Browsing by Subject "Nestin"

Now showing 1 - 5 of 5
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    Histological differences in healing following experimental transmural infarction in rats
    (Murcia : F. Hernández, 2010) Aljinović, Jure; Vukojevic, Katarina; Košta, Vana; Marinović Guić, Maja; Saraga-Babić, Mirna; Grković, Ivica
    Mechanisms of cardiac regeneration following transmural myocardial infarction were analysed in rat hearts using immunohistochemistry for α-SMA, caspase-3, Ki-67 and nestin markers. Seven weeks after experimental myocardial infarction, two different types of healing processes were revealed in rats with and without aneurysmatic bulging of the left ventricular wall. Besides thinning of the ventricular wall, three zones characterized both types of scars: the scar zone (divided into central and peripheral parts), the peri-infarct zone and the border zone. The main difference between the types of scars was the presence of a central necrotic zone inside the aneurysmatic wall, while connective tissue with myofibroblasts characterized the same zone in nonbulging wall. Apoptotic caspase-3 positive cells were found in the granulation tissue of the border zone in aneurysmatic scar, while in non-bulging scar they characterized all three zones. Proliferating Ki-67 positive cells displayed reverse expression pattern compared to apoptotic cells. Quantification of α-SMA positive cells revealed 60% α-SMA positive cells inside the central part of the aneurysmatic scar zone and 39% in invaginating areas, versus 19% in non-invaginating areas of the peripheral zone, but only 30% in the peripheral part of the non-bulging scar zone. Nestin positive cells were found in both types of scars, but with different distribution. These results suggest that even seven weeks after myocardial infarction, the healing processes in non-bulging scars are in chronic phase, while aneurysmatic scars are still in subacute phase. Histological differences in scar healing might be important for functional properties of the heart wall and for heart recovery prognosis.
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    Nestin 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, Gianandrea
    Introduction. 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.
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    Nestin and WT1 expression in small-sized vasa vasorum from human normal arteries
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Vasuri, Francesco; Fittipaldi, Silvia; Buzzi, Mariana; Degiovanni, Alessio; Stella, Aandrea; D’Errico-Grigioni, Antonia; Pasquinelli, Gianandrea
    Introduction. Vasa vasorum (VV) neovasculogenic potential is now widely accepted, and possibly related to the presence of progenitor cells. We studied the morphology of VV in healthy arteries and their immunohistochemical (IHC) expression of Nestin and WT1, two markers of endothelial progenitor cells. Materials and Methods. Twenty arteries from 16 multiorgan donors were analyzed; IHC was performed manually (CD34, CD31, Nestin) or automatically (WT1). Microvessel positivity “density” for each antibody was calculated dividing vascular adventitia in 1-mm2 fields with an ocular micrometer. Double immunofluorescence was used to investigate Nestin and WT1 co-localization in VV. Results. The mean positivity “densities” for CD31, CD34, Nestin and WT1 were 13.63, 12.20, 8.90 and 7.98/mm2 respectively. Mean Nestin/CD31 and WT1/CD31 ratios were 0.69 and 0.63 respectively. VV <50 µm in diameter showed a higher percentage of Nestin/WT1-positive cells than larger ones, especially in “hot spots”, characterized by several small-sized arteriolar VV, often together with nerva vasorum. Immunofluorescence indentified Nestin and WT1 in the same endothelial cells. WT1 nuclear expression was mainly seen in <50 µm VV. Discussion. We describe Nestin and WT1 in adult VV, especially <50 µm and gathered in “hot spots”. The nuclear localization of WT1 could express an increasing transcriptional activity in progenitor-committed Nestin-positive cells. The “hot spot” could therefore represent a valid model for the vasculogenic niche in normal arteries and could potentially represent the main source for neovasculogenesis during atherosclerosis
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    Nestin expression in normal adrenal gland and adrenocortical tumors
    (Murcia : F. Hernández, 2005) Toti, P.; Regoli, M.; Nesi, G.; Occhini, R.; Bartolommei, S.; Fonzi, L.; Bertelli, E.
    Human adrenocortical cells have been shown to express cytokeratins and vimentin. Nestin is an intermediate filament protein that is mainly expressed in the developing nervous system and that has been recently reported in rat adrenal gland as well. Using immunohistochemical and biochemical approaches, the present study demonstrates that nestin is constantly expressed in situ in the cortex of normal human adrenal glands. Nestin expressing cells were prevalently located in the zona reticularis but some positive cells could be spotted in the zona fasciculata as well. Moreover, patches of nestin-positive cells have been constantly detected on sections of cortical adenomas. In contrast, adrenal carcinomas displayed a variable number of nestin-immunoreactive cells that in some cases were virtually absent. Samples of renal clear cell carcinoma metastasis in the adrenals were also examined which did not show nestin-immunoreactivity. We propose that a positive nestin-immunoreaction could be useful in differential diagnosis of clear cell tumors in adrenal glands.
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    Nestin+cells forming spheroids aggregates resembling tumorspheres in experimental ENU-induced gliomas
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) García Blanco, Alvaro; Bulnes, Susana; Pomposo, Iñigo; Carrasco, Alex; Lafuente, José Vicente
    Nestin+cells from spheroid aggregates display typical histopathological features compatible with cell stemness. Nestin and CD133+cells found in glioblastomas, distributed frequently around aberrant vessels, are considered as potential cancer stem cells. They are possible targets for antitumoral therapy because they lead the tumorigenesis, invasiveness and angiogenesis. However, little is known about their role and presence in low-grade gliomas. The aim of this work is to localize and characterize the distribution of these cells inside tumors during the development of experimental endogenous glioma. For this study, a single dose of Ethyl-nitrosourea was injected into pregnant rats. Double immunofluorescences were performed in order to identify stem-like and differentiated cells. Low-grade gliomas display Nestin+cells distributed throughout the tumor. More malignant gliomas show, in addition to that, a perivascular location with some Nestin+cells co-expressing CD133 or VEGF, and the intratumoral spheroid aggregates of Nestin/CD133+ cells. These structures are encapsulated by welldifferentiated VEGF/GFAP+cells. Spheroid aggregates increase in size in the most malignant stages. Spheroid aggregates have morphological and phenotypic similarities to in vitro neurospheres and could be an in vivo analogue of them. These arrangements could be a reservoir of undifferentiated cells formed to escape adverse microenvironments.