Histology and histopathology Vol.29, nº 5 (2014)

Ir a Estadísticas

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    Morphological and immunohistochemical evaluation of ganglion cysts. Cross-sectional study of 354 cases
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) O’Valle, Francisco; Hernández-Cortés, Pedro; Aneiros Fernández, José; Caba Molina, Mercedes; Gómez-Morales, Mercedes; Cámara, Miguel; Payá, Jorge A.; Aguilar, David; Del Moral, Raimundo G.; Aneiros, Jose
    The aim of this study was to characterize the morphology and immunophenotype of ganglion cysts (GCs) and explore their histogenetic origin. Material and Methods: A cross-sectional morphological and immunohistochemical study of 354 GCs used the following antibody panel: vimentin, specific actin, ß- actin, smooth-muscle actin, smoothelin, h-caldesmon, ß- catenin, desmin, calponin, podoplanin, keratins 5/6, Ecadherin, cyclooxygenase 2 (COX-2), lysozyme, CD10, CD31, CD33, CD34, CD68, Ki-67, and PCNA. Doubleblind semi-quantitative analyses were conducted to evaluate the immunopositivity on a 4-point scale. Samples from 10 synovial membranes and 10 scapholunate ligaments were compared. GCs showed a hyalinized wall with mesenchymal spindle cells and were intensely positive for vimentin, actins, h-caldesmon, calponin in all cases and for podoplanin in 53% of cases, suggesting features of early muscle differentiation, without ruling out a myofibroblastic origin. Focal cavity lining of nonsynovial flat or raised cells (CD34/CD31/CD10/Ecadherin-negative and podoplanin-positive in 34% of cases) was detected in 93% of cases, showing differential expression with synovial membrane and scapholunate ligament cells. Nuclear positivity for proliferative markers was observed in GC wall cells (258.1±255; 1019.3±316 positive cells/mm2, Ki-67 and PCNA, respectively) but positivity for these markers was significantly lower (p<0.001 Mann Whitney U-test) in scapholunate ligament samples. Conclusion: In this first immunohistochemical study of GCs, focal cellular lining of the cavity was observed in almost all cases, and the immunophenotype was identical to that of GC wall cells. These cells are immunohistochemically different from synoviocytes and scapholunate ligament cells and show characteristics of myofibroblasts or mesenchymal cells undergoing early muscle differentiation.
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    Changes of calcium/calmodulin-dependent protein kinase II expression in dorsal root ganglia during maturation in long-term diabetes
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Ferhatovic, Lejla; Jelicic Kadic, Antonia; Boric, Matija; Puljak, Livia
    Calcium/calmodulin-dependent protein kinase II (CaMKII) is considered one of the key intracellular signaling proteins for development of neuropathy. We analyzed the expression of total CaMKII (tCaMKII) and its alpha, beta, gamma and delta isoforms in dorsal root ganglia (DRG) in a rat model of Diabetes mellitus type I (DM1), 6 months and 1 year after diabetes induction. Diabetes was induced with streptozotocin and confirmed by measuring glucose levels and weight increase. Immunohistochemistry was performed for detection of tCaMKII and its isoforms in L4 and L5 DRGs. A significant decrease of CaMKII alpha and beta isoforms was noted 6 months after diabetes induction, while CaMKII gamma and delta were significantly decreased after 12 months in diabetic rats compared to controls. Analysis of neuronal subgroups based on the neuronal diameter revealed that the expression of alpha, beta and delta isoforms decreased only in small-diameter neurons. In conclusion, a significant decrease of specific CaMKII isoforms in small-diameter DRG neurons may suggest involvement of CaMKII alpha, beta and delta in the development of complex events responsible for the development of neuropathy in long-term diabetes during maturation. CaMKII is a part of the neuronal pathway that regulates the firing properties of excitable cells, especially neurons, and decreased CaMKII activity may be responsible for generation of aberrant signals, hyperalgesia and neuropathic pain.
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    Immunohistochemical expression of RECK protein in placental membranes of the preterm delivery with and without chorioamnionitis
    (2014) Benzon, Zdeslav; Kuzmiç Prusac, Ivana; Zekic, Sandra; Vulic, Marko Vulic
    Objective: To compare the immunohistochemical expression of RECK protein in placental membranes of late preterm delivery in women with and without histologically proven chorioamnionitis. Study design: Fetal membranes were collected from women who had late preterm delivery with (n=8) and without (n=9) histologic chorioamnionitis. Immunohistochemistry for RECK protein was performed on formalin fixed and paraffin-embedded sections. The two groups were matched for age, body mass index and parity. SPSS Version 13.0 was used for statistical analysis. Results: There was weaker immunohistochemical expression of RECK protein in placental membranes of women with histologic chorioamnionitis compared to control subjects (P=0.0498). Conclusions: Chorioamnionitis has an impact on immunohistochemical expression of RECK protein in placental membranes in late preterm delivery
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    Bromodeoxyuridine (BrdU)-label-retaining cells in mouse terminal bronchioles
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Kameyama, Hiroki; Kudoh, Shinji; Udaka, Naoko; Kagayama, Motoko; Hassan, Wael; Hasegawa, Kohki; Niimori-Kita, Kanako Niimori-Kita; Ito, Takaaki
    Adult male mice were continuously treated with bromodeoxyuridine (BrdU) for 1, 2, or 4 weeks by an osmotic pump. To detect BrdU-label-retaining cells (LRCs), putative progenitor/stem cells, other animals were continuously treated with BrdU for 2 weeks, and were then kept without any treatments for 2, 6, or 18 months. The lungs were fixed with 4% paraformaldehyde, and were paraffin-embedded. We observed terminal bronchioles with BrdU immunostaining alone or with BrdU immunostaining accompanying immunostaining for Clara cell secretory protein (CCSP), forkhead box protein J1 (FoxJ1), or calcitonin gene-related peptide (CGRP). The average incidences of BrdU-incorporated cells in the terminal bronchioles after 1, 2, and 4 weeks of continuous BrdU infusion were 6.2%, 11.9%, and 23.1%, respectively. Most BrdU-incorporated cells in these periods were CCSP-immunoreactive (91.7%, 91.3%, and 88.2%, respectively), which means progenitor function of Clara cells. FoxJ1-immunoreactive BrdU-incorporated cells were fewer (5.4%, 3.0%, 2.7%, respectively). The average incidences of BrdU-LRCs in the terminal bronchioles after 2, 6, and 18 months were 7.2%, 4.3, and 2.7%, respectively. Most BrdU-LRCs were CCSP-immunoreactive (91.0%, 92.7%, and 89.6%, respectively), and FoxJ1- immunoreactive BrdU-LRCs were fewer (6.0%, 5.7%, and 2.1%, respectively). CGRP-positive BrdUincorporated cells were occasional. CGRP-positive BrdU-LRCs were detected in 17.6% of neuroepithelial bodies (NEBs) at 2 months, but disappeared at 6 months. BrdU-positive stem cell candidates, which locate at the brochiolo-alveolar duct junction or cover NEB, were few throughout this study. In conclusion, in the lungs treated only with BrdU, CCSP-immunoreactive cells are important to maintain homeostasis in the terminal bronchiolar epithelium.
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    Induction of high temperature requirement A1, a serine protease, by TGF-beta1 in articular chondrocytes of mouse models of OA
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Xu, Lin; Golshirazian, Imanoel; Asbury, Brian J.; Li, Yefu
    The goal of this study is to determine whether transforming growth factor beta 1 (Tgf-ß1) induces the high temperature requirement A1 (HtrA1) in articular chondrocytes of two mouse models of osteoarthritis (OA). Early onset articular cartilage degeneration in the mouse models was characterized by histology. Expression profiles of Tgf-ß1, p-Smad1, pSmad2/3 and HtrA1 in knee joints of the mouse models were examined by immunofluorescene. By in vitro and ex vivo experiments, human primary chondrocytes and articular cartilages from femoral condyles of mice were treated with recombinant human TGF-ß1 and an ALK5 chemical inhibitor, SB431542. The level of HTRA1 mRNA in human and mouse articular chondrocytes was examined by real-time PCR. Chondrocyte clusters were present in the articular cartilage of knee joints in the mouse models. Increased expressions of Tgf-ß1, pSmad2/3 and HtrA1 were detected in the articular chondrocyte of knee joints in the mouse models. The increased expressions of p-Smad2/3 and HtrA1 were colocalized in the articular chondrocyte of the knee joints. The expression of p-Smad1 was hardly detectable in the mouse models and their corresponding wild-type littermates. The level of HTRA1 mRNA was increased in human and mouse articular chondrocytes treated with TGF-ß1, compared with that in chondrocytes without the treatment of TGF-ß1. The TGF-ß1-induced expression of HTRA1 in human and mouse articular chondrocytes was inhibited by SB431542. These results suggest that the Tgf-ß1 canonical signaling was activated to induce HtrA1 in the articular chondrocytes of the mouse models of OA.