Histology and histopathology Vol.33,nº10 (2018)
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- PublicationOpen AccessSulfur dioxide ameliorates rat myocardial fibrosis by inhibiting endoplasmic reticulum stress(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Wang, Xin Bao; Cui, Hong; Du, Jun BaoMyocardial remodeling occurs after myocardial infarction (MI), the leading cause of mortality worldwide. Although myocardial fibrosis plays an important role in the process of myocardial remodeling, there is not yet an effective method of reducing it. The aim of the present study was to determine the effects of sulfur dioxide (SO2) on myocardial fibrosis and the possible mechanisms of these effects. SO2 treatment reduced the extent of myocardial fibrosis and post-MI levels of collagens I and III in the left-ventricular myocardium. SO2 also improved MI-induced thinning of the left ventricular wall while enlarging the left ventricular internal diameter. SO2 was able to reduce matrix metalloproteinase (MMP)-9 activity and increase tissue matrix metalloproteinase inhibitor (TIMP)-1 content in myocardium after MI. However, the mechanism underlying these effects of SO2 on myocardial fibrosis are unknown. Western blot analysis of endoplasmic reticulum (ER) stress-related proteins showed that glucose-regulated protein 78, C/EBP homologous protein, caspase-12, and phosphorylated eukaryotic initiation factor 2α expression levels were significantly increased in MI rats and decreased by SO2 treatment. The ER stress promoter dithiothreitol reversed these effects of SO2. In conclusion, SO2 alleviated myocardial fibrosis in MI rats through a mechanism related to inhibition of excessive ER stress.
- PublicationOpen AccessButylated hydroxytoluene induces type-V collagen and overexpression of remodeling genes/proteins in experimental lung fibrosis(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Martins, Vanessa; Teodoro, Walcy Rosolia; Pereira Velosa, Ana Paula; Andrade, Priscila; Farhat, Cecília; Fabro, Alexandre Todorovic; Capelozzi, Vera LuizaAnomalous histoarchitecture with increased levels of type-V collagen (Col V) in lungs of human idiopathic pulmonary fibrosis (IPF) and bleomycin (BLM) airway-centered interstitial fibrosis suggest that this collagen can be a possible trigger involved in the pathogenesis of these diseases. Butylated hydroxytoluene (BHT) injury model revealed a distal involvement of lung parenchyma with significant endothelial injury and fibrotic response, contrasting with the BLM airway-centered insult. We undertook this study to analyze whether BHT alters distal airway/alveolar epithelial cells (AECs) and extracellular matrix (ECM) signaling involved in the initiation and progression of pulmonary fibrosis in a different pathway concerning overexpression of Col V. Female mice C57BL/6 (n=6) were instilled intraperitoneally with 400mg/kg of BHT dissolved in 1 mL of corn oil and euthanized at day 14 or 21 after BHT administration. Morphometry, immunohistochemistry and transmission electron microscopy were performed to characterize microscopic and submicroscopic changes of AECs and endothelial cells through transforming growth factor beta (TGF-β) basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) expression. Immunofluorescence and immunogold electron microscopy were performed to characterize Col V. Quantitative polymerase chain reaction (qPCR) was used to confirm differential levels of RNA messenger. BHT lungs showed marked fibrotic areas and hyperplastic AECs. The alveolar damage caused destruction of elastic fibers and a critical increase of Col V in ECM of distal lung parenchyma. Fibrogenesis-promoting markers TGF-β, bFGF and VEGF were also overexpressed in situ, coinciding with up-regulation in remodeling enzymes, growth factors, cytokines, transduction and transcription genes. BHT alters distal lung parenchyma signaling involved in pulmonary fibrosis highlighted similarities to human IPF in a pathway involving Col V arising as a promissory model to identify effective therapeutic targets.
- PublicationOpen AccessQuantification of the heterogeneity of cytokeratin 18 immunoexpression in prostate adenocarcinoma and normal prostate: Global and local features(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Santamaría, Luis; Ingelmo, Ildefonso; Sinues, Bryan; Martínez, Laura; Teba, FernandoThere are few studies comparing global versus local changes in spatial patterns in prostate cancer. In this study, stereological tools have been applied to find out if the cytokeratin18 (ck18) immunoexpression shows local changes in cancer compared to normal prostate. To verify if these changes are relevant to ascertain differences between normal (CTR) and cancer (Ca) cases, several parameters were estimated. Volume fraction of epithelium immunostained for ck18 (VV ck18), dispersion index of VV ck18, positional variance of VV ck18, and multiscale entropy analysis (MSE) to measure the tissue heterogeneity. The MSE values showing significant differences between CTR and Ca were employed in a discriminant analysis to determine if MSE was able to classify the cases in CTR and Ca groups. The findings obtained indicate that changes in the expression of ck18 by the cancer prostate are heterogeneous. The increase in local variability of ck18 immunoexpression can be related to the increase in heterogeneity of shape and size of the tumor acini. The asymmetry of distribution of the local values of VV ck18 along the axis of the space series may indicate the existence of anisotropy in the distribution of tumor acini. The increase in scale-dependent entropy for VV ck18 in cancer at the morphological level could be interpreted as the macroscopic expression of the same increase at the molecular level already described. The discriminant analysis shows that the dependence on the resolution for MSE values need to be taken into account to characterize the prostate cancer better
- PublicationOpen AccessHistomorphometric analysis with a proposed tissue lesion index in ischemia-reperfusion induced gastric mucosa damage(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Peña Mercado, Eduardo; Garcia Lorenzana, Mario; Beltran, Nohra E.Damage to the gastrointestinal mucosa caused by ischemia - reperfusion is a significant clinical problem associated with various physiopathological conditions. Our group has conducted various studies in patients in critical conditions and in animal models to identify early damage to the gastric mucosa under ischemia using impedance spectroscopy. It is important to perform a quantitative histopathological analysis which can be linked to changes in impedance of the gastric mucosa under conditions of ischemia and I/R. Aim. To propose a tissue lesion index which considers pathological alterations inherent to the inflammatory process and cell damage which may be directly related to changes in impedance under conditions of ischemia and I/R. Methods. The animals were randomly distributed into 4 groups: control, ischemia (30 min), and I/R (30 and 60 min). Qualitative histopathological analysis was performed; the vascular area, glandular lumen area, the number of damaged cells, and the depth of the erosion were also quantified to obtain a scale to propose a tissue lesion index (TLI). Results. Under ischemic conditions, histopathological analysis showed edema and necrosis in epithelial cells, and vascular congestion. In I/R (30 and 60 min) conditions, areas of epithelial erosion were generated. Damage was classified based on the TLI. A TLI threshold of 3 showed a predictive value of tissue lesion. Conclusion. The proposed gastric lesion index allows us to objectively quantify and classify damage to the gastric mucosa produced by I/R.
- PublicationOpen AccessIdentification of protein kinase C α- and tyrosine hydroxylase-immunoreactive cells in the microbat retina(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Park, Eun Bee; Jeon, Joo Yeong; Jeon, Chang JinA growing number of studies have revealed the functional neuroarchitecture of the microbat retina and suggested that microbats can see using their eyes. To better understand the organization of the microbat retina, quantitative analysis of protein kinase C alpha (PKCα)- and tyrosine hydroxylase (TH)-immunoreactive (IR) cells was conducted on the greater horseshoe bat (Rhinolophus ferrumequinum) retina. As a result, PKCα immunoreactivity was observed in rod bipolar cells, consistent with previous studies on other mammalian retinas. PKCα-IR cell distribution in the inner nuclear layer showed regional differences in density, with the highest density found in the nasal retina. The average density of PKCα-IR cells was 10,487±441 cells/mm2 (mean ± SD; n=4), with a total of 43,077±1,843 cells/retina. TH-IR cells in the Rhinolophus ferrumequinum retina could be classified into four types based on soma location and ramification in the inner plexiform layer: conventional amacrine, displaced amacrine, interplexiform, and intercalated cells. The majority of TH-IR cells were conventional amacrine cells. TH-IR cells were nonrandomly distributed at low density over the retina. The average density was 29.7±3.1 cells/mm2 (mean ± SD; n=3), with a total of 124.0±11.3 cells/retina. TH-IR processes showed varicosities and formed ring-like structures encircling AII amacrine cells. Our study provides the foundation for understanding the neurochemical architecture of the microbat retina and supports the notion that the eyes do play a role in the visual system of microbats.