Histology and histopathology Vol.30, nº4 (2015)
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- PublicationOpen AccessA surgical model of short bowel syndrome induces a long-lasting increase in pancreatic beta-cell mass(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Pérez-Arana, G.; Camacho-Ramírez, A.; Segundo-Iglesias, M.C.; Lechuga-Sancho, A.M.; Sancho-Maraver, E.; Aguilar-Diosdado, M.Several surgical techniques are used nowadays as a severe treatment for obesity and diabetes mellitus type 2. These techniques are aggressive due to drastic changes in the nutrient flow and non-reversible modifications on the digestive tube. In this paper we present the effects of a massive intestinal resection on the pancreas. Results have shown that short bowel technique is less aggressive to normal anatomy and physiology of the intestinal tract than Gastric bypass or biliopancreatic diversion (e.g.). In this paper we reproduce a model of short bowel syndrome (SIC), with similar surgical conditions and clinical complications as seen in human cases. This work was conducted on normal Wistar rats, with no other concurrent factors, in order to determine the effects on normal pancreas islets. We measured pancreatic implications by histomorphometric studies, which included beta-cell mass by immunocytochemistry, and apoptosis/proliferation test with TUNEL technique and Ki-67. Briefly, we reported on an increased relative area of the islets of the pancreas, as well as an increase in the average size of islets in the SIC versus the control group. Furthermore we stated that this increase in size of the pancreatic islets is due to the mechanisms of proliferation of beta cells in animals undergoing SIC. These goals could reveal a direct influence of surgical modification of the digestive tract over the pancreatic beta cell homeostasis. In this sense, there are many potential stimulators of intestinal adaptation, including peptide hormones and growth components which are associated or involved as effectors of the endocrine pancreas.
- PublicationOpen AccessDifferential effects of intestinal ischemia and reperfusion in rat enteric neurons and glial cells expressing P2X2 receptors(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Marosti, Aline Rosa; Da Silva, Marcos Vinícius; Palombit, Kelly; Mendes, Cristina Eusébio; Tavares de Lima, Wothan; Castelucci, PatriciaBackground. Intestinal ischemia followed by reperfusion (I/R) may occur following intestinal obstruction. In rats, I/R in the small intestine leads to structural changes accompanied by neuronal death. Aim. The objective was to analyze the impact of I/R injury on different neuronal populations in the myenteric plexus of the rat ileum after different periods of reperfusion. Methods. The superior mesentery artery was occluded for 45 minutes, and animals were euthanized after 24 hours and 1 week of reperfusion. Immunohistochemical analyses were performed with antibodies against the P2X2 receptor in combination with antibodies against nitric oxide synthase (NOS), choline acetyltransferase (ChAT), calbindin, calretinin, the panneuronal marker anti-HuC/D, or S100β (glial marker). Results. Dual immunolabeling demonstrated that approximately 100% of NOS-, ChAT-, calbindin-, and calretinin-immunoreactive neurons in all groups expressed the P2X2 receptor. Following I/R, the neuronal density decreased in the P2X2 receptor-, ChAT- , calretinin-, and HuC/D-immunoreactive neurons at 24 hours and 1 week following injury compared to the densities in the control and sham groups. The calbindinimmunoreactive neuron density was not reduced in any of the groups. The density of enteric glial cells increased by 40% in the I/R group compared to the density in the sham groups. We also observed increases of 12%, 16%, and 23% in the neuronal cell body profile areas of the NOS-, ChAT-, and calbindin-immunoreactive neurons, respectively, at 1 week following I/R. However, the average size of the calretinin-immunoreactive neurons was reduced by 12% in the I/R group at 24 hours. Conclusions This work demonstrates that I/R is associated with a significant loss of different classes of neurons in the myenteric plexus accompanied by morphological changes and an increased density of enteric glial cells; all of these effects may underlie conditions related to intestinal motility disorder.
- PublicationOpen AccessMorphological adaptation and protein modulation of myotendinous junction following moderate aerobic training(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Curzi, Davide; Baldassarri, Valentina; De Matteis, Rita; Salamanna, Francesca; Bolotta, Alessandra; Frizziero, Antonio; Fini, Milena; Marini, Marina; Falcieri, ElisabettaMyotendinous junction is the muscle-tendon interfacethrough which the contractile force can be transferred from myofibrils to the tendon extracellular matrix. At the ultrastructural level, aerobic training can modify the distal myotendinous junction of rat gastrocnemius, increasing the contact area between tissues. The aim of this work is to investigate the correlation between morphological changes and protein modulation of the myotendinous junction following moderate training. For this reason, talin, vinculin and type IV collagen amount and spatial distribution were investigated by immunohistochemistry and confocal microscopy. The images were then digitally analyzed by evaluating fluorescence intensity. Morphometric analysis revealed a significant increased thickening of muscle basal lamina in the trained group (53.1±0.4 nm) with respect to the control group (43.9±0.3 nm), and morphological observation showed the presence of an electron-dense area in the exercised muscles, close to the myotendinous junction. Protein concentrations appeared significantly increased in the trained group (talin +22.2%; vinculin +22.8% and type IV collagen +11.8%) with respect to the control group. Therefore, our findings suggest that moderate aerobic training induces/causes morphological changes at the myotendinous junction, correlated to the synthesis of structural proteins of the muscular basal lamina and of the cytoskeleton.
- PublicationOpen AccessDifferent expression of protein kinase A (PKA) regulatory subunits in normal and neoplastic thyroid tissues(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Ferrero, Stefano; Vaira, Valentina; Del Gobbo, Alessandro; Vicentini, Leonardo; Bosari, Silvano; Beck-Peccoz, Paolo; Mantovan, Giovanna; Spada, Anna; Lania, Andrea G.The four regulatory subunits (R1A, R1B, R2A, R2B) of protein kinase A (PKA) are differentially expressed in several cancer cell lines and exert distinct roles in both cell growth and cell differentiation control. Mutations of the PRKAR1A gene have been found in patients with Carney complex and in a minority of sporadic anaplastic thyroid carcinomas. The aim of the study was to retrospectively evaluate the expression of different PKA regulatory subunits in benign and non benign human thyroid tumours and to correlate their expression with clinical phenotype. Immunohistochemistry demonstrated a significant increase in PRKAR2B expression in both differentiated and undifferentiated (anaplastic) thyroid tumors in comparison with normal thyroid tissues. Conversely, a significant increase in PRKAR1A expression was only demonstrated in undifferentiated thyroid carcinomas in comparison with normal thyroid tissue and differentiated thyroid tumors. In thyroid cancers without lymph nodal metastases PRKAR1A expression was higher in tumours of more than 2 cm in size (T2 and T3) compared to smaller ones (T1). In conclusion, our data shows that an increased PRKAR1A expression is associated with aggressive and undifferentiated thyroid tumors.
- PublicationOpen AccessPresence of MUC1 in the epidermal thickening of psoriatic plaques(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Arciniegas, Enrique; Carrillo, Luz Marina; Páez, Erika; Rojas, Héctor; Ramírez, Richard; Reales, Eysi; Chopite, MarinaMucin 1 (MUC1) is a transmembrane glycoprotein that protects epithelial cells from injury caused by external stimuli. In addition to this role, MUC1 is involved in cell-cell adhesion, proliferation, motility, invasion and survival. In epithelial cells, MUC1 expression is regulated by binding of TNFα to TNFR1 and activation of the NFκB pathway. In human skin, MUC1 is not expressed in normal epidermis but rather in pre-malignant and malignant conditions. Nevertheless, the expression of MUC1 and its implication in psoriasis vulgaris has not been considered. Here, we show that MUC1 was present in the epidermis of psoriatic plaques observed in 11 biopsies from patients diagnosed with psoriasis vulgaris which were compared with 5 normal human skin. Interestingly, MUC1 in addition to being localized at the apical surface of some suprabasal keratinocytes, was also localized over the entire cell surface of some of these cells and some basal keratinocytes. Conversely, no MUC1 immunoreactivity was detected in the epidermis of normal skin. Additionally, we demonstrated that activated TNFR1, cSrc, IKKα/β and p50/p65 were present in the epidermal thickening. This study demonstrates the presence of MUC1 in psoriatic plaque and suggests a possible role for MUC1 during the motility, migration and survival of human keratinocytes, where activated TNFR1, c-Src and NFκB seem to be required.
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