Histology and histopathology Vol.25, nº5 (2010)

Permanent URI for this collection

http://hdl.handle.net/10201/177376

Browse

Now showing 1 - 13 of 13

Open Access
Impact of hepatitis virus and aging on DNA methylation in human hepatocarcinogenesis
(Murcia : F. Hernández, 2010) Nishida, Naoshi
Hepatocellular carcinoma (HCC) usually develops on the basis of chronic hepatitis and liver cirrhosis, where inactivation of several tumor suppressor genes (TSGs) takes place via methylation of the promoter. Interestingly, these methylation events are more prevalent in a background liver at high risk of HCC than one at low risk. Abnormal methylation is also observed in precancerous nodules such as dysplastic nodules and adenomas, suggesting that epigenetic alteration is an early event for HCC carcinogenesis. It is possible that infection with the hepatitis virus induces alteration of methylation at promoters of TSGs. Some studies suggested that viral proteins interfere with DNA methyltranferase in chronic hepatitis B. Induction of epigenetic alteration in chronic hepatitis C might, however, might be a consequence of oxidative stress. In addition, we proposed age should be taken into consideration for HCC development via epigenetic pathways. Further investigations are required to understand the mechanism of inducing epigenetic instability during hepatocarcinogenesis
Open Access
Sex-dependent effect of liver growth factor on atherosclerotic lesions and fatty liver disease in apolipoprotein E knockout mice
(Murcia : F. Hernández, 2010) Surra, Joaquin C.; Guillén, Natalia; Barranquero, Cristina; Arbonés Mainar, José M.; Navarro, María A.; Gascón, Sonia; Arnal, Carmen; Godino, Javier; Guzmán, Mario A.; Díaz-Gil, Juan J.; Osada, Jesús
Objective: Since the hepatic mitogen, liver growth factor (LGF), improves vascular structure and function in a hypertensive rat model and exhibits antioxidant activity, it may play a role in the development of atherosclerosis. Methods: To test this hypothesis, 14 male and 11 female apolipoprotein E (apoE)-deficient mice with a C57BL/6J genetic background were injected intraperitoneally twice a week with 1.7 µg of LGF per mouse for ten weeks. Plasma carbohydrates, inflammatory and lipid parameters, apolipoproteins A-I and A-II and paraoxonase activity were assessed at the end of the experimental period. Histological and chemical analyses of the livers and quantification of aortic atherosclerotic lesions were also carried out. Results: LGF administration changed neither plasma lipid nor inflammatory parameters. ApoA-I and arylesterase activity were not affected by LGF either, while apoA-II decreased significantly in males but not in females. Plasma apoA-II correlated positively with liver fat in males but negatively in females. Atherosclerotic area lesions in males receiving LGF were 25% lower than in control mice. Likewise, a significant reduction of fatty liver disease was also observed in males in association with decreased levels of insulin, leptin and resistin. Conclusion: These results indicate that administration of LGF modulates atherosclerotic lesions in a sex-dependent manner. This effect is independent of plasma cholesterol, triglycerides, IL-6, MCP-1 and TNF-α and is related to a remodelling of HDL particles characterised by a decrease in apoA-II induced by changes in hepatic mRNA expression. Hence, LGF administration could be used as a safe alternative to control fatty liver disease and atherosclerosis in males
Open Access
Vitamin E action on oxidative state, endothelial function and morphology in long-term myocardial preservation
(Murcia : F. Hernández, 2010) Álvarez-Ayuso, Lourdes; García Gómez-Heras, Soledad; Jorge, Eduardo; Guardiola, José M.; Torralba, Amalia; Granado, Fernando; Millán, Isabel; Roda, Jorge R.; Calero, Patricia; Fernández-García, Héctor; García-Poblete, Eduardo
. This study assesses the effects of a vitamin E analogue, Trolox, on the oxidative state, endothelial function and morphology in experimental heart transplantation. Heterotopic heart transplantation was carried out in pigs: untreated after 2 and 24 hours of ischemia and treated with Trolox after 24 hours of ischemia. Prolonged preservation of donor hearts was achieved with continuous perfusion and University of Wisconsin solution, in which acid-base balance and enzymes were determined during the procedure. In recipients, hemodynamic and biochemical parameters were determined at baseline and during reperfusion. Trolox diminished the pH of the preservation solution (p<0.01), the left ventricle of the transplanted heart recovered a systolic pressure equaling that of the 2h group and higher than that of the untreated 24h group (p<0.01), the antioxidant levels were not decreased and the glutathione reductase level was maintained throughout the first part of reperfusion. In this group also there was a direct correlation between the concentration of this enzyme and the antioxidant levels (p<0.001). Although the endothelin concentrations increased, the change was less marked in the Trolox group than in the untreated 24h group (p<0.01). Morphologically, mitochondria and myocardial vessels presented a normal structure in the Trolox group, and interstitial edema, inflammatory infiltrate and contraction bands were less prominent than in the untreated group. All these effects indicate that Trolox protected the transplanted heart, at least partially, against ischemia-reperfusion injury
Open Access
Pericentriolar material analyses in normal esophageal mucosa, Barrett’s metaplasia and adenocarcinoma
(Murcia : F. Hernández, 2010) Segat, Daniela; Cassaro, Mauro; Dazzo, Emanuela; Cavallini, Lucía; Romualdi, Chiara; Salvador, Renato; Vitale, María Pia; Vitiello, Libero; Fassan, Matteo; Rugge, Massimo; Zaninotto, Giovanni; Ancona, Ermanno; Baroni, Mauricio David
Barrett’s esophagus metaplasia is a pre-cancerous condition caused by chronic esophagitis. Chromosomal instability (CIN) is common in Barrett’s cells: therefore, we investigated the possible presence of centrosomal aberrations (a main cause of CIN) by centrosomal protein immunostaining in paraffined esophageal samples of patients who developed a Barrett’s adenocarcinoma. In most (55%) patients, alterations of the pericentriolar material (PCM) signals were evident and consistently marked the transition between normal epithelium to metaplasia. The alterations could even be found in adjacent native squamous epithelium, Barrett’s mucosa and submucosal gland cells, as well as in the basal/epibasal layers of the mucosa and submucosal gland duct, which are the regions hosting esophageal stem and progenitor cells. These findings strongly support the hypothesis that the three esophageal histotypes (one being pathological) can have a common progenitor. Surprisingly, PCM defective signal eventually decreased with neoplastic progression, possibly to enhance the genome stability of advanced cancer cells. Importantly, PCM altered signals in Barrett’s mucosa and their apparent evolution in successive histopathological steps were correlated to adenocarcinoma aggressiveness, suggesting PCM as a possible prognostic marker for tumor relapse. Extending our observations in a prospective study might help in the development of new prevention protocols for adenocarcinoma patients
Open Access
Targeting the renin angiotensin system for remission-regression of chronic kidney disease
(Murcia : F. Hernández, 2010) Macconi, Daniela
In the last few years great progress has been made in the search for the cellular and molecular mechanisms of chronic kidney disease and its progression to end-stage renal failure. The possibility of remission/regression of chronic nephropathy has become a reality for some patients on therapy based on renin-angiotensin system blockade – an example of how a public health concern can be successfully addressed by translational medicine. This review describes experimental and clinical investigations documenting the advances achieved in the management of chronic kidney diseases by targeting angiotensin II.
Open Access
The phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin signaling network and the control of normal myelopoiesis
(Murcia : F. Hernández, 2010) Martelli, Alberto M.; Chiarini, Francesca; Evangelisti, Camila; Grimaldi, Cecilia; Ognibene, Andrea; Manzoli, Lucia; Billi, A.M.; McCubrey, James A.
he phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway plays a central role in cell growth, proliferation, differentiation, and survival under physiological conditions. Aberrant regulation of the PI3K/Akt/mTOR signal transduction network has been observed in a wide range of neoplasias, including malignant hematological disorders. This observation suggests that this signaling cascade could also play a critical role during normal hematopoiesis, a highly regulated process which results in the formation of all blood lineages. The development of blood cells comprises a complex series of events which are mainly regulated through the actions of cytokines, a large family of extracellular ligands than can stimulate many biological responses in a wide array of cell types. Several of these cytokines are known to activate the PI3K/Akt/mTOR signal transduction network and thus regulate proliferation, survival, and differentiation events during hematopoiesis. Moreover, hematopoiesis is strictly dependent on the correct functions of the bone marrow microenvironment. Here, we review the evidence which links the signals emanating from the PI3K/Akt/mTOR cascade with the functions of hematopoietic stem cells and the process of lineage commitment, which then gives rise to myeloid lineage-restricted cells. We then further highlight the key role played by the PI3K/Akt/mTOR network during erythropoiesis, megakaryocytopoiesis, and granulo-cytopoiesis/monocytopoiesis
Open Access
The internal thoracic artery as a transitional type of artery: a morphological and morphometric study
(Murcia : F. Hernández, 2010) Labudović Borović, Milica; Borović, Saša; Perić, Miodrag; Vuković, Petar; Marinković, Jelena; Todorovic, Vera; Radak, Ðorde; Lackovic, Vesna
Coronary artery by-pass grafting (CABG) with arterial grafts is widely accepted as the procedure of choice in the treatment of coronary ischemic disease. It brings back focus on morphological studies of arteries used as conduits in this procedure. One of the most frequently used CABG grafts is the internal thoracic artery with an excellent graft prognosis and patency rate. The aim of the study was a detailed morphological and morphometric description of the internal thoracic artery with an emphasis on its basic histological structure and its changes in aging and atherosclerosis. Therefore, 42 full-length arteries were obtained during forensic autopsies from 27 persons, aged between 20 and 81 years, who had died from non-vascular causes. The arteries were classified into three different age groups. Analysis of the serial arterial segments has shown that the internal thoracic artery is an artery of the transitional type whose media is organized into two layers: the internal, muscular layer and the external layer with spirally oriented elastic lamellae and smooth muscle cells in between. The number of elastic lamellae progressively decreases throughout the length of the examined arteries. As opposed to previous assumptions, we have proven that the grade of atherosclerosis is independent of the number of elastic lamellae in the external media. Perfectly formed elastic lamellae are not a persistent feature of the internal thoracic artery, as previously claimed. We have confirmed that the thickness of elastic lamellae decreases, while the number and the size of their fenestrations steadily increase with aging
Open Access
Vascular wall-resident stem cells
(Murcia : F. Hernández, 2010) Klein, Diana; Hohn. Hans-Peter; Kleff, Veronika; Tilki, Derya; Ergün, Süleyman
New vessels in the adult have been considered to be formed not only by angiogenesis, but also by postnatal vasculogenesis via endothelial progenitor cells (EPCs). However, it is still a matter of debate as to what extent the EPCs contribute to new vessel formation in the adult. While the role of the circulating and bone marrow-derived EPCs has intensively been studied, the contribution of the vascular wall itself was neglected for a long time. Evidence published in the last few years strongly suggests the existence of different stem and progenitor cell types in the vascular wall. Particularly, the presence of EPCs and smooth muscle progenitor cells (SMPCs) in distinct zones of the vascular wall supports the hypothesis that not only BM- or C-EPCs, but also vascular wall-resident stem cells (VW-SCs) might contribute to new vessel formation and vascular wall morphogenesis. However, the differentiation potential of the VW-SCs, e.g. whether a VW-SC is able to give rise to a complete hierarchy of vascular progenitors still remains to be studied. This review will provide a survey about the VW-SCs and their potential impact in vascular biology
Open Access
Specification of arterial, venous, and lymphatic endothelial cells during embryonic development
(Murcia : F. Hernández, 2010) Kume, Tsutomu
The groundbreaking discovery about arterial and venous expression of ephrinB2 and EphB4, respectively, in early embryonic development has led to a new paradigm for vascular research, providing compelling evidence that arterial and venous endothelial cells are established by genetic mechanisms before circulation begins. For arterial specification, vascular endothelial growth factor (VEGF) induces expression of Notch signaling genes, including Notch1 and its ligand, Delta-like 4 (Dll4), and Foxc1 and Foxc2 transcription factors directly regulate Dll4 expression. Upon activation of Notch signaling, the Notch downstream genes, Hey1/2 in mice or gridlock in zebrafish, further promote arterial differentiation. On the other hand, the orphan nuclear receptor COUP-TFII is a determinant factor for venous specification by inhibiting expression of arterial specific genes, including Nrp1 and Notch. After arterial and venous endothelial cells differentiate, a subpopulation of venous endothelial cells is thought to become competent to acquire lymphatic endothelial cell fate by progressively expressing the transcription factors Sox18 and Prox1 to differentiate into lymphatic endothelial cells. Therefore, it has now evident that arterial-venous cell fate determination and subsequent lymphatic development are regulated by the multi-step regulatory system associated with the key signaling pathways and transcription factors. Furthermore, new signaling molecules as additional regulators in these processes have recently been identified. As the mechanistic basis for a link between signaling pathways and transcriptional networks in arterial, venous and lymphatic endothelial cells begins to be uncovered, it is now time to summarize the literature on this exciting topic and provide perspectives for future research in the field.
Open Access
Role of HTRA1, a serine protease, in the progression of articular cartilage degeneration
(Murcia : F. Hernández, 2010) Polur, Llona; Lee, Peter L.; Servais, Jacqueline M.; Xu, Lin; Li, Yefu
This study is to investigate the possible role of high temperature requirement A 1 (HtrA1) in the articular cartilage degeneration. Paraffin sections were prepared from the knee and temporomandibular (TM) joints of four mouse OA models; two of the models had a genetic mutation (type IX collagen-deficient and type XI collagen-haploinsufficient) and two were surgically induced (destabilization of the medial meniscus of knee joint and discectomy of TM joint). The HtrA1 protein expression profiles of the prepared sections were examined by immunohistostaining. The level of HtrA1 mRNA in the articular cartilage taken from the knee joints of one of the genetically mutated OA models was determined by real-time PCR. Double immunohistostaining was used to examine the expression of co-localization of HtrA1 with type VI collagen and HtrA1 with discoidin domain receptor 2 (Ddr2) in the articular cartilage of knee joints from the genetically mutated OA model. The expression of HtrA1 was found to be increased in the knee and TM joints of these four models at early stages of the disease. An examination of the knee joint of a mutant mouse indicated an 8-fold increase in the level of HtrA1 mRNA, when compared to the levels observed in the knee joints of its wild-type littermates. Pericellular type VI collagen was not present in chondrocytes expressing HtrA1. Meanwhile, the expression of HtrA1 was associated with the expression of Ddr2 in the chondrocytes. Results indicate that HtrA1 may disrupt the pericellular matrix network, resulting in alteration of chondrocyte metabolisms. This eventually leads to OA
Open Access
Galectin fingerprinting in Warthin`s tumors: lectin-based approach to trace its origin?
(Murcia : F. Hernández, 2010) Saussez, Sven; Leval, Laurence de; Decaestecker, Christine; Sirtaine, Nicolas; Cludts, Stéphanie; Duray, Anaelle; Chevallier, Dominique; André, S.; Gabius, H.J.; Remmelink, Myriam; Leroy, Xavier
Warthin’s tumor of the parotid gland is assumed to originate from the proliferation of epithelial inclusions within parotid lymph nodes. In that case, these cells are supposed to retain characteristics similar to common salivary gland ductal cells. Using immunohistochemical fingerprinting with four members of the family of adhesion/growth-regulatory galectins and comparison to intra- and interlobular ducts, marked similarities were noted for presence of galectins-3, -7 and -8. Notably, profiles of lectin binding, determined by applying human lectins as probes, were also similar when testing biotinylated galectins-3 and -8. Besides defining the galectin histochemical parameters in Warthin’s tumors this study adds support to the hypothesis of heterotopia
Open Access
Immunoexpression of gelatinase (MMP-2 and MMP-9) in the seminal vesicles and ventral prostate of Libyan jird (Meriones libycus) during the seasonal cycle of reproduction
(Murcia : F. Hernández, 2010) Belhocine, M.; Gernigon-Spychalowicz, T.; Jacob, M.P.; Benazzoug, Y.; Exbrayat, Jean Marie
An immunohistochemical study of matrix metalloproteinases (MMP-2 and MMP-9) or gelatinase (gelatinase A and gelatinase B) was performed on the seminal vesicles and ventral prostate of the Libyan jird (Meriones libycus) collected in the Beni-Abbes area during breeding period (spring and early summer), during resting phase (late summer, autumn, winter) and from castrated animals in the spring. The work was done using the indirect immunohistochemistry protocol by amplification with streptavidin-biotin-peroxidase and AEC as chromogen. In the seminal vesicles, during the breeding period, an important immunohistochemical signal of MMP-2 and MMP-9 was observed in epithelial cells and smooth muscle cells (SMC) without any immunoexpression in the extracellular matrix (ECM) and secretion. During resting phase and in thirty days castrated Meriones libycus, the MMP-2 and MMP-9 immunoexpression was weak in the epithelial cells and persisted with the same intensity in the SMC. The ECM, with no immunostaining in active season, showed a pronounced immunoresponse of both the two gelatinase. Three days after castration, the MMP-9 immunohistochemical reaction in epithelial cells and SMC was as intense as during active season. A prolonged castration of 50 and 90 days resulted in the maintenance of the MMP-9 immunostaining in epithelial cells and SMC and its disappearance from the ECM, suggesting a slow process of regression. During the breeding period, in the ventral prostate, MMP-2 immunostaining was more important in the SMC than in epithelial cells. The MMP-9 immunoexpression pattern was the opposite, the epithelial cells showed a higher immunoreaction than SMC. ECM and secretion lacked MMP-2 and MMP-9 immunostaining. The ventral prostate lumen contained a granular secretion without any gelatinase immunolabelling and was hollowed by empty circular forms reflecting the disappearance of the product in these areas. Part of the secretion showed a positive MMP-2 and MMP-9 immunoreaction. The latter was subsequently filled and seemed involved in the progression of the secretion in the tubules, preventing their filling. In resting phase and in animals castrated since thirty days, the immunoreactivity of both the two gelatinases was maintained in the epithelial cells and in the SMC, and was absent in the ECM. The gelatinases are involved in the seasonal reproductive cycle of Meriones libycus
Open Access
Catecholamine-induced heart injury in mice: differential effects of isoproterenol and phenylephrine
(Murcia : F. Hernández, 2010) Navarro Sobrino, Míriam; Lorita, Jordi; Soley, María; Ramírez, Ignasi
-

Browse

Browsing Histology and histopathology Vol.25, nº5 (2010) by Issue Date

Results Per Page

Sort Options