Previous studies have indicated that paracrine factors (conditioned medium) increase wound closure and reduce reactive oxygen species in a traumatic brain injury in vitro model. Although the beneficial effects of conditioned medium from human adipose tissue-derived mesenchymal stem cells (hMSCA-CM) have been previously suggested for various neurological diseases, their actions on astrocytic cells are not well understood. In this study, we have explored the effect of hMSCA-CM on human astrocyte model (T98G cells) subjected to scratch assay. Our results indicated that hMSCA-CM improved cell viability, reduced nuclear fragmentation, attenuated the production of reactive oxygen species, and preserved mitochondrial membrane potential and ultrastructural parameters. In addition, hMSCA-CM upregulated neuroglobin in T98G cells and the genetic silencing of this protein prevented the protective action of hMSCA-CM on damaged cells, suggesting that neuroglobin is mediating, at least in part, the protective effect of hMSCA-CM. Overall, this evidence suggests that the use of hMSCA-CM is a promising therapeutic strategy for the protection of astrocytic cells in central nervous system (CNS) pathologies.
Platelet-derived growth factor, subtype BB (PDGF-BB) is a mitogenic growth factor produced in different cell types such as platelets, fibroblasts, neurons, and astrocytes. Previous reports have shown that different PDGF isoforms exert a neuroprotective effect in neurons and astrocytes against multiple degenerative insults. Previously, we showed that pretreatment with PDGF-BB for 24 h increased cell viability, preserved nuclear morphology and mitochondrial membrane potential following stimulation with rotenone, and reduced free radical production nearly to control conditions. In the present study, we explored the potential mechanisms associated with PDGF-BB protection against oxidative damage. Our results showed that PDGF-BB protected astrocytic cells through multiple responses, including decrease in the expression of cytoskeleton proteins, attenuated free radicals (reactive oxygen species (ROS)) production, preservation of mitochondrial ultrastructure, and improved expression of neuroglobin (Ngb1). In summary, these findings point out that PDGF-BB protects astrocytic cells by a reduction in ROS production and activation of antioxidant mechanisms.
Background Foods prone to deteriorate renal function are rich in fat and in phosphorus (P), but the interaction between these two factors is not well studied. Method Detailed structural and ultrastructural histopathological studies were performed on the kidneys of rats fed different amounts of fat and P: low (4%) fat (LF) and normal (0.6%) P (NP), LF and high (1.2%) P (HP), high (35%) fat (HF) and NP, HF and HP, and HF with low (0.2%) P (LP) for 28 weeks. Results Glomeruli of the HF groups showed segmental areas of retraction, sclerosis and thickening of the Bowman’s capsule and basal membranes, which were more accentuated in the HF–HP group. Ultrastructural lesions in the glomeruli also were prominent in rats fed HF, particularly in the HF–HP group, and included thickening of the capillary membrane, endothelial damage, mesangial matrix hypercellularity and podocyte effacement. P restriction reduced the severity of endothelial damage, mesangial matrix hypercellularity, thickening of capillary basement membrane and podocyte effacement. The kidneys of rats fed HP showed significant tubular atrophy and dilatation, focal tubular hyperplasia, thickening of the tubular basal membrane, interstitial edema, inflammation and calcification. All groups fed HF also showed tubular lesions that were more prominent in the HF–HP group. P restriction had a beneficial effect on inflammation and calcification. Conclusions Intake of both HF and HP damages the kidneys and their noxious effects are additive. HF intake was preferentially associated with glomerular lesions, while lesions related to HP intake were located mainly in the tubuli and in the interstitium.
The role of the P. multocida lipopolysaccharide (LPS) as a putative adhesin during the early stages of infection with this bacterium in the respiratory epithelium of rabbits was investigated. By light microscopy and double enzyme labeling of nasal septa tissues, the amount of bacteria attached to the respiratory epithelium and the amount of LPS present in goblet cells at different experimental times were estimated. Transmission electron microscopy (TEM) and LPS labeling with colloidal gold particles were also used to determine the exact location of LPS in the cells. Septa that were challenged with LPS of P. multocida and 30 minutes later with P. multocida showed more adherent bacteria and more severe lesions than the other treatments. Free LPS was observed in the lumen of the nasal septum, forming bilamellar structures and adhering to the cilia, microvilli, cytoplasmic membrane, and cytoplasm of epithelial ciliated and goblet cells. The above findings suggest that P. multocida LPS plays an important role in the process of bacterial adhesion and that it has the ability of being internalized into host cells.
An ultrastructural comparison between the nasal cavities of healthy rabbits and those suffering from two forms of spontaneous infection with Pasteurella multocida was undertaken. Twelve commercially produced rabbits of different ages and respiratory health status were divided into four groups: healthy from 0 to 21 days (G1, n = 2); healthy from 23 to 49 days (G2, n = 2); healthy from 51 to 69 days (G3, n = 2); diseased rabbits with septicemia and the rhinitic form of P. multocida infection (G4, n = 3). The main ultrastructural changes observed were a widening of the interepithelial spaces, increased activity and number of goblet cells, the formation of two types of vacuoles in epithelial cells, the degranulation and migration of heterophils between the epithelial cells, and the association of this migration with some of the other changes. No bacteria were observed adhering to the epithelium, and very few were observed free in the mucus. Scant inter-epithelial spaces were found in healthy rabbits, but they were not as large and numerous as those found in diseased animals. We discuss the origin and meaning of these changes but, we focus on the significance of the inter-epithelial spaces and goblet cells for the defense of the upper respiratory airways against the bacterium and its lipopolysaccharide.
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