Histology and histopathology Vol.29, nº12 (2014)
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- PublicationOpen Access‘Green Mice’ display limitations in enhanced green fluorescent protein expression in retina and optic nerve cells(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Caminos, Elena; Vaquero, Cecilia F.; García-Olmo, Dolores C.Characterization of retinal cells, cell transplants and gene therapies may be helped by prelabeled retinal cells, such as those transfected with vectors for green fluorescent protein expression. The aim of this study was to analyze retinal cells and optic nerve components from transgenic green mice (GM) with the ‘enhanced’ green fluorescent protein (EGFP) gene under the control of the CAG promoter (a chicken β-actin promoter and a cytomegalovirus enhancer). The structural analysis and electroretinography recordings showed a normal, healthy retina. Surprisingly, EGFP expression was not ubiquitously located in the retina and optic nerve. Epithelial cells, photoreceptors and bipolar cells presented high green fluorescence levels. In contrast, horizontal cells, specific amacrine cells and ganglion cells exhibited a null EGFP expression level. The synaptic terminals of rod bipolar cells displayed a high green fluorescence level when animals were kept in the dark. Immature retinas exhibited different EGFP expression patterns to those noted in adults. Axons and glial cells in the optic nerve revealed a specific regional EGFP expression pattern, which correlated with the presence of myelin. These results suggest that EGFP expression might be related to the activity of both the CAG promoter and β-actin in mature retinal neurons and oligodendrocytes. Moreover, EGFP expression might be regulated by light in both immature and adult animals. Since GM are used in numerous retina bioassays, it is essential to know the differential EGFP expression in order to select cells of interest for each study.
- PublicationOpen AccessDemonstration of an add-on effect of probucol and cilostazol on the statin-induced anti-atherogenic effects(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Wang, Yanli; Bai, Liang; Lin, Yan; Guan, Hua; Zhu, Ninghong; Chen, Yulong; Li, Yafeng; Gao, Shoucui; Zhao, Sihai; Fan, Jianglin; Liu, EnqiStatins are often prescribed for treatment of cardiovascular diseases, although there are still many patients who cannot be effectively treated by statins alone. Both probucol and cilostazol exhibit antiatherogenic effects. In the current study, we attempted to investigate whether a probucol and cilostazol combination had any add-on effects on atorvastatin. To examine this hypothesis, we fed Japanese white rabbits with a cholesterol-rich diet supplemented with atorvastatin alone (Statin group), probucol and cilostazol (PC group), atorvastatin, probucol and cilostazol (APC group), and compared their effects on plasma lipids and aortic atherosclerosis. All three drug-treated groups had lowered total cholesterol levels compared with the vehicle group but high-density lipoproteins cholesterol levels of the atorvastatin group were higher than other groups. Although aortic atherosclerosis was significantly reduced in all drug-treated groups, the most prominent atheroprotective effect was seen in APC group (APC: 67% reduction> PC: 43% reduction> Statin group: 42% reduction over the vehicle). Morphometric analysis revealed that the reduced aortic atherosclerosis in all three groups was mainly attributed to the reduction of intimal macrophages and smooth muscle cells. These results suggest that a combination of probucol and cilostazol with statin enhances statin’s anti-atherogenic functions, which may be beneficial for those patients who are less responsive to statin therapy alone.
- PublicationOpen AccessModulation of renin angiotensin system predominantly alters sclerotic phenotype of glomeruli in HIVAN(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Plagov, Andrei; Lan, Xiqian; Rai, Partab; Kumar, Dileep; Lederman, Rivka; Rehman, Shabina; Malhotra, Ashwani; Ding, Guohua; Chander, Praveen N.; Singhal, Pravin C.HIV-associated nephropathy (HIVAN) is a common complication of HIV-1 infection in patients with African ancestry in general and with APOL1 gene risk variants in particular. Although collapsing glomerulopathy is considered a hallmark of HIVAN, significant numbers of glomeruli in patients with HIVAN also display other variants of focal segmental glomerulosclerosis (FSGS). We propose that collapsed glomeruli as well as glomeruli with other variants of FSGS are manifestations of HIVAN and their prevalence depends on associated host factors. We explored the role of the renin-angiotensin system (RAS) in the manifestation of any specific glomerular phenotype in HIVAN. To evaluate the role of the RAS we have used a genetically engineered mouse model of HIVAN (Tg26) with two and four copies of angiotensinogen (Agt) gene (Tg26/Agt2 and Tg26/Agt4). In Tg26/Agt2, 1 out of 6 glomeruli exhibited sclerosed phenotype, whereas 1 out of 25 glomeruli displayed collapsed phenotype; on the other hand, in Tg26/Agt4, 1 out of 3 glomeruli exhibited sclerotic phenotype and only 1 out of 7 glomeruli showed collapsed phenotype. To inhibit the effect of RAS, Tg26/Agt2 were administered captopril, aliskiren, aliskiren plus captopril or aliskiren plus telmisartan by miniosmotic pumps for 4 weeks. In all experimental groups there was a significant reduction in percentage of sclerosed glomeruli and only minimal reduction in collapsed glomeruli compared to normal saline receiving Tg26/Agt2. These findings suggest that the manifestation of the sclerosed phenotype in HIVAN is predominantly dependent on activation of the RAS.
- PublicationOpen AccessCystic gastrointestinal stromal tumors of the pancreas simulating cystoadenocarcinoma. Report of three cases and short review of the literature(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Ambrosio, Maria Raffaella; Rocca, B.J.; Mastrogiulio, M.G.; Pesci, A.; De Martino, A.; Mazzei, M.A.; Volterrani, L.; Arcuri, F.; Cintorino, M.; Tripodi, S.A.Gastrointestinal stromal tumors (GISTs) represent a distinct subset of mesenchymal tumours of the gastrointestinal tract. They are more common in the stomach and small intestine, and are characterized by the proliferation of spindle or epithelioid cells and by the expression of CD117. Extra-gastrointestinal stromal tumors are rare and only 13 cases of pancreatic GISTs have been reported in the literature, only 1 of which presented as a cystic lesion. Mutational analysis of KIT and Platelet derived growth factor receptor-α genes was performed only in two out of the 13 cases. We report 3 cases of cystic GISTs of the pancreas, radiologically mimicking a cystoadenocarcinoma. Routine histopathology and molecular characterization of the tumours have been performed. In two of them, molecular analysis showed unusual genetic alterations (the internal repeat of codon 502 and 503 in exon 9 of the KIT gene and the KIT exon 9 single nucleotide substitution c.1427G>T). Pancreatic GIST should be included in the differential diagnosis of both cystic and solid masses of the pancreas. The diagnosis should be accomplished by a combination of radiology, histology, immunohistochemistry and molecular biology. The evaluation of CD117 expression and the sequence analysis of KIT and Platelet derived growth factor receptor-α gene is mandatory for therapy.
- PublicationOpen AccessNestin and WT1 expression in atheromatous plaque neovessels: association with vulnerability(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Fittipaldi, Silvia; Vasuri, Francesco; Degiovann, Alessio; Pini, Rodolfo; Mauro, Raffaella; Faggioli, Gianluca; D'Errico-Grigioni, Antonia; Stella, Andrea; Pasquinelli, GianandreaIntroduction. Neoangiogenesis is crucial for the progression and vulnerability of atheromasic lesions. Since adult vasa vasorum, which represent the neoangiogenetic burden of healthy arteries, constitutively express Nestin and Wilms Tumor (WT1), the aims of the present study are: i) to describe and quantify Nestin and WT1 in plaque neovessels; ii) to investigate the relationship between neovessel phenotype and plaque instability. Methods. We prospectively evaluated 49 consecutive carotid endarterectomy specimens. Histopathological characteristics were separately collected, particularly the intraplaque histological complications. Immunohistochemistry was carried out for CD34, Nestin and WT1; the density of positivity was evaluated for each marker. RT-PCR was performed to assess Nestin and WT1 mRNA levels on the first 10 plaques and on 10 control arteries. Results. Six (12.2%) plaques showed no neoangiogenesis. In the others, the mean immunohistochemical densities of CD34, Nestin, and WT1-positive structures were 41.88, 28.84 and 17.68/mm2. Among the CD34+ neovessels, 68% and 42% expressed Nestin and WT1 respectively, i.e., nearly 36% of the neovessels resulted to be Nestin+/WT1-. Furthermore, complicated plaques (n=30) showed significantly more CD34 and Nestin-positive vessels than uncomplicated plaques (n=13; P=0.045 and P=0.009), while WT1 was not increased (P=0.139). RT-PCR confirmed that WT1 gene expression was 3-fold lower than Nestin gene in plaques (p=0.001). Conclusions. Plaque neoangiogenesis shows both a Nestin+/WT1- and a Nestin+/WT1+ phenotype. The Nestin+/WT1- neovessels are significantly more abundant in complicated (vulnerable) plaques. The identification of new transcription factors in plaque neoangiogenesis, and their possible regulation, can open new perspectives in the therapy of vulnerable plaques.