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41.
Akira Hirata Masaru Inatani Yasuya Inomata Naoko Yonemura Takahiro Kawaji Megumi Honjo Hidenobu Tanihara 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》2008,246(1):51-59
Purpose Transient retinal ischemia induces the death of retinal neuronal cells. Postischemic damage is associated with the infiltration
of leukocytes into the neural tissue through vascular endothelia. The current study aimed to investigate whether this damage
was attenuated by the inhibition of Rho/ROCK (Rho kinases) signaling, recently shown to play a critical role in the transendothelial
migration of leukocytes.
Methods Y-27632, a selective inhibitor of ROCK, was injected intravitreally into rat eyes with transient retinal ischemia. Cell loss
of the ganglion cell layer (GCL) and thinning of the inner plexiform layer (IPL) with and without the administration of Y-27632
were evaluated by histological anaysis, TUNEL assay and retrograde labeling of retinal ganglion cells (RGCs). To examine the
attenuation of leukocyte infiltration in postischemic retinas with the administration of Y-27632, silver nitrate staining
and immunohistochemistry using an anti-LCA antibody were performed.
Results Cell loss of the GCL and thinning of the IPL were significantly attenuated when 100 nmol Y-27632 was administered within three
hours of the induction of ischemia. TUNEL assay and retrograde labeling of RGCs showed a decreased number of apoptotic cells
and an increased number of RGCs in Y-27632-injected retinas. Moreover, silver nitrate staining and immunohistochemical analysis
using an anti-LCA antibody showed that Y-27632 injection dramatically inhibited leukocyte infiltration and endothelial disarrangement.
Conclusions Our data suggest that inhibition of Rho/ROCK signaling offers neuroprotective therapy against postischemic neural damage,
by regulating leukocyte infiltration in the neural tissue. 相似文献
42.
43.
SC1 is an extracellular matrix glycoprotein that is related to the multifunctional protein SPARC. These matricellular members play regulatory roles in modulating cellular interactions. SC1 expression is enriched in the central nervous system during embryonic and postnatal development as well as in the adult brain. In the rat cerebellum, SC1 is expressed at high levels in Bergmann glial cells and their radial fibers which project into the synaptic-rich molecular layer. At specific stages of development and in the adult, SC1 mRNA is selectively transported into cellular processes of these cells. In the present study, we have examined the effect of whole-body hyperthermia on the transport of SC1 mRNA in Bergmann glial cells of the rat cerebellum. Our results show that SC1 mRNA transport is diminished at 10 and 15 h post-hyperthermia, but returns to control levels by 24 h after heat shock. One of the characteristics of a heat shock on cells grown in tissue culture is a collapse of the cytoskeletal network. Intact components of the cytoskeleton are necessary for the transport of mRNA into peripheral processes of cells. However, in vivo hyperthermia does not appear to affect the morphology of the intermediate filament proteins GFAP, vimentin, or the beta-tubulin component of microtubules in Bergmann glial cell processes. During the hyperthermic time course, levels of vimentin protein increase, which is reflected by immunoreactivity of activated astrocytes and microvasculature in cerebellar white matter. 相似文献
44.
Induction of peripherin expression in subsets of brain neurons after lesion injury or cerebral ischemia 总被引:6,自引:0,他引:6
Peripherin is a type III intermediate filament predominantly expressed in neurons having direct axonal projections toward peripheral structures. Here, we report that brain injuries can trigger expression of peripherin and the formation of peripherin accumulations in neurons that are normally silent for this gene. Stab lesions made with nitrocellulose implants induced within 4 days the formation of peripherin accumulations, devoid of neurofilament proteins, in thalamic neurites at the site of the lesion. The local administration of interleukin-6 or leukemia inhibitory factor at the site of the stab lesion extended the expression pattern of peripherin to other neuronal subsets in areas of the cortex and/or of the hippocampus adjacent to injury. We also show that transient focal ischemia in mice, a model of stroke, can trigger within 72 h the formation of neuronal peripherin accumulations in neurons of the cortex, thalamus and hippocampus. This new type of potentially noxious intermediate filament protein accumulations, composed of peripherin, may be of relevance to many brain degenerative disorders with occurrence of proinflammatory cytokines. 相似文献
45.
组织工程化神经研究进展 总被引:1,自引:0,他引:1
近年来,组织工程化周围神经研制工作取得了很大的进展。自体神经、同种异体神经和合成材料均可作为桥接神经缺损的神经导管,以化学萃取的同种异体神经及可降解的生物材料导管较为理想。同时,经培养和纯化后的雪旺细胞具有分泌多种神经营养因子活性,是提高修复神经损伤效果的关键。 相似文献
46.
Katia Sabrina Paludo Luiza Helena Gremski Silvio Sanches Veiga Olga Meiri Chaim Waldemiro Gremski Dorly de Freitas Buchi Helena Bonciani Nader Carl Peter Dietrich Clia Regina Cavichiolo Franco 《Toxicon》2006,47(8):844-853
Spiders of the Loxosceles genus have been responsible for severe clinical cases of envenomation worldwide. Accidents involving brown spiders can cause dermonecrotic injury, hemorrhage, hemolysis, platelet aggregation and renal failure. Histological findings of animals treated by venom have shown subendothelial blebs, vacuoles and endothelial cell membrane degeneration of blood vessel walls, as well as fibrin and thrombus formation. The mechanisms by which the venom causes these disorders are poorly understood. In this work, with an endothelial cell line derived from rabbit aorta, we were able to demonstrate that venom binds to the cell surface and the extracellular matrix. Moreover, we observed that the venom also induced morphological alterations, such as cell retraction, homophilic disadhesion and an increasing in filopodia projections. We also demonstrated that toxins present in the venom disorganized focal adhesion points and actin microfilaments of endothelial cells. Nevertheless, endothelial cell viability showed no alterations compared to controls. Additionally, venom treatment changed the fibronectin matrix profile synthesized by these cells as well as cell adhesion to fibronectin. These results suggest that the deleterious effects of venom on blood vessel walls could be a consequence of the direct effect on the endothelial cell surface and adhesive structures involved in blood vessel stability. These effects indirectly lead to leukocyte and platelet activation, disseminated intravascular coagulation and an increase in vessel permeability. 相似文献
47.
Neurofilaments assume a less random architecture at nodes and in other regions of axonal compression
Neurofilament distributions were mathematically characterized in four chicken somatic motor axons at each of four histologically distinct regions: compact myelinated regions, compact myelinated regions associated with Schwann cell nuclei, Schmidt-Lanterman clefts, and nodes of Ranvier. Compact myelinated regions had the largest cross-sectional areas, the lowest neurofilament densities, and the most random neurofilament organizations — nodes of Ranvier had the smallest cross-sectional areas, the highest neurofilament densities, and the most ordered architectures. In these myelinated axons, the closest natural neurofilament spacing was 25 nm. Mathematical analyses of serial sections suggested that neurofilament interactions are sufficiently weak and transient to permit a full range of variation from random to ordered cytoskeletal architectures as the neurofilaments move longitudinally through the few micron span of the paranodal-nodal region of a single axon. 相似文献
48.
Dolfini E Roncoroni L Elli L Fumagalli C Colombo R Ramponi S Forlani F Bardella MT 《World journal of gastroenterology : WJG》2005,11(48):7597-7601
AIM: To evaluate the interplay between gliadin and LoVo cells and the direct effect of gliadin on cytoskeletal patterns. METHODS: We treated LoVo multicellular spheroids with digested bread wheat gliadin in order to investigate their morphology and ultrastructure (by means of light microscopy and scanning electron microscopy), and the effect of gliadin on actin (phalloidin fluorescence) and the tight-junction protein occludin and zonula occluden-1. RESULTS: The treated spheroids had deep holes and surface blebs, whereas the controls were smoothly surfaced ovoids. The incubation of LoVo spheroids with gliadin decreased the number of intracellular actin filaments, impaired and disassembled the integrity of the tight-junction system. CONCLUSION: Our data obtained from an "in vivo-like" polarized culture system confirm the direct noxious effect of gliadin on the cytoskeleton and tight junctions of epithelial cells. Unlike two-dimensional cell culture systems, the use of multicellular spheroids seems to provide a suitable model for studying cell-cell interactions. 相似文献
49.
50.
Parkinson's disease is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra and a marked reduction of dopamine (DA) levels in the striatum. Binding to its specific receptors, DA switches on a complex program of intracellular signaling that regulates gene expression. We evaluated the changes in striatal gene expression in a mouse model of Parkinson's disease, using differential display analysis. The mRNA for the cytoskeleton family proteins, radixin, cofilin and centractin/ARP-1, was abnormally expressed in the striatum of these MPTP-treated mice. Moreover, we also found that radixin mRNA and its protein levels are under DA control through specific D1-dopaminergic receptors in a dose- and time-dependent manner in the GT1-7 neural cell line. These findings suggest a role for DA for regulation of cytoskeletal proteins involved in the integrity and function of synapsis. 相似文献