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ABSTRACT. The immediate early gene exhibits activation markers in the nervous system consisting of ARC, EGR-1, and c-Fos and is related to synaptic plasticity, especially in the hippocampus. Immediate early gene expression is affected by physical exercise, which induces direct ARC, EGR-1, and c-Fos expression. Objective: To assess the impact of exercise, we conducted a literature study to determine the expression levels of immediate early genes (ARC, c-Fos, and EGR-1). Methods: The databases accessed for online literature included PubMed-Medline, Scopus, and ScienceDirect. The original English articles were selected using the following keywords in the title: (Exercise OR physical activity) AND (c-Fos) AND (Hippocampus), (Exercise OR physical activity) AND (ARC) AND (Hippocampus), (Exercise OR physical activity) AND (EGR-1 OR zif268) AND (Hippocampus). Results: Physical exercise can affect the expression of EGR-1, c-Fos, and ARC in the hippocampus, an important part of the brain involved in learning and memory. High-intensity physical exercise can increase c-Fos expression, indicating neural activation. Furthermore, the expression of the ARC gene also increases due to physical exercise. ARC is a gene that plays a role in synaptic plasticity and regulation of learning and memory, changes in synaptic structure and increased synaptic connections, while EGR-1 also plays a role in synaptic plasticity, a genetic change that affects learning and memory. Overall, exercise or regular physical exercise can increase the expression of ARC, c-Fos, and EGR-1 in the hippocampus. This reflects the changes in neuroplasticity and synaptic plasticity that occur in response to physical activity. These changes can improve cognitive function, learning, and memory. Conclusion: c-Fos, EGR-1, and ARC expression increases in hippocampal neurons after exercise, enhancing synaptic plasticity and neurogenesis associated with learning and memory.
RESUMO. O gene precoce imediato (GPI) exibe marcadores de ativação no sistema nervoso constituídos por ARC, EGR-1 e c-Fos e está relacionado à plasticidade sináptica, especialmente no hipocampo. A expressão do GPI é afetada pelo exercício físico, que induz a expressão direta de ARC, EGR-1 e c-Fos. Objetivo: Para avaliar o impacto do exercício físico, realizamos um estudo de literatura para determinar os níveis de expressão dos GPIs (ARC, c-Fos e EGR-1). Métodos: A base de dados utiliza literatura on-line, PubMed-Medline, Scopus e ScienceDirect. O artigo original em inglês usa as seguintes palavras-chave em seu título: (Exercise) AND (c-Fos) AND (Hippocampus), (Exercise) AND (ARC) AND (Hippocampus), (Exercise) AND (EGR-1) AND (Hippocampus). Resultados: O exercício físico pode afetar a expressão de EGR-1, c-fos e ARC no hipocampo, uma parte importante do cérebro envolvida na aprendizagem e na memória. O exercício físico aumenta a expressão do gene c-Fos; sua alta intensidade pode aumentar a expressão de c-Fos, indicando ativação neural. Além disso, a expressão do gene ARC aumentou devido ao exercício físico, onde ARC é um gene que desempenha um papel na plasticidade sináptica e na regulação da aprendizagem e da memória, nas mudanças na estrutura sináptica e no aumento das conexões sinápticas, enquanto o EGR-1 também desempenha um papel na plasticidade sináptica, uma mudança genética que afeta o aprendizado e a memória. De maneira geral, o exercício físico regular pode aumentar a expressão de ARC, c-fos e EGR-1 no hipocampo. Isso reflete as mudanças na neuroplasticidade e na plasticidade sináptica que ocorrem em resposta à atividade física. Essas mudanças podem melhorar a função cognitiva, o aprendizado e a memória. Conclusão: A expressão de c-Fos, EGR-1 e ARC aumenta após o exercício físico nos neurônios do hipocampo, para aumentar a plasticidade sináptica, a neurogênese associada ao aprendizado e à memória.
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Objective:To investigate the effects of c-fos antisence olioneucleotide on the intimal proliferation of autogrfted veins with antisence technology.Methods:The external jugule veins were grafted into common carotid arteries in 20 rabbits and were divided into test group and control group randomly.The anastomosis and transplanted vein were coated with c-fos antisence olioneucleotide glue gel in the test group,while the contral group were merely coated with glue gel.The autografted veins were removed and measured by means of pathology and immunohistochemistry two weeks later.Results:The results show that the thickness of the venous intima,the degree of the vascular stricture,the expression of PCNA and the numbers of vascular smooth muscle cell were decreased in test group.Conclusion:The results suggest the c-fos antisence olioneucleotide can inhibit the intimal proliferation of the autografted veins.It is a prospective and idea genetic prophylactic therapy to intimal hyperplasia.
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To elucidate the endocrine mechanism of human parturition, the expression of c-Jun and c-Fos mRNA were examined in relation to estrogen receptor (ER) and progesterone receptor (PR) in human myometrium. c-Jun mRNA was detected in all myometrial tissues (n=5) during labor but not before labor (n=5) and in oxytocin-resistant postterm pregnancy (n=3). c-Fos mRNA was detected in only one myometrial tissue from a woman in labor. The distribution and intensity of immunostaining for ER and PR were semiquantitatively scored. During the late pregnancies, no significant difference was seen in the receptor scores for myometrial ER and PR between the patients who experienced labor and those who did not. Receptor scores for ER and PR were significantly lower in postterm pregnancy than in late pregnancy, regardless of the labor status. These data suggest that there are no changes in ER and PR in human myometrium during parturition. On the other hand, postterm pregnancy is associated with low ER and PR. c-Jun, induced during labor without changes in ER and PR, may play a role as a signaling mechanism in human myometrium.
Subject(s)
Adult , Female , Humans , Pregnancy , Blotting, Northern , Genes, jun/genetics , Immunohistochemistry , Labor, Obstetric/metabolism , Myometrium/metabolism , Myometrium/cytology , RNA, Messenger/analysis , Receptors, Estrogen/metabolism , Receptors, Progesterone/metabolism , Reference ValuesABSTRACT
Objective To detect the c fos proto oncogene expression in the hypothalamus of the mice which underwent water immersion and the effects of propofol Methods Twenty four mice were divided randomly into three groups:group A (normal control), group B (water immersion) and group C (water immersion+propofol) The group C was subdivided into two sub groups: in group C1 3mg/kg propofol was administered intraperitoneally 10min after water immersion; in group C2 3mg/kg propofol was given intraperitoneally 10min before water immersion The cerebral c fos positive cells were detected by S P immunohistochemical assay and the gastric ulcer index was calculated using Guth method Results Animal in group A had no gastric mucosa injury The gastric ulcer index increased significantly (6 2?2 1) with the obvious bleeding points in gastric mucosa and the rate of c fos gene positive cell increased markedly (64 2%?2 1%) in group B as compared with those in group A The gastric ulcer index and c fos gene expression rate decreased greatly in group C1 (3 2?1 0, 21 8%?3 2%) and group C2 (2 1?0 9, 18 4%?3 5%) respectively (P
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AIM: To investigate the role of D1 and D3 dopamine receptor on MAPK signal transduction and c-fos gene expression after acute cocaine treatment. METHODS: Activations of extracellular signal-regulated kinase (ERK), the c-Jun N-terminal kinase (JNK), p38 activation and expression of c-fos in wild type and D1 and D3 receptor mutant mice after acute cocaine treatment were checked by Western blotting. RESULTS: ERK activation and c-fos induction was enhanced in D3 mutant mice and abolished in D1 mutant mice by acute cocaine treatment, while p38 and JNK activation was not obviously modulated by the D1 and D3 receptors by acute cocaine treatment. Meanwhile, c-fos induction was inhibited when SL327, a specific MEK inhibitor, was injected before cocaine treatment. CONCLUSION: D1 and D3 receptors play opposite roles in the regulation of ERK activation and c-fos gene expression after acute cocaine treatment. The expression of c-fos gene depends on ERK signal pathway after acute cocaine treatment.
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Objective Proliferation and apoptosis play a major role in the development of tumor cells,and the intranuclear transcriptional factor c-fos is significantly up-regulated in the primary hepatocellular carcinoma and involved in early carcinogenesis.The purpose of the present study is to investigate the apoptotic effect of c-fos antisense oligodeoxynucleotide(ASO) on human hepatocellular carcinoma HepG2 cells and the participation of Caspase3 in this process.Methods Cell culture,Hoechst 33258 staining,real-time PCR and Western blotting were used in present study.Cultured HepG2 cells were divided into 3 groups: 1) control group: cultured with 10?l saline;2) sense oligodeoxynucleotide(SO,used as a negative control) treated group: co-cultured with 10?l SO(5?g/?l);3) ASO treated group: co-cultured with ASO 10?l(5?g/?l).The subsequent experiments were performed 1h after cultivation for each group.Hoechst 33258 staining was performed to detect the apoptosis by observing the staining of nuclear chromatin.Real-time PCR and Western blotting were used respectively to detect the expression of Caspase 3 at mRNA and protein levels after different treatments.Results Hoechst 33258 staining revealed that the nuclei of HepG2 cells showed diffuse and adqulis fluorescence in control and SO-treated groups,while dense and dark fluorescence was observed in ASO-treated group,which indicated that c-fos ASO had significantly induced apoptosis of HepG2 cells.The expression of Caspase 3 in ASO group was enhanced both at mRNA and protein levels compared to that in control groups.Conclusions C-fos ASO significantly induces apoptosis in human hepatocellular carcinoma HepG2 cells,as shown by Hoechst 33258 staining and higher expression of Caspase 3 mRNA and protein.Moreover,Caspase 3 activation is involved and probably plays an important role in c-fos ASO-induced apoptosis of HepG2 cells.