human breast.
  • Thumbnail Image
    Publication
    Open Access
    Analysis of pRb, p16INK4A proteins and proliferating antigens, PCNA, Ki-67 and MCM5 expression in aggressive fibromatosis (desmoid tumor)
    (Murcia : F. Hernández, 2009) Stalinska, Lilliana; Turant, María; Tosik, Dariusz; Sygut, Jacek; Kulig, Andrzej; Kopczynski, Janusz; Dziki, Adam; Ferenc, Tomasc
    Aggressive fibromatosis (desmoid tumor) is a mesenchymal lesion originating from fascial, aponeurotic and muscular connective tissue. It rarely becomes histologically malignant. In this study we analyzed the cell cycle regulation proteins: pRb, p16, and proliferating antigens: Ki-67, PCNA, MCM5 with immunohistochemical method in archival material derived from 27 extra-abdominal (E-AD), 18 abdominal (AD) and 5 intra-abdominal (I-AD) cases of desmoid tumor. None of the examined cases (n=50) of aggressive fibromatosis was pRb-immunonegative. Heterogeneous expression of pRb was observed in 51.85% (14/27) of Group AD cases and in 5.56% (1/18) of Group E-AD cases; positive expression in 48,15% (13/27) of Group AD cases, in 94.44% (17/18) of Group E-AD cases, and in 100% (5/5) of Group I-AD cases. There were no negative cases for p16 staining in any of the examined groups. The number of heterogeneous cases in individual groups was: 33.33% (9/27) in Group AD, 50% (9/18) in Group E-AD and 40% (2/5) in Group I-AD, and positive cases: 66.67% (18/27), 50% (9/18) and 60% (3/5), respectively. Overexpression of PCNA was noted in 98% (49/50) of cases. The positive staining for Ki-67 protein was noted in 25.93% (7/27) in Group AD, in 16.67% (3/18) in Group E-AD and in 60% (3/5) in Group I-AD. None of the examined cases was immunopositive for MCM5 protein. The noted levels of pRb and p16 expression in desmoid cells reflect their function in cell cycle regulation. Probably the unsettled cell cycle progression, especially in G1 phase, is not the cause of aggressive fibromatosis pathogenesis.
  • Thumbnail Image
    Publication
    Open Access
    Lymph node lymphangiogenesis, a new concept for modulating tumor metastasis and inflammatory process
    (Murcia : F. Hernández, 2009) Ji, R.C.
    The proliferation of lymphatic endothelial cells (LECs) occurs not only in tumor and inflamed tissues, but also in regional draining lymph nodes (LNs). The lymph node lymphangiogenesis (LNLG) has recently emerged as a prominent area in biomedical research, because it is involved in the pathogenesis of several human diseases. The LEC functional features and lymphatic remodeling regulated by lymphangiogenic factors actively promote tumor metastasis and the inflammation process. VEGFA/ VEGFR-2 and VEGF-C/-D/VEGFR-3 have been implicated as the prime mediators in inflammation- or tumor-induced LNLG. This knowledge may provide a foundation for further understanding of specific modification in the gene expression, cell migration, and differentiation of LECs and other cells in lymphaticassociated diseases. Importantly, it should be taken into consideration that inflammation and lymphangiogenesis are strongly linked in the formation and metastasis of cancer when designing therapeutic strategies.
  • Thumbnail Image
    Publication
    Open Access
    Pulmonary expression of vascular endothelial growth factor (VEGF) and alveolar septation in a newborn rat model exposed to acute hypoxia and recovered under conditions of air or hyperoxia
    (Murcia : F. Hernández, 2009) Remesal, Ana; Pedraz, Carmen; San Feliciano, Laura; Ludeña, Dolores
    Vascular endothelial growth factor (VEGF) is an endothelial cell growth factor expressed in normal lung tissue. The aim of the study was to investigate the expression of VEGF and its repercussions as regards alveolarization in the developing rat lung. We studied pulmonary VEGF expression at 0 and 14 days of life in Wistar rats. Rat pups were exposed to hypoxia for two hours during the first hours of life and recovered under conditions of hyperoxia or normoxia for a further two hours, or not recovered. The animals of the control group were only exposed to conditions of normoxia. Our results showed that VEGF was increased in the lungs of the animals that were exposed to hypoxia but we did not find any correlation with the septation. The VEGF was decreased in the lungs of animals exposed to hyperoxia after neonatal hypoxia. We observed this at 0 and 14 days of life, and it was correlated with a lower degree of alveolarization at 14 days of life. Our data suggest that hyperoxia after neonatal hypoxia at birth may give rise to a decrease in the expression of VEGF, possibly permanently, together with a reduction in alveolar development.