Histology and histopathology Vol.23, nº8 (2008)
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- PublicationOpen AccessDegenerative changes of the interface membrane as a possible reason for prosthesis loosening(Murcia : F. Hernández, 2008) Krohmer, Gerhard; Koleganova, Nadezda; Hadjicostas, Panayiotis T.; Fink, Bernd; Berger, I.Objective: The aim of the present study was to perform a comparative evaluation of septic and aseptic interface membranes, assessing histological features, inflammatory infiltrate, and expression of inflammatory cytokines. Methods: Septic and aseptic interface membranes from 102 patients were examined by histology, histochemistry, and immunohistochemistry (tissue arrays). The cell subpopulations were characterized by quantification of CD3, CD4, CD8, CD20, and CD163 positive cells. Additionally, a semiquantitative evaluation of inflammatory cytokines (TNFa, TGF-ß1, IL-1, IL-6, CRP, MMP-1, MMP-6) was performed to complete the analysis of inflammatory infiltrates. Results: The histological analysis revealed three different types of aseptic interface membranes: wear particle, degenerative, and mixed type. The expression of inflammatory molecules did not differ between septic and wear particle interface membranes. Significantly lower expression of cytokines, MMPs and CRP was observed, however, in degenerative interface membranes compared to other types. No expression of TNFa was observed in the degenerative interface membranes. Over 88% of patients with degenerative interface membranes had had a clinical record of osteoarthritis. Conclusion: Aseptic interface membranes were represented by wear particle, degenerative and mixed type. The expression of inflammatory factors in wear particle type is similar to this in septic membranes and can contribute to the bone destruction and prosthesis loosening. These factors seem not to play a major role in the degenerative membranes.
- PublicationOpen AccessP53, CD95, cathepsin and survivin pathways in Fuchs dystrophy and pseudophakic bullous keratopathy corneas(Murcia : F. Hernández, 2008) Szentmáry, Nora; Szende, Béla; Süveges, IldikoOur purpose was to elucidate the pathways of apoptosis of corneas with Fuchs’ dystrophy and pseudophakic bullous keratopathy. Sixteen corneal buttons (14 patients, median age 73 years) with Fuchs’ dystrophy, 13 with pseudophakic bullous keratopathy (PBK) (13 patients, median age 69 years) and 8 buttons (8 patients, median age 59 years) from enucleated eyes with chorioideal melanoma (controls) were analysed histologically. Immunohistochemical analysis was performed to investigate the expression of p21, p27, p63, survivin, CD95, cathepsin, bax, bcl-2 and Ki67. Positive immunohistochemical reactions were detected in epithelial cells of the corneas, but keratocytes and endothelial cells were not positive in any of the groups or stainings. The number of p27 and survivin positive epithelial cells was significantly lower (p=0.048 and 0.041) and the number of cathepsin positive epithelial cells was significantly higher (p=0.004) in Fuchs’ dystrophy corneas compared to controls. In pseudophakic bullous keratopathy, p21 and p27 positive epithelial cells were present in a significantly lower (p=0.02 and 0.005) number than in controls. We conclude that genetically programmed cell death is related to the p27, cathepsin and survivin pathways in Fuchs’ dystrophy and to the p21 and p27 pathways in pseudophakic bullous keratopathy.
- PublicationOpen AccessRECK, a novel matrix metalloproteinase regulator(Murcia : F. Hernández, 2008) Meng, N.; Li, Y.; Zhang, H.; Sun, X-F.Extracellular matrix (ECM) macromolecules are important for creating the cellular environments required during development and morphogenesis of tissues. Matrix metalloproteinases (MMPs) are a family of Zn-dependent endopeptidases that collectively are capable of cleaving virtually all ECM substrates, and play an important role in some physiological and pathological processes. MMP activity can be inhibited by some natural and artificial inhibitors. A newly found membrane-anchored regulator of MMPs, the reversioninducing- cysteine-rich protein with kazal motifs (RECK), is downregulated when the cells undergo a process of malignant transformation, and is currently the subject of considerable research activity because of its specific structure and function. In this review, we have chosen to concentrate our efforts on the structure, function, regulation, and future prospect of RECK in order to provide a new target for prevention and treatment of tumours.
- PublicationOpen AccessExpression of K+ channels in normal and cancerous human breast(Murcia : F. Hernández, 2008) Brevet, Marie; Ahidouch, Ahmed; Sevestre, Henri; Merviel, Philippe; El Hiani, Yassine; Robbe, Micheline; Ouadid-Ahidouch, HalimaPotassium (K+) channels contribute to the regulation of cell proliferation and apoptosis and are also involved in tumor generation and malignant growth. Using immunohistochemical analysis, we investigated the expression of four K+ channels GIRK1 (G-Protein Inwardly Rectifying Potassium Channel 1), Ca2+-activated K channel (KCa1.1), voltage activated K+ channels (KV 1.1 and KV 1.3) and of the anti-apoptotic protein Bcl2 in normal and cancerous breast tissues and compared their expression with clinicopathological data. GIRK1 was overexpressed in carcinomatous tissues. In contrast, KV 1.1 and KV 1.3 were less expressed in cancerous tissue. The expression of Bcl-2 was similar in both tissues. As to the clinicopathological data, a correlation between KCa1.1 channel and estrogen receptor (ER) expression was observed. GIRK1 was overexpressed in breast carcinoma suggesting its involvement in proliferation and oncogenesis and its possible use as a putative pharmaceutigal target. The correlation between KCa1.1 channel and ER suggests the involvement of this channel in proliferation. The loss of expression of the two channels KV 1.1 and KV 1.3 may correspond to their role in apoptosis.
- PublicationOpen AccessApolipoprotein D expression absence in degenerating neurons of human central nervous system(Murcia : F. Hernández, 2008) Navarro, Ana; Ordóñez, Cristina; Martinez, Eva; Pérez, Cristina; Astudillo, Aurora; Tolivia, JorgeApolipoprotein D (apo D), a lipocalin transporter of small hydrophobic molecules could play an important role in several neurodegenerative diseases. However, its role in those diseases remains unclear. There has been reported increments of apo D in relation with different neuropathologic diseases. Recently, we reported the absence of apo D in neurons of substantia nigra which can contribute to the lability of neurons to oxidative damage. In order to determine the relationship between apo D expression and neuronal death, we studied the expression of apo D in various regions of human brains from patients without any neurological or psychological disorders, in relation with the neuronal damage revealed by Fluoro-Jade B staining. The absence of expression for apo D in injured neurons and the negative staining for Fluoro-Jade B of neurons that express apo D was observed in all sections studied. These findings are in accordance with the role possibly played by apo D in the neuroprotection of the nervous system.
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