Histology and histopathology Vol.30, nº7 (2015)
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- PublicationOpen AccessThe postulated mechanism of the protective effect of ginger on the aspirin induced gastric ulcer: Histological and immunohistochemical studies(Universidad de Murcia. Departamento de Biología Celular e Histología, 2015) Salah Khalil, MahmoudThere are many available drugs for treating gastric ulcer, but they have various side effects. Ginger is a folk, herbal medicine, which is used for treatment of various diseases including gastric ulcer. This study investigates the possible mechanism of the protective effect of ginger on aspirin induced gastric ulcer. Forty adult male albino rats were randomized into four groups (10 animals per each group) and orally received the followings once daily for 5 days: Group I: 3 ml of 1% carboxymethyl cellulose; Group II: ginger powder (200 mg/kg body weight) suspended in 3 mL of 1% carboxymethylcellulose; Group III: aspirin (400 mg/kg body weight) suspended in 3 ml of 1% carboxymethylcellulose in water. Group IV: ginger and 30 minutes later, received aspirin suspended in 1% carboxymethylcellulose, in similar doses as received in groups II and III. On day 6, rats were sacrificed. The animals were anesthetized and the stomach was removed for the macroscopic, histological (Haematoxylin and Eosin and Periodic Acid Shiff) and immunohistochemical investigations (Bax, inducible nitric oxide synthase and heat shock protein 70). Aspirin induced a significant increase of the macroscopic ulcer score, shed and disrupted epithelium, mucosal hemorrhage, submucosal edema and leukocyte infiltration, loss of the mucus of the mucosal surface significantly increased expression of apoptosis regulator Bax, inducible nitric oxide synthase (iNOS) and heatshock protein 70 (HSP70). Ginger ameliorated the histological changes by reducing Bax and iNOS and increasing HSP70 expressions.
- PublicationOpen AccessReduced innervation in the human pharynx in patients with obstructive sleep apnea(Universidad de Murcia. Departamento de Biología Celular e Histología, 2015) de Carlos, Félix; Cobo, Juan; Macías, Emilio; Feito, Jorge; González, Mónica; Cobo, Teresa; Fernández-Mondragón, María P.; García-Suárez, Olivia; Vega, José A.Obstructive sleep apnea is a disease characterized by repetitive breathing during sleep that lead to reduced oxygen saturation and sleep disturbance among other symptoms. Obstructive sleep apnea is caused by blockade of the upper respiratory airway, although the pathogenic mechanism underlying this occlusion remains unknown. In these studies we explored the hypothesis that alterations in the innervation, especially mechanosensory innervation, of the pharynx may contribute to obstructive sleep apnea. We tested this hypothesis by analyzing the innervation of the human pharynx in normal individuals and in subjects clinically diagnosed with obstructive sleep apnea. Using immunohistochemistry for axon and Schwann cells, as well as for two putative mechanoproteins (ASIC2 and TRPV4), we observed a significant reduction in the density of nerve fibers in the submucosa of patients with obstructive sleep apnea as well as morphological abnormalities in mechanosensory corpuscles. Importantly, while ASIC2 and TRPV4 expression was regularly found in the axons of mechanosensory corpuscles distributed throughout the muscular layer in the control subjects, it was absent in patients with obstructive sleep apnea. These findings support that neurological alterations are important contributors to the pathogenesis of obstructive sleep apnea.
- PublicationOpen AccessMutation stability in primary and metastatic melanoma: what we know and what we don’t(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Varada, Sowmya; Mahalingam, MeeraDespite the efficacy and success of targeted therapies, a significant number of patients with melanoma exhibit either intrinsic or acquired resistance to these drugs. Numerous mechanisms for the development of resistance have been postulated, but the precise reason for this is not known. In this review, we examine the incidence of mutations in select genes (BRAF, NRAS, C-KIT, and GNAQ) known to occur in melanoma, specifically in primary tumors and their paired metastases, to understand the significance of intratumoral heterogeneity by assessing how changes in mutation status alters the process of metastatic spread. Our data revealed a small yet consistent degree of discordance of mutations in the MAPK pathway commonly occurring in melanoma indicating that failed targeted therapy may be a consequence of this.
- PublicationOpen AccessMarkers of squamocolumnar junction cells in normal tonsils and oropharyngeal cancer with and without HPV infection(Universidad de Murcia. Departamento de Biología Celular e Histología, 2015) Morbini, Patrizia; Capello, Gianluca; Alberizzi, Paola; Benazzo, Marco; Paglino, Chiara; Comoli, Patrizia; Pedrazzoli, Paoloy. HPV infection has been identified recently as the causative agent of a subset of squamous cell carcinomas arising in oropharyngeal tonsils. Factors influencing the susceptibility of tonsillar epithelium to HPV-induced oncogenesis are far from being elucidated. A 5-protein signature including cytokeratin (CK)7, anterior gradient (AGR)2, cluster differentiation (CD)63, matrix metalloproteinase (MMP)7, and guanine deaminase (GDA) has recently been found to identify a residual embryonic cell population in the squamocolumnar (SC) junction of the cervix, susceptible to HPV infection, and cancers originating from these cells. The expression of SC junction markers was investigated with immunohistochemistry in normal tonsils and in oropharyngeal carcinomas (OPC) fully characterised for HPV. All markers were constantly expressed in the reticulated epithelial cells of the tonsillar crypts, with variable diffusion and intensity; in OPC, positivity was observed in 36.5%, 29.2%, 39%, 17%, and 25% of cases with respectively AGR2, CK7, GDA, CD63, and MMP7 antibodies. No OPC was positive for all markers; 6 were completely negative. AGR2 and CK7 showed significant association with tumor- and HPV-related parameters. AGR2 expression was associated with tumor origin in the tongue base (p=0.013); CK7 was associated withnon-keratinising morphology (p=0.013). p16 tumor cell expression was associated with AGR2 (p=0.021); transcriptionally active HPV infection was associated with AGR2 and CK7 (p=0.024 and 0.043). Expression of SC junction markers in tonsillar crypt cells might be related to the embryological development of tonsillar structures; their partial association with HPV oncogenic infection could help to identify HPVsusceptible cells and related OPC.
- PublicationOpen AccessThe pivotal role of PDGF and its receptor isoforms in adipose-derived stem cells(Universidad de Murcia. Servicio de publicaciones, 2015) Kim, Won-Serk; Park, Hyoung-Sook; Sung, Jong-HyukPlatelet-derived growth factor (PDGF) is one of the growth factors that reportedly regulates cell growth and division of mesenchymal cells. Although PDGF isoforms and their receptors reportedly play a pivotal role in mesenchymal stem cell regulation, there is a paucity of literature reviewing the role of PDGF in adipose-derived stem cells (ASCs). Therefore, we summarized previous reports on the expression and functional roles of PDGF and its receptor isoforms in this review. In addition, we examined findings pertaining to underlying molecular mechanisms and signaling pathways with special focus on PDGF-D/PDGFRβ. ASCs only express PDGF-A, -C, -D, PDGFRα, and PDGFRβ. PDGFRα expression decreases with adipocyte lineage, while PDGFRβ inhibits white adipocyte differentiation. In addition, PDGFRβ induces proliferation, migration, and angiogenesis and upregulates the expression of paracrine factors in ASCs. Although PDGF-B and -D mediate their functions mainly by PDGFRβ and ROS generation, there are many differences between them in terms of regulating ASCs. PDGF-D is endogenous, generates ROS via the mitochondrial electron transport system, and regulates the autocrine loop of ASCs in vivo. Furthermore, PDGFD has stronger mitogenic effects than PDGF-B.
- PublicationOpen AccessPurkinje fibers after myocardial ischemia-reperfusion(Universidad de Murcia. Departamento de Biología Celular e Histología, 2015) García Gómez-Heras, Soledad; Álvarez-Ayuso, Lourdes; Torralba Arranz, Amalia; Fernández-García, HéctorThe purpose of this study was to evaluate the effects of ischemia-reperfusion on Purkinje fibers, comparing them with the adjacent cardiomyocytes. In a model of heterotopic heart transplantation in pigs, the donor heart was subjected to 2 hours of ischemia (n=9), preserved in cold saline, and subjected to 24 hours of ischemia with preservation in Wisconsin solution, alone (n=6), or with an additive consisting of calcium (n=4), Nicorandil (n=6) or Trolox (n=7). After 2 hours of reperfusion, we evaluated the recovery of cardiac electrical activity and took samples of ventricular myocardium for morphological study. The prolonged ischemia significantly affected atrial automaticity and AV conduction in all the groups subjected to 24 hours of ischemia, as compared to 2 hours. There were no significant differences among the groups that underwent prolonged ischemia. Changes in the electrical activity did not correlate with the morphological changes. In the Purkinje fibers, ischemia-reperfusion produced a marked decrease in the glycogen content in all the groups. In the gap junctions the immunolabeling of connexin-43 decreased significantly, adopting a dispersed distribution, and staining the sarcolemma adjacent to the connective tissue. These changes were less marked in the group preserved exclusively with Wisconsin solution, despite the prolonged ischemia. The addition of other substances did not improve the alteredmorphology. In all the groups, the injury appeared to be more prominent in the Purkinje fibers than in the neighboring cardiomyocytes, indicating the greater susceptibility of the former to ischemia-reperfusion injury.
- PublicationOpen AccessProgress in histopathologic and pathogenetic research in a retinitis pigmentosa model(Universidad de Murcia. Servicio de publicaciones, 2015) Liu, Xin; Zhang, Yan Zhang; He, Yuxi; Zhao, Jinsong; Su, GuanfangRetinitis pigmentosa is a major cause of visual impairment and blindness, affecting millions of people worldwide. The mechanisms of and effective treatments for the disease, however, remain to be further investigated. The Royal College of Surgeons rat is one of the most widely used animal models for the study of retinal degeneration diseases. The mutation in the mer tyrosine kinase proto-oncogene of this model leads to deficient phagocytosis in the retinal pigment epithelium cells and the accumulation of photoreceptor out segments in the subretinal space, ultimately resulting in retinal degeneration. The retina begins to change as early as 17 days after birth and becomes gradually thinner with the death and remodeling of cells and blood vessels. Retinal cell apoptosis plays a dominant role in this degeneration, with some cells being activated by the secondary alterations of the retinal neurotransmitter and other related factors.
- PublicationOpen AccessCXCR3 in carcinoma progression(Universidad de Murcia. Servicio de publicaciones, 2015) Ma, Bo; Khazali, Ahmad; Wells, AlanCXCR3 is a G-protein coupled receptor which binds to ELR-negative CXC chemokines that have been found to impact immune responses, vascular develop, and wound repair. More recently, CXCR3 has been examined in the context of cancer and increased expression in many human tumors has been correlated with poor prognosis in breast, melanoma, colon and renal cancer patients. Three variants of CXCR3 are identified so far (CXCR3-A, CXCR3-B and CXCR3-alt) with the two primary ones, CXCR3-A and CXCR3-B, considered to induce opposite physiological functions. Generally, CXCR3-A, the predominant form in hematopoietic cells, appears to mediate tumor “go” signaling via promoting cell proliferation, survival, chemotaxis, invasion and metastasis; while CXCR3-B, the main form on formed elements including epithelial cells, appears to mediate tumor “stop” signaling via promoting growth suppression, apoptosis and vascular involution. Thus, aberrant expression of the isoforms CXCR3-A and CXCR3-B could affect tumor progression. In this review, we have discussed the profiles of CXCR3 variants and related signaling, as well as the role of CXCR3 variants in cancer.
- PublicationOpen AccessAerobic training attenuates nicotinic acetylcholine receptor changes in the diaphragm muscle during heart failure(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) de Souza, Paula Aiello Tomé; de Souza, Rodrigo Wagner Alves; Campos Soares, Luana; Piedade, Warlen Pereira; Campos, Dijon Henrique S.; Carvalho, Robson Francisco; Padovani, Carlos Roberto; Okoshi, Katashi; Cicogna, Antônio Carlos; Michelin Matheus, Selma Maria; Dal-Pai-Silva, MaeliIntroduction: Heart failure (HF) is a progressive myopathy, with clinical signs of fatigue and limb weakness that can damage the nerve-muscle interaction, altering synaptic transmission and nicotinic acetylcholine receptors (nAChR) in neuromuscular junctions (NMJs). The diaphragm is composed of a mixed proportion of muscle fibres, and during HF, this muscle becomes slower and can alter its function. As exercise training is an accepted practice to minimise abnormalities of skeletal muscle during HF, in this study, we evaluated the hypothesis that aerobic training attenuates alterations in the expression of nAChR subunits in NMJs diaphragm during heart failure. Objective: The aim of this study was to evaluate the distribution and expression of nAChR subunits in the diaphragm muscle fibres of rats subjected to an aerobic training programme during HF. Methods: Control (Sham), control training (ShamTR), aortic stenosis (AS) and aortic stenosis training (ASTR) groups were evaluated. The expression of nAChR subunits (γ, α1, ε, β1 and δ) was determined by qRT-PCR, and NMJs were analysed using confocal microscopy. Results: We observed increased expression of the γ, α1 and β1 subunits in the AS group compared with the ASTR group. The distribution of NMJs was modulated in these groups. Discussion: HF alters the mRNA expression of nAChR subunits and the structural characteristics of diaphragm NMJs. In addition, aerobic training did notalter NMJs morphology but attenuated the alterations in heart structure and function and in nAChR subunit mRNA expression. Our findings demonstrate the beneficial effects of aerobic exercise training in maintaining the integrity of the neuromuscular system in the diaphragm muscle during HF and may be critical for non-pharmacological therapy to improve the quality of life for patients with this syndrome.
- PublicationOpen AccessKeratin-chitosan membranes as scaffold for tissue engineering of human cornea(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Vázquez, Natalia; Chacón, Manuel; Meana, Álvaro; Menéndez-Menénde, Yolanda z; Ferrero-Gutierrez, Amaia; Cereijo-Martín, David; Naveiras, Miguel; Merayo-Lloves, JesúsPurpose: To study the attachment and growth of human corneal cells on keratin-chitosan membranes. The end goal is to develop a bioengineered cornea based on this material. Methods: Keratin-chitosan membranes were prepared as previously described by Tanabe et al., 2002. Briefly, 7.15 mg/cm2 of keratin dialysate was mixed with 10wt% chitosan solution and 20 wt% glycerol. The solution was cast into a silicone mold and dried at 50°C for 36 hours. Eyes were attained from a local eye bank after penetrant-keratoplastic surgery. Human epithelial, stromal and endothelial cells were obtained of the limbal, stromal and endothelial regions. Cells were cultured on keratin-chitosan membranes, as well as on plastic dishes as controls. When cultured cells reached confluence, they were fixed, incubated with primary antibodies (E-cadherin, cytokeratin high molecular weight (CK), vimentin and Na+/K+ ATPase) and visualized by indirect immunocytochemistry. Results: Epithelial, stromal and endothelial cells were able to attach and grow on keratin-chitosan membranes. All the cells maintained their morphology and cellular markers, both in the membrane and on the culture plate. Epithelial cells stained positively for CK and Ecadherin. A positive vimentin stain was observed in all stromal cells, while endothelial cells were positive forvimentin and Na+/K+ ATPase, but negative for Ecadherin. Conclusions: Keratin-chitosan membranes have been shown to be a good scaffold for culturing epithelial, stromal and endothelial corneal cells; therefore, future applications of keratin-chitosan membranes may be developed for reconstruction of the cornea.
- PublicationOpen AccessCcdc85C, a causative protein for hydrocephalus and subcortical heterotopia, is expressed in the systemic epithelia with proliferative activity in rats(Universidad de Murcia. Departamento de Biología Celular e Histología, 2015) Tanaka, Natsuki; Izawa, Takeshi; Takenaka, Shigeo; Yamate, Jyoji; Kuwamura, Mitsuru. Coiled-coil domain containing 85c (Ccdc85c) is a causative gene for spontaneous mutant mouse with non-obstructive hydrocephalus and subcortical heterotopia. Detailed functions of Ccdc85C protein have not been clarified. To reveal roles of Ccdc85C, we examined the distribution and expression pattern of Ccdc85C in the systemic developing organs in rats. Ccdc85C was expressed in various simple epithelia but not stratified epithelia. In the various epithelia, Ccdc85C was localized at cell-cell junctions and its expression was strong at apical junctions. Furthermore, intense expression was seen at developing period and gradually decreased with advancing development. Distribution of Ccdc85C coincides with that of proliferating epithelial cells. These results suggest that Ccdc85C plays an important role in the proliferative property of simple epithelia.