Histology and histopathology Vol.30, nº4 (2015)
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- 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 AccessLeptomeninges: a novel stem cell niche harboring ischemia-induced neural progenitors(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Nakagomi, Takayuki; Nakano-Doi, Akiko; Matsuyama, TomoiroIt is well known that neural stem cells (NSCs) are present in many parts of the central nervous system (CNS), including the subventricular zone (SVZ) of the lateral ventricle, subgranular zone (SGZ) of the hippocampal dentate gyrus, cortex, and spinal cord. Using a mouse model of cortical infarction, we demonstrated for the first time that NSCs, which can differentiate into neural lineage cells, could be induced in the meninges (leptomeninges) of ischemic brain areas as well. However, such ischemia-induced NSCs (iNSCs) were not observed in the leptomeninges of non-ischemic areas. This suggests the leptomeninges, which surround the CNS, might be a novel stem cell niche harboring endogenous iNSCs following brain injury. In this review, we introduce the characterization and possible origin of leptomeningeal iNSCs based on our reports and recent findings. We also refer to the potential of leptomeningeal iNSCs for cortical neurogenesis.
- PublicationOpen AccessVersatile hemidesmosomal linker proteins: Structure and function(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Chaudhari, Pratik R.; Vaidya, Milind M.Hemidesmosomes are anchoring junctions which connect basal epidermal cells to the extracellular matrix. In complex epithelia like skin, hemidesmosomes are composed of transmembrane proteins like α6β4 integrin, BP180, CD151 and cytoplasmic proteins like BPAG1e and plectin. BPAG1e and plectin are plakin family cytolinker proteins which anchor intermediate filament proteins i.e. keratins to the hemidesmosomal transmembrane proteins. Mutations in BPAG1e and plectin lead to severe skin blistering disorders. Recent reports indicate that these hemidesmosomal linker proteins play a role in various cellular processes like cell motility and cytoskeleton dynamics apart from their known anchoring function. In this review, we will discuss their role in structural and signaling functions.
- PublicationOpen AccessRespiratory syncytial virus receptor expression in the mouse and viral tropism(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Shakeri, Aria; Mastrangelo, Peter; Griffin, Jennifer K.; Moraes, Theo J.; Hegele, Richard G.Human respiratory syncytial virus (RSV) infects airway epithelium and can cause serious illnesses such as bronchiolitis and pneumonia. With the discovery of cell-surface nucleolin as a fusion receptor for RSV, the question arose as to whether nucleolin could explain RSV tropism in vivo. Here, we report the distribution of cell-surface nucleolin expression in tissues of normal mice and how this distribution of expression relates to what is known about RSV tropism and its clinical manifestations. Our results show evidence of cellsurface nucleolin expression in the respiratory tract. In addition, cell-surface nucleolin is expressed in tissues outside of the respiratory tract, many of which correspond to previous reports of tissue-specific RSV infection, and others that may allude to additional potential sites for RSV infection in vivo. Furthermore, our work provides a foundation for the investigation of nucleolin’s physiological function in various healthy mammalian tissues.
- 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.
- PublicationOpen AccessSmall cell carcinoma of the prostate: Molecular basis and clinical implications(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Wang, Lisha; Davidson, Darrell D.; Montironi, Rodolfo; Lopez-Beltran, Antonio; Zhang, Shaobo; Williamson, Sean R.; MacLennan, Gregory T.; Wang, Chaofu; Wang, Mingsheng; Emerson, Robert E.; Du, Xiang; Cheng, LiangSmall cell carcinoma of the prostate (PSCC) is a rare and highly aggressive malignancy with a dismal prognosis. Most patients present with advanced disease, including metastases to bone, viscera, and the central nervous system. Histologically, PSCC is indistinguishable from its pulmonary counterpart. Although PSCC may occur in pure form, as in small cell lung carcinoma, it also occurs in conjunction with conventional glandular prostate carcinoma, and may evolve from conventional adenocarcinoma during the course of hormonal therapy. Immunohistochemical staining is extremely helpful in establishing the diagnosis, a prerequisite, as in small cell lung cancer, for optimal therapeutic strategy. Currently, combinations of surgical resection, chemotherapy, and radiation therapy represent the main treatment options. Improvement in survival may depend upon the identification of new molecular markers to facilitate earlier diagnosis and the development of novel targeted therapies. This review will discuss general aspects of PSCC, focusing on ways in which our understanding of PSCC has been advanced by studies of the histopathologic, immunohistochemical and molecular alterations in this disease.
- 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 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 AccessEvaluation of CART-, glucagon-, and insulinimmunoreactive cells in the pancreas of an experimental rat model of unilateral renal artery stenosis(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Kasacka, I.; Janiuk, I.; Piotrowska, Z.Hypertension is one of the most frequently occurring diseases worldwide. Approximately 10% of the population with hypertension reveal the secondary type of hypertension. The aim of this study was to evaluate the cells containing CART, insulin and glucagon in the pancreas of rats with renovascular hypertension. An experimental model of hypertension in rats according to Goldblatt (2K1C model of hypertension) was used in the study. The experimental material (pancreas) was collected in the 6th week of the study. Cells containing CART, insulin and glucagon were evaluated using immunohistochemical and morphometric methods. Pancreatic islet cells were evaluated based on the number and intensity of staining. The investigation showed an increase in the number and immunoreactivity of CART containing cells, 6 weeks after partial unilateral ligation of the renal artery. There was a significant decrease in the number of glucagon-IR cells. Although intensity of staining these cells did not change. No differences were observed in the number and staining affinity of insulin-containing cells. On the basis of the study it can be stated that the endocrine system of pancreas undergoes changes in the course of renovascular hypertension. This may affect the production of hormones and contribute to the development of possible hypertension complications.
- PublicationOpen AccessLong-term type 1 diabetes alters the deposition of collagens and proteoglycans in the early pregnant myometrium of mice(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Favaro, Rodolfo R.; Raspantin, Priscila R.; Salgado, Renato M.; Forte, Zuleica B.; Zorn, Telma M.T.troduction: We have previously shown that long-term type 1 diabetes affects the structural organization, contractile apparatus and extracellular matrix (ECM) of the myometrium during early pregnancy in mice. Objective: This study aimed to identify which myometrial ECM components are affected by diabetes, including fibril-forming collagen types I, III and V, as well as proteoglycans, decorin, lumican, fibromodulin and biglycan. Methods: Alloxaninduced type 1 diabetic female mice were divided into subgroups D1 and D2, formed by females that bred 90- 100 and 100-110 days after diabetes induction, respectively. The deposition of ECM components in the myometrium was evaluated by immunohistochemistry/immunofluorescence. Results: The subgroup D1 showed decreased deposition of collagen types I and III in the external muscle layer (EML) and decreased collagen types III and V in the internal muscle layer (IML). Collagen types I and III were decreased in both muscle layers of the subgroup D2. In addition, increased deposition of collagen types I and III and lumican as well as decreased collagen type V were observed in the connective tissue between muscle layers of D2. Lumican was decreased in the EML of the subgroups D1 and D2. Fibromodulin was repressed in the IML and EML of both D1 and D2. In contrast, decorin deposition diminished only in muscle layers of D2. No changes were noticed for biglycan. Conclusions: Subgroups D1 and D2 showed distinct stages of progression of diabetic complications in the myometrium, characterized by both common and specific sets of changes in the ECM composition.
- 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.