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Coactosin-like protein 1 (Cotl1), a member of the actin-depolymerizing factor (ADF)/cofilin family, was first purified from a soluble fraction of Dictyostelium discoideum cells. Neuronal migration requires cytoskeletal remodeling and actin regulation. Although Cotl1 strongly binds to F-actin, the role of Cotl1 in neuronal migration remains undescribed. In this study, we revealed that Cotl1 overexpression impaired migration of both early- and late-born neurons during mouse corticogenesis. Moreover, Cotl1 overexpression delayed, rather than blocked, neuronal migration in late-born neurons. Cotl1 expression disturbed the morphology of migrating neurons, lengthening the leading processes. This study is the first to investigate the function of Cotl1, and the results indicate that Cotl1 is involved in the regulation of neuronal migration and morphogenesis.
Subject(s)
Animals , Humans , Mice , Actins , Dictyostelium , Morphogenesis , NeuronsABSTRACT
Stem cell research has become a frontier in the field of life sciences, and provides an ideal model for exploring developmental biology problems such as embryogenesis, histiocytosis, and gene expression regulation, as well as opens up new doors for clinical tissue defective and inheritance diseases. Among them, menstrual blood-derived stem cells (MenSCs) are characterized by wide source, multi-directional differentiation potential, low immune rejection characteristics. Thus, MenSCs can achieve individual treatment and have the most advantage of the clinical application. The central nervous system, including brain and spinal cord, is susceptible to injury. And lethality and morbidity of them tops the list of all types of trauma. Compared to peripheral nervous system, recovery of central nervous system after damage remains extremely hard. However, the treatment of stem cells, especially MenSCs, is expected to solve this problem. Therefore, biological characteristics of MenSCs and their treatment in the respect of central nervous system diseases have been reviewed at home and abroad in recent years, so as to provide reference for the treatment of central nervous system diseases.
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Objective:To investigate the influence of acrylamide ( ACR) on adult neurogenesis and expression of GSK 3βin mouse.Methods:Method Adult male Kunming mice were used and divided into two groups:control group and experimental poisoning groups,that were exposured to acrylamide by intraperitoneal injection.Brdu labeling and immunohistochemistry were used to investigate the proliferation of adult neural stem cells in the subgranular zone ( SGZ).BrdU/NeuN/GFAP triple labeling to investigate the survival and differentiation of newly generated cells.Detecting GSK3βexpression and distribution in Neuro-2a cells,the expression of GSK3βwas examined by using Western blot.Results:Compared with control mice ,lower number of BrdU-positive cells and less differentiated into neurons in ACR mice.Less neural stem cells survived ,but more glia cells were generated in the subgranular zone of acrylamide mice.Moreover,higher phosphorylated GSK 3β( Ser9 ) were detected in Neuro-2a cells and mouse dentate gyrus in ACR mice respectively .Conclusion:These results suggested that acrylamide inhibits neural stem cells proliferation and influences the survival and differentiation of newly generated cells.Acrylamide inhibits neurogenesis maybe through GSK 3βsignaling pathway.
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Molecular mechanisms underlying the effects of Fyn on cell morphology, pseudopodium movement, and cell migration were investigated. The Fyn gene was subcloned into pEGFP-N1 to produce pEGFP-N1-Fyn. Chinese hamster ovary (CHO) cells were transfected with pEGFP-N1-Fyn. The expression of Fyn mRNA and proteins was monitored by reverse transcription-PCR and Western blotting. Additionally, transfected cells were stained with 4',6-diamidino-2-phenylindole and a series of time-lapse images was taken. Sequences of the recombinant plasmids pMD18-T-Fyn and pEGFP-N1-Fyn were confirmed by sequence identification using National Center for Biotechnology Information in USA, and Fyn expression was detected by RT-PCR and Western blotting. The morphology of CHO cells transfected with the recombinant vector was significantly altered. Fyn expression induced filopodia and lamellipodia formation. Based on these results, we concluded that overexpression of mouse Fyn induces the formation of filopodia and lamellipodia in CHO cells, and promotes cell movement.
Subject(s)
Animals , Cricetinae , Mice , Blotting, Western , CHO Cells , Cricetulus , Genetic Vectors , Green Fluorescent Proteins/genetics , Proto-Oncogene Proteins c-fyn/genetics , Pseudopodia/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Time-Lapse Imaging , TransfectionABSTRACT
Objective In order to investigate the influence of reelin deficiency on the hippocampal development, the histochemical characteristics of hippocampal pyramidal cells and granule cells of reeler mice were analyzed, therefore, reelin's function would be better understood with more morphological evidences. Methods With immunofluorescent double labeling, the pyramidal cells, granule cells and mossy cells in hippocampi between wild type and reeler mice were labeled. Results The development and lamination of hippocampal cortical plate were in disorder. Pyramidal cells and granule cells dispersed, and moreover, granule cells proliferated rapidly and migrated into hilus, so that the bound between granule layer and hilus disappeared. Conclusion As a stop signal and regulatory signal, reelin plays important roles in neuronal migration of developing cortical plate, especially in the regulation of granule cell proliferation.
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Objective In order to make a epileptic model in organotypic slice culture and to further investigate the epileptic pathology. Methods Immunohistochemistry, Fluoro-Jade B staining and BrdU labeling were carried out in the hippocampal slices with domoic acid treatment after 7 days of culture.Results Domoic acid could induce a series of pathological changes, such as, dispersion of granule cells(0.105±0.063) mm vs (0.057±0.012) mm, t = 4.8, P<0.01), neurogenesis in granular layer and cell loss of pyramidal cell and Mossy cell as well. Conclusions In hippocampal organotypic slices, domoic acid induced such pathological changes as human temporal lobe epilepsy and epileptic animal model. It is an ideal epileptic model for pathological, pharmacological and electronic physiological studies with great applicable prospect.