Histology and histopathology Vol.25, nº5 (2010)

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https://hdl.handle.net/10201/46248

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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
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
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
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
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

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