Histology and histopathology Vol.23, nº2 (2008)
Permanent URI for this collection
Browse
Browsing Histology and histopathology Vol.23, nº2 (2008) by Issue Date
Now showing 1 - 13 of 13
Results Per Page
Sort Options
- PublicationOpen AccessMedial and adventitial macrophages are associated with expansive atherosclerotic remodeling in rabbit femoral artery(Murcia : F. Hernández, 2008) Yamashita, A.; Shoji, K.; Tsuruda, T.; Furukoji, E.; Takahashi, M.; Nishihira, K.; Tamura, S.; Asada, YujiroExpansive vascular remodeling is considered a feature of vulnerable plaques. Although inflammation is upregulated in the media and adventitia of atherosclerotic lesions, its contribution to expansive remodeling is unclear. We investigated this issue in injured femoral arteries of normo- and hyperlipidemic rabbits fed with a conventional (CD group; n=20) or a 0.5% cholesterol (ChD group; n=20) diet. Four weeks after balloon injury of the femoral arteries, we examined vascular wall alterations, localization of macrophages and matrix metalloproteases (MMP)-1, -2, -9, and extracellular matrix. Neointimal formation with luminal stenosis was evident in both groups, while expansive remodeling was observed only in the ChD group. Areas immunopositive for macrophages, MMP-1, -2 and -9 were larger not only in the neointima, but also in the media and/or adventitia in the injured arterial walls of the ChD, than in the CD group. Areas containing smooth muscle cells (SMCs), elastin and collagen were smaller in the injured arterial walls of the ChD group. MMP-1, -2 and -9 were mainly localized in infiltrating macrophages. MMP-2 was also found in SMCs and adventitial fibroblasts. Vasa vasorum density was significantly increased in injured arteries of ChD group than in those of CD group. These results suggest that macrophages in the media and adventitia play an important role in expansive atherosclerotic remodeling via extracellular matrix degradation and SMC reduction.
- PublicationOpen AccessDown-regulation of lysyl oxydase-like in aging and venous insufficiency(Murcia : F. Hernández, 2008) Pascual, G.; Mendieta, C.; Mecham, R.P.; Sommer, P.; Bellón, J.M.; Buján, J.Background: Elastin expression is higher in tissues where elastic fibres are essential for the correct maintenance of function such as blood vessels. Elastin expression usually diminishes with age, however, it may be re-expressed in response to injury or repair processes. Some authors attribute the characteristic loss of elasticity of the varicose vein to a drop in the population of smooth muscle cells in the media layer. A reduction in elastin has been observed in chronic venous insufficiency, but little is known about some of the factors involved in elastin synthesis such as lysyl oxidases. The aim of this study was to examine the in vivo expression of the elastin precursor, tropoelastin (TE), and lysyl oxidase-like 1 (LOXL1), a cross-linking enzyme responsible for elastin polymer deposition. The effects of age on these expression patterns were also evaluated. Methods: Saphenous vein segments were obtained during surgery from organ donors (controls, n=20) and subjects with venous insufficiency (varicose veins, n=20). Both these groups were subdivided according to subject age into <50 years (n=10) and ³ 50 years (n=10). Control and varicose vein tissue specimens were immunolabelled using anti-tropoelastin and antiLOXL1 antibodies and also subjected to Western blot analysis. Results: Our results indicate that the levels of these markers of elastin synthesis (LOXL/tropoelastin) in the vein wall diminish in a significant way (p<0.05) with the age factor. Excluding the age factor, LOXL1 was significantly decreased in the varicose condition (p<0.05). In the younger pathological population they showed an inverse relationship (LOXL decreased, tropoelastin increased). Conclusions: The already established reduction in elastin in the varicose condition may be related, at least in part, to the decreased LOXL1 levels observed here. These events could reduce spontaneous reticulation of elastin and the partial loss of tissue elasticity in this group of patients.
- PublicationOpen AccessAnalysis of Epstein-Barr virus strains and variants in classical Hodgkin s lymphoma by laser microdissection(Murcia : F. Hernández, 2008) García-Cosío, Mónica; Santón, Almudena; Martín, Paloma; Reguero, María Eugenia; Cristóbal, Eva; Bellas, CarmenEpstein-Barr virus (EBV) seems to have an etiological role in the pathogenesis of classical Hodgkin’s lymphoma (cHL). Studies of whole tissue DNA by polymerase-chain reaction (PCR) have shown a considerable number of cHL cases with co-infections by different EBV strains and variants, which apparently contradict the clonality of EBV in cHL previously demonstrated by Southern blot analysis. Due to the paucity of HRS cells in HL tissues, studies on single cell DNA are necessary to identify the specific cellular location (HRS cells and/or bystander B lymphocytes) of the EBV strains and variants present in tissue specimens. In the current study, the presence of EBV was determined by PCR of the 3’ end of the LMP-1 gene and EBNA-3C gene in whole tissue and, consecutively, in isolated cells from 26 cases of cHL: 10 HIV-positive and 16 sporadic cHL cases. EBV EBERs were present in all but 2 sporadic cHL cases, which were used as negative controls. At isolated cell level, EBNA-3C gene PCR was more sensitive. Indeed, from the cHL cases in which dual-infection was present, it was observed that, in most of them, HRS cells were infected by type 1 virus, and B lymphocytes were co-infected by both types, which points towards EBV infection occurring early in cHL development. Moreover, the finding of 2 cases with dual-infection in HRS may suggest that, in a small percentage of cHL cases, HRS cells derive from different neoplastic clones, or that HRS cells are superinfected by other viral types after the establishment of the neoplastic clone.
- PublicationOpen AccessHuman galectin-2: nuclear presence in vitro and its modulation by quiescence/stress factors(2008) Dvoránková, B.; Smetana, K. Jr.; Lacina, L.; Lensch, M.; Manning, J.C.; André, S.; Gabius, H.J.
- PublicationOpen AccessImmunohistochemical localization of renin, NO synthase-1, and cyclooxygenase-2 in rodent kidney(Murcia : F. Hernández, 2008) Ichii, Osamu; Yabuki, Akira; Ojima, ToshimichiThe renin-angiotensin system (RAS) and tubuloglomerular feedback (TGF) are central to the maintenance of blood pressure and body fluid composition. Renin, NO synthase-1 (NOS-1), and cyclooxygenase-2 (COX-2) are key regulators of the RAS and TGF. In the present study, to investigate species-specific differences in the RAS and TGF, we immunohistochemically and morphometrically investigated the localization of renin, NOS-1, and COX- 2 in the kidneys of various laboratory rodents and comparing males with females (DBA/2Cr mice, F344/N rats, Syrian hamsters, MON/JmsGbs gerbils and Hartley guinea pigs). In all animals, renin-positive immunoreactions were observed in the vascular walls of afferent arterioles. Renin immunoreactions appeared to be more widely distributed in mice. Mice had a greater number of renin-positive arterioles than other species. NOS-1-positive reactions were detected in the macula densa (MD) of all animals. Mice had the greatest number of NOS-1-positive MD cells. In addition to NOS-1- positive reactions, COX-2-positive reactions were observed in the MD of mice, rats, hamsters and gerbils. Interestingly, guinea pigs had no COX-2-positive MD cells. Rats had the greatest number of COX-2-positive MD cells. In nephron segments excluding the MD, the immunohistochemical localization of NOS-1 and COX-2 differed markedly among not only species but also sexes within the same species. In conclusion, we determined that localization of renin, NOS-1, and COX-2 showed large species- and sex-related differences. These data suggest that the regulation mechanisms of the RAS and TGF via renin, NOS-1, and COX-2 differ among rodents.
- PublicationOpen AccessEffects of hypothyroidism on anti-mullerian hormone expression in the prepubertal rat testis(Murcia : F. Hernández, 2008) Chamindrani Mendis-Handagama, S.M.L.; Siril Ariyaratne, H.B.Differentiation of adult Leydig cells (ALC) in the prepubertal rat testis is stimulated by thyroid hormone (Thy) and inhibited by the Anti-Mullerian Hormone (AMH) produced by the immature Sertoli cell (SC). As Thy induces SC maturation in the prepubertal rat testis, we hypothesized that Thy stimulation of ALC differentiation is mediated via inhibition of AMH production by the SC with their maturation. If this hypothesis is true, AMH production by the prepubertal Sertoli cells in hypothyroid rats should not decline immediately after birth as in euthyroid rats, but should be maintained throughout the hypothyroid period at a similar or higher level to that of day 1 rats. This concept was tested using control rats of postnatal days (pd) 1, 7 and 14 and hypothyroid (fed 0.1% propyl thiouracil/PTU to lactating mothers) rats of pd7 and pd14. Presence of AMH in SC was examined by immunocytochemistry for AMH. Results demonstrated that testes of pd1 rats had intense AMH positive labeling exclusively in cytoplasm of SC. In testes of pd7 and pd14 control and PTU rats, a positive but weak labeling was also observed in cytoplasm of some SC; Germ cells and testicular interstitial cells were negative for AMH at all tested ages in both experimental groups. These findings suggest that AMH production by the prepubertal SC is independent of Sertoli cell maturation and not regulated by Thy. Therefore, Thy regulation of ALC differentiation in the prepubertal rat testis is unlikely to be mediated via inhibition of AMH produced by the SC with their maturation.
- PublicationOpen AccessHistochemical demonstration of aluminum and iron deposition in pulmonary bony tissues in three cases of diffuse pulmonary ossification(Murcia : F. Hernández, 2008) Ohtsuki, Yuji; Yamanaka, Akira; Ohyama, Hideki; Yamada, Eiji; Terada, Nobuyuki; Fujita, Jiro; Lee, Gang-Hong; Furihata, MutsuoDiffuse pulmonary ossification is a rare condition. We examined three cases of it in Japan, and attempted histochemically to stain for deposition of aluminum and iron in bony tissues. The patients were all female, and in their mid-twenties, mid- eighties, and later teen years. One of the patients had been exposed to heavy metals in her work involving heavy-metal analyses for 18 months. Aluminum staining and Berlin blue staining for iron were performed with dewaxed, undecalcified sections of pulmonary tissues from these three cases. Interestingly, all pulmonary bony tissues from the three cases examined exhibited linear regions of both aluminum and iron deposition in the calcifying fronts or the cement lines of bones. The patient exposed to heavy metals exhibited the most severe aluminum and iron deposition, and also exhibited positive reaction for both aluminum and iron in elastic fibers of blood vessels. Foreign body granulomas with multinucleated giant cells exhibiting elastophagia were also found in this case. This phenomenon, “endogenous pneumoconiosis”, appeared to have been the cause of pulmonary hemorrhage in this case, resulting in focal heavy hemosiderosis. It is of great interest that identical patterns of aluminum and iron deposition in hemodialysis patients were found in these three cases, This is the first report on histochemical demonstration of aluminum and iron deposition in diffuse pulmonary ossification, and detailed analysis of additional cases is needed.
- PublicationOpen AccessThe urokinase-system - role of cell proliferation and apoptosis(Murcia : F. Hernández, 2008) Hildenbrand, Ralf; Gandhari, Mukesh; Stroebel, Philipp; Marx, Alexander; Allgayer, Heike; Arens, NorbertThe serine protease urokinase-type plasminogen activator (uPA) and its receptor (uPAR) are involved in the control of extracellular matrix turnover, cell migration, invasion and cell signalling leading to a variety of different responses, under both physiological and pathological conditions. The urokinase receptor, binding to the growth factor-like domain of uPA, directs membrane-associated extracellular proteolysis and signals through transmembrane proteins, thus regulating tissue regeneration, angiogenesis, cancer growth and metastasis. Since these physiological and pathophysiological processes of the uPA-system are known, less informations concerning uPA-induced cell proliferation and anti-apoptotic effects of the uPAsystem are available. Recent studies show a close relationship of the uPA-system and cell proliferation/ apoptosis. uPA is responsible for the activation and release of different growth factors and modulates the cell proliferation/apoptosis ratio through the dynamic control of cell-matrix interactions. This article focuses on the important role of the uPA/uPAR-system for cell proliferation and apoptosis.
- PublicationOpen AccessImmunohistochemical and in situ hybridization observations favor a local catecholamine production in the human Achilles tendon(Murcia : F. Hernández, 2008) Bjur, Dennis; Danielson, Patrik; Alfredson, Hàkan; Forsgren, StureResults of recent studies using immunohistochemistry show evidence of an occurrence of catecholamine production in the cells (tenocytes) of patellar tendons exhibiting tendinopathy (tendinosis). In the present study, antibodies against the catecholaminesynthesizing enzyme tyrosine hydroxylase (TH) and a1- adrenoreceptors were applied to sections of specimens of normal and tendinosis Achilles tendons. In situ hybridization using a probe detecting human TH mRNA was also utilized. It was found that sympathetic innervation was very scarce. On the other hand, there were distinct a1-adrenoreceptor immunoreactions in blood vessel walls. Interestingly, tenocytes, particularly from tendinosis samples in which the tenocytes showed an abnormal shape (not the typical slender appearance), displayed TH immunoreactions and reactions for TH mRNA. Of further interest was the finding of a1- adrenoreceptor immunoreactions in tenocytes. The observations show not only evidence of local catecholamine production at the protein level, which was the case in recent studies for the patellar tendon, but also at the mRNA level. The observations suggest that the tenocytes, especially those with disfigured appearances in tendinosis, can produce catecholamines and also that they can respond to sympathetic transmitters. This is of interest as adrenergic stimulation in other parts of the body is known to induce degenerative/apoptotic and proliferative events, features which are seen in Achilles tendinosis. These observations are completely new findings concerning the human Achilles tendon. It is likely that locally produced catecholamines and the occurrence of autocrine/paracrine effects of these substances are of great relevance during the process of tendinosis.
- PublicationOpen AccessPathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages(Murcia : F. Hernández, 2008) Nishimura, Toshico; Hirata, Hitoshi; Tsujil, Masaya; Iida, Ryu; Hoki, Yoko; Iino, Takahiro; Ogawa, Satoru; Uchida, AtsumasaTo examine the pathomechanism of entrapment neuropathy associated with diabetes with special emphasis on the roles of mast cells and Tenascin- C using a rat model of Streptozotocin-induced diabetes. The roles of mast cells and Tenascin-C in development of tarsal tunnel syndrome were analyzed electrophysiologically and histologically in 20 male Ws/Ws-/-rats (mast cell deficient) and 20 of their male wild type counterparts (12-16 weeks old; 250-300g). Rats were assigned randomly to one of the following three groups; diabetic group and nondiabetic group reared in cages with a wire grid flooring; non-diabetic group in cages with sawdust covered plastic flooring. No significant role for mast cells in entrapment neuropathy was found in the rats with streptozotocin-induced diabetes. Distal latency was prolonged in diabetic rats compared with nondiabetic rats, and positively correlated with increases in blood glucose levels. Tenascin-C expression levels in the endoneurium at the tarsal tunnel in diabetic rats were found to be correlated with distal latency. The anti-alpha-smooth muscle actin (a-SMA) positive myofibroblast was scattered in nerve fascicles overexpressing Tenascin-C. It seems likely that Tenascin-C expressing myofibroblasts constrict axons by inducing collagen contraction of the endoneurium. Our data indicate that metabolic and phenotypic abnormalities of endoneurium and perineurum lie behind the vulnerability of diabetic patients to entrapment neuropathy.
- PublicationOpen AccessHuman postmenopausal ovary - hormonally inactive fibrous connective tissue or more(Murcia : F. Hernández, 2008) Laszczynska, M.; Brodowska, A.; Starczewski, A.; Masiuk, M.; Brodowski, J.The ovary undergoes several changes after the menopause. In this period, the main structural changes in both the cortex and medulla were observed. In the cortex, they included: 1) reduction of its thickness; 2) epithelial inclusions forming cysts; 3) blurring the line between medulla and cortex; 4) reduction of follicles number; 5) tendency to fragmentation of corpora albicantia; 6) surface epithelium invaginations. Whereas the changes in the medulla included: 1) fibrosis and scars in stroma; 2) architectonical changes in blood vessels with hyalinization of walls and constriction of lumen. The loss of follicles and several changes in the ovary are due to apoptotic processes. Despite age related atrophic changes, the postmenopausal ovary is not devoid of hormonal activity. Our results are coherent with the reports of other researchers, and reveal that postmenopausal ovary produces trace quantities of steroid hormones, mainly androgens, and confirm the presence of steroid receptors and activity of main enzymes involved in steroidogenesis process.
- PublicationOpen AccessTherapeutic perspectives for the treatment of Huntington s disease, Treating the whole body(Murcia : F. Hernández, 2008) Martin, Bronwen; Golden, Erin; Keselman, Alex; Stone, Matthew; Mattson, Mark P.; Egan, Josephine M.; Maudsley, StuartHuntington’s disease (HD) is a tremendously debilitating disorder that strikes relatively young individuals and progresses rapidly over the next ten to fifteen years inducing a loss of cognitive and motor skills and eventually death occurs. The primary locus of the disorder is a polyglutamine expansion of the protein product of the huntingtin (htt) gene. The htt protein appears to be a scaffolding protein that orchestrates the complex assembly of multiple intracellular proteins involved in multiple processes, including vesicular movement and cell metabolism. The htt protein is ubiquitously expressed in human tissues but the predominance of the interest in the pathology lies in its effects on the central nervous system (CNS). Most of the current therapeutics for HD thus have been targeted at preventing neuronal damage in the CNS, however, a considerable body of evidence has been accumulating to suggest that the maintenance of a healthy nervous system is tightly linked with peripheral physiological health. Therefore treatment of both the peripheral and central pathophysiologies of HD could form the basis of a more effective HD therapeutic strategy.
- PublicationOpen AccessThymidine phoshorylase expression in breast cancer, the prognostic significance and its association with other angiogenesis(Murcia : F. Hernández, 2008) Loachim, E.Thymidine phosphorylase (TP)/plateletderived endothelial cell growth factor, stimulates chemataxis of endothelial cells and is involved in the angiogenesis of human solid tumours. In this study we investigated tissue sections from 93 breast carcinomas for the immunohistochemical expression of thymidine phosphorylase protein and in relationship to several clinicopathological parameters. The possible relationship to tumour neovascularization, VEGF expression, extracellular matrix components (tenascin, fibronectin, collagen type IV and laminin) and cathepsin D was also estimated. Nuclear and/or cytoplasmic TP expression was observed in tumour cells. Immunoreactivity was also often present in the stroma, endothelium and tumour-associated macrophages. High cytoplasmic TP expression, was observed in 35.5%, moderate in 30.1%, mild in 18.3%, while 16.1% of the cases were negative for TP expression. Moderate and high nuclear TP expression was observed in 30.1% of the tumours, low in 43%, while 26.9% did not show nuclear TP expression. High tumour stroma TP expression was expressed in 23.7% of the cases, moderate in 21.5%, mild in 45.2%, while 9.7% did not show stromal TP expression. TP expression did not correlate with the conventional clinicopathological features as well as with the microvessel density and the VEGF expression. Patients with high levels of tumour cell TP expression were significantly associated with a favorable outcome in univariate method of analysis. A positive correlation of TP expression with Cathepsin D expression was noticed. In addition, tumour cell TP expression was correlated with the extracellular matrix component tenascin, while stromal cell TP expression was correlated with the growth fraction of the tumour. Our data suggests that TP expression does not seem to affect directly the neovasculatur of breast carcinoma, although it seems to be implicated in the remodeling of breast cancer tissue, through the interaction with other extracellular matrix components or proteolytic enzymes. In addition, tumour cell TP expression could be considered as a prognostic indicator of breast cancer patients.