Histology and histopathology Vol.21, nº 2 (2006)
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- PublicationOpen AccessImmunocytochemical localization of metabotropic (mGluR2/3 and mGluR4a) and ionotropic (GluR2/3) glutamate receptors in adrenal medullary ganglion cells(Murcia : F. Hernández, 2006) Sarría, R.; Díez, J.; Losada, J.; Doñate-Oliver, F.; Kuhn, R.; Grandes, P.The localization of metabotropic glutamate receptors of groups II (mGluR2/3) and III (mGluR4a) and the subunits 2 and 3 of alfa-amino-3-hydroxy-5- methyl-4-isoxazolepropionic acid (AMPA) ionotropic glutamate receptors (GluR2/3) was investigated with immunocytochemical methods in the rat adrenal gland. MGluR2/3, mGluR4a and GluR2/3 immunoreactivities were observed in large-sized, centrally located type I adrenal medullary ganglion neurons. Furthermore, the small-sized type II adrenal ganglion neurons identified by their immunoreactivity to brain nitric oxide synthase (bNOS), also expressed mGluR2/3, mGluR4a and GluR2/3. These cells were disposed in the peripheral portion of the adrenal medulla. None of the type I neurons were positively labeled for bNOS. These morphological observations suggest that activation of glutamate receptors in ganglion neurons may be instrumental in the control of adrenal endocrine systems as well as blood regulation.
- PublicationOpen AccessExpression and function of cell cycle proteins in rheumatoid arthritis synovial tissue(Murcia : F. Hernández, 2006) Taranto, E.; Leech, M.Rheumatoid Arthritis (RA) is a chronic disease characterised by synovial lining hyperplasia and progressive destruction of joint tissues. Experimental data suggests that abnormal alterations in the expression of proteins involved in maintaining homeostatic control of the cell cycle is involved in disease progression in RA. By contributing to the overgrowth of synovial tissue, factors such as dysregulated proliferation or reduced apoptosis of cells can directly influence the pathological outcome of RA.
- PublicationOpen AccessStress proteins expression in rat kidney and liver chronically exposed to aluminium sulphate(Murcia : F. Hernández, 2006) Stacchiotti, A.; Rodella, L.F.; Ricci, F.; Rezzani, R.; Lavazza, A.; Bianchi, R.Aluminium (Al) is the third most widespread metal in the environment. It is toxic for the brain, bone and haematological system but unfortunately very little data exist for other organs. Stress proteins are induced or enhanced against metal toxicity with an essential role in the recovery of organules and other cellular proteins. This immunohistochemical study was performed to analyze the distribution of three stress proteins (HSP25, HSP72, GRP75) in rat kidney and liver orally exposed to Al sulphate daily for 3 and 6 months. Al-induced alterations were further studied by histopathology (H&E, PAS, Perl’s, Masson) and ultrastructural morphometry. In the kidney: HSP25 was enhanced in proximal tubules after 6 months Al-exposure when abnormal brush borders were observed; HSP72 was induced in proximal tubules only after long Al-treatment; GRP75 was raised in midcortical area sometimes within nuclei. Furthermore, lysosomal and lipofuscins densities increased in the juxtamedullary tubules after 3 months Al exposure with respect to controls. In the liver: Perl’spositive deposits and fibrosis became evident after Al treatment. HSP25 was very weak; HSP72 focal in pericentral hepatocytes at 3 months and induced also in Kupffer cells at 6 months; GRP75 diffuse in periportal hepatocytes and non parenchymal cells at 6 months. Prolonged Al exposure stimulated stress proteins strictly organ-dependently in the rat. Their distribution in kidney and liver seems related to cumulative sublethal effects induced by metal and could be a sensitive index of Al susceptibility of these organs.
- PublicationOpen AccessRhoB in cancer suppression(Murcia : F. Hernández, 2006) Huang, M.; Prendergast, G.C.RhoB is a mainly endosomal small GTPase that regulates actin organization and vesicle trafficking. Expression of RhoB is elevated rapidly by many stimuli, including growth factors, cytokines, and genotoxic stress. In cancer, RhoB can limit cell proliferation, survival, invasion, and metastasis, and during malignant progression its levels are attenuated commonly. In support of its role as a negative modifier of cancer progression, targeted deletion of RhoB in mice can increase tumor formation initiated by Ras mutation. How RhoB acts to suppress different aspects of cancer pathophysiology has emerged as a question of significant interest.
- PublicationOpen AccessAlterations of the cerebrospinal fluid proteins and subcommissural organ secretion in the arterial hypertension and ventricular dilatation. A study in SHR rats(Murcia : F. Hernández, 2006) Martínez de la Peña y Valenzuela, Isabel; Carmona-Calero, E.; Pérez-González, H.; Ormazabal-Ramos, C.; Fernández-Rodríguez, P.; Gonzalez-Marrero, I.; Castañeyra Perdomo, A.; Ferres Torres, R.The aim of this work was to analyze the proteins in the cerebrospinal fluid (CSF) of spontaneously hypertensive rats, to study their possible role in the relationship between hydrocephalus, arterial hypertension and alterations in the subcommissural organ. Brains from control Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) sacrificed with chloral hydrate were used. Antiserums against some cerebrospinal fluid protein bands and Reissner’s fiber (RF) were used for immunohistochemical study of the SCO. Ventricular dilation was observed in the lateral and third ventricle of the SHR. Third ventricle ependyma showed immunoreactive material (IRM) for antibody against 141kDa protein band anti-B1 and 117 protein band anti-B2 and the SCO of the SHR showed a decrease of the IRM when compared with WKY rats. An alteration in the expression of anti-RF was found to compare the SCO of the WKY and SHR groups. Our results demonstrate that hydrocephalus and hypertension are interconnected in this kind of rat which produce alterations in SCO secretions and some proteins of the CSF.
- PublicationOpen AccessIdentification of gene networks modulated by activin in LßT2 cells using DNA microarray analysis(Murcia : F. Hernández, 2006) Mazhawidza, W.; Winters, S.J.; Kaiser, U.B.; Kakar, S.S.Activins, members of the TGFß family of proteins, are widely expressed in a variety of tissues. First identified based on their ability to regulate biosynthesis and secretion of follicle-stimulating hormone (FSH), activins have also been shown to modulate development, cell growth, apoptosis, and inflammation. Despite their many known functions, the precise mechanisms and downstream signaling pathways by which activins mediate their diverse effects remain unknown. We have used a DNA microarray assay to identify genes that are regulated by activin, alone or in combination with gonadotropin-releasing hormone (GnRH), another major regulator of FSH, in a murine gonadotrope-derived cell line (LßT2). We used mRNA from these cells to screen Affymetrix Mu74av2 mouse Gene Chip oligonucleotide microarrays, representing approximately 12,400 mouse genes. Treatment of LßT2 cells with activin A, a gonadotropin-releasing hormone agonist (GnRHA) or activin A plus GnRHA resulted in alterations in levels of gene expression that ranged in magnitude from 15 to 67-fold. Data analysis identified 268 transcripts that were up- or down-regulated by twofold or more. Distinct sets of genes were affected by treatment with activin, GnRHA and activin plus GnRHA, suggesting interactions between activin and GnRHA. Changes in expression of seven randomly selected representative genes identified by the microarray technique were confirmed by real-time quantitative PCR and semi-quantitative reverse transcription/PCR (RT/PCR). Modulation of expression of genes by activin suggests that activin may mediate its effects through a variety of signaling pathways.
- PublicationOpen AccessATM gene expression is associated with differentiation and angiogenesis in infiltrating breast carcinomas(Murcia : F. Hernández, 2006) Cuatrecasas, M.; Santamaria, G.; Velasco, M.; Camacho, E.; Hernandez, L.; Sanchez, M.; Orrit, C.; Murcia, C.; Cardesa, Antonio; Campo, Elías; Fernandez, P.L.The product of the ATM gene, mutated in the human genetic disorder ataxia-telangiectasia (A-T) plays a key role in the detection and repair of DNA doublestrand breaks. A-T is defined by progressive cerebellar ataxia, telangiectasia, sensitivity to ionising radiation and genomic instability with cancer predisposition. On the other hand, increased angiogenesis is essential for tumor growth and metastasis. The aim of this study was to investigate ATM expression in breast carcinomas and its relationship to neoangiogenesis. Methods and Results: Fifty-two breast tumors from 51 patients, 38 of them with concomitant in situ component (CIS), were analyzed by immunohistochemistry for the expression of ATM. CD34 expression was used for the morphometric evaluation of vasculature. ATM was positive in 1 to 10% of normal epithelial cells. ATM expression was reduced in 55.8% of infiltrating carcinomas, non-reduced in 34.6%, and increased in 9.6%. Expression of ATM in CIS was similar to the infiltrating component in 71% of cases and reduced in 23.7% of them. High-grade ductal infiltrating carcinomas showed lower ATM expression than lowgrade ones. Reduced ATM expression also correlated with increased microvascular area. Conclusions: Reduced ATM expression in breast carcinomas correlated with tumor differentiation and increased microvascular parameters, supporting its role in neoangiogenesis and tumor progression in breast carcinogenesis.
- PublicationOpen AccessMolecular alterations of monophasic synovial sarcoma: loss of chromosome 3p does not alter RASSF1 and MLH1 transcriptional activity(Murcia : F. Hernández, 2006) Pazzaglia, L.; Benassi, M.S.; Ragazzini, P.; Gamberi, G.; Ponticelli, F.; Chiechi, A.; Hattinger, C.M.; Morandi, Luca; Alberghini, M.; Zanella, L.; Picci, P.; Mercuri, MarioDifferential diagnosis of monophasic synovial sarcoma requires the detection of specific biological markers. In this study we evaluated the presence of molecular alterations in 15 monophasic synovial sarcomas. Multiple changes affecting chromosome arms were detected by CGH-array in all microdissected cases available, and an association between gain or loss of specific regions harbouring cancer progression-associated genes and aneuploid status was found. The most frequent alteration was loss of 3p including 3p21.3-p23 region that, however, did not involve the promoter regions of the corresponding genes, RASSF1 and MLH1. Using Real-Time PCR, mRNA levels of both resulted moderately high compared to normal tissue; however, the weak to absent protein expression suggests RASSF1 and MLH1 posttranscription deregulation. Moreover, immunohistochemical analysis revealed that both mesenchymal and epithelial antigens were present in diploid tumours. These findings confirm the genetic complexity of monophasic synovial sarcoma and underline the need to integrate different analyses for a better knowledge of this tumour, essential to investigate new diagnostic and prognostic markers.
- PublicationOpen AccessMolecular pathology of endometrial carcinoma, Transcriptional signature in endometrioid tumors(Murcia : F. Hernández, 2006) Abal, M.; Planaguma, J.; Gil-Moreno, A.; Monge, M.; Gonzalez, M.; Baró, Teresa; Garcia, A.; Castellvi, J.; Ramón y Cajal, S.; Xercavins, J.; Alameda, F.; Reventos, J.A dualistic model, which has been established on a morphological basis and that differentiates type I endometrioid from type II nonendometrioid endometrial cancer, is widely accepted. Molecular genetics have provided us with data supporting the dualistic model of endometrial tumorigenesis and with some clues to speculate about the sequence of the molecular alterations defining the tumorigenesis pathways. In type I endometrioid endometrial cancer, PTEN gene silencing, microsatellite instability associated with defects in DNA mismatch repair genes, or mutations in the K-ras gene are the known major alterations defining the progression from normal endometrium to hyperplasia and then on to carcinoma. Recently, cDNA microarray technology for identifying the differences in gene expression patterns between the histological types of endometrial cancer have permitted the identification of differentially expressed genes that could help us to understand differences in the biology and the clinical outcome between histiotypes. Genes involved in the mitotic checkpoint as a major mechanism of carcinogenesis in non-endometrioid endometrial cancer, or altered genes associated with the initial steps of myometrial infiltration in endometrioid endometrial cancer, represent examples of how useful large genetic screenings can be for understanding the tumorigenesis process and the future directions in the molecular pathogenesis of endometrial cancer.
- PublicationOpen AccessDetection of anti-mullerian hormone receptor II protein in the postnatal rat testis from birth to sexual maturity(Murcia : F. Hernández, 2006) Mendis-Handagama, S.M.L.C.; Di Clementi, N.; Ariyaratne,H.B.S.; Mrkonjich, L.Anti-Mullerian hormone (AMH) produced by the immature Sertoli cells negatively regulates the postnatal Leydig cell (i.e. adult Leydig cells/ALC) differentiation, however, the mechanism is sparsely understood. AMH negatively regulates the steroidogenic function of fetal Leydig cells (FLC) and ALC. However, when this function is established in the ALC lineage and whether AMH has a function in FLC in the postnatal testis are not known. Therefore, the objectives of this study were to examine the presence of AMH receptor type II (AMHR-II) in FLC and cells in the ALC lineage in the postnatal mammalian testis using the rat model Male Sprague Dawley rats of days 1, 5, 7-21, 28, 40, 60 and 90 were used. AMHR-II in testicular interstitial cells was detected in testis tissue using immunocytochemistry. Findings showed that the mesenchymal and the progenitor cells of the ALC lineage, were negative for AMHR-II. The newly formed ALC were the first cell type of the ALC lineage to show positive labeling for AMHR-II, and the first detection was on postnatal day 13, although they were present in the testis from day 10. From days 13-28, labeling intensity for AMHR-II in the ALC was much weaker than those at days 40-90. FLC were also positive. The time lag between the first detection of the newly formed ALC in the testis and the first detection of AMHR-II in them suggests that the establishment of the negative regulatory role of AMH on ALC steroidogenesis does not take place immediately upon their differentiation; no change in cell size occurs during this period. The absence of AMHR-II in mesenchymal cells suggests that it is unlikely that the negative regulatory effect of AMH on ALC differentiation in the postnatal testis is achieved via a direct action of AMH on mesenchymal cells. The presence of AMHR-II in postnatal FLC suggests a possible role by AMH on FLC, which warrants future investigations.
- PublicationOpen AccessAntioxidant enzymes in renal cell carcinoma(Murcia : F. Hernández, 2006) Soini, Y.; Kallio, J.P.; Hirvikoski, P.; Helin, H.; Kellokumpu-Lehtinen, P.; Tammela, T.L.J.; Peltoniemi, M.; Martikainen, P.M.; Kinnula, V.L.The aim of the study was to estimate the significance of oxidative/nitrosative damage and expression of antioxidant enzymes in renal cell carcinomas (RCC). For this we investigated immunohistochemically six antioxidant enzymes (AOEs) including MnSOD, ECSOD, thioredoxin, thioredoxin reductase, and gammaglutamyl cysteine synthetase heavy and light chain in 138 RCCs. As an indicator of oxidative/nitrosative damage, sections were stained with an antibody to nitrotyrosine. The extent of apoptosis was evaluated by TUNEL method and proliferation by immunohistochemistry to Ki67. Variable expression of all AOEs could be seen in RCC with expression of MnSOD being strongest. Nitrotyrosine was significantly associated with high grade tumors. MnSOD was associated with tumors of a lower stage. Cases showing ECSOD reactivity had higher and cases expressing thioredoxin lower apoptotic index than other tumors. No association with patient prognosis was observed. According to the results renal cell carcinomas show oxidative/nitrosative damage which, according to nitrotyrosine staining, was higher in high grade tumors. Of AOEs, MnSOD was more abundantly expressed in low stage tumors suggesting that its antioxidant function could play a main role to prevent development of oxidative damage leading to more aggressive tumors.