OBJECTIVETo explore the mechanism of electroacupuncture at "Neiguan" (PC 6) improving acute myocardial ischemia.

METHODSThe rats were randomly divided into a sham operation group, a myocardial ischemia model group and a myocardial ischemia model plus electroacupuncture group. The acute myocardial ischemia model was developed byligation of the descending anterior branch of the coronary artery, and electroacupuncture was given at bilateral "Neiguan" (PC 6). Serum myocardial enzymes was determined by biochemical method and the expression of c-fos mRNA in myocardium was detected by using reverse transcription polymerase chain reaction (RT-PCR).

RESULTSThe activities of serum myocardial enzymes and the expression of c-fos mRNA in ischemic myocardium were significantly increased as compared with those in the sham operation group (P < 0.05), and after electroacupuncture they were significantly decreased (P < 0.05).

CONCLUSIONThe mechanism of electroacupuncture at "Neiguan" (PC 6) improving acute myochadial ischemia is possibly related with down-regulation of expression of c-fos mRNA in myocardium.

Acupuncture Points ; Animals ; Electroacupuncture ; Genes, fos ; Humans ; Myocardial Ischemia ; genetics ; Myocardium ; metabolism ; Rats

OBJECTIVETo investigate the effects of transforming growth factor beta (TGF ) on c-fos gene expression in hepatic stellate cells.

METHODSHepatic stellate cells (HSC-T6) were cultured in the medium containing different concentrations of TGF (0.2, 1, and 5 ng/ml), and cells were collected at different time points of incubation (8, 24, 48, and 72 h). The total RNA of the HSCs was isolated and c-fos gene expression level were measured by reverse transcription polymerase chain reaction.

RESULTSc-fos gene expression levels of HSCs cultured in the presence of low (0.2 ng/ml), moderate (1 ng/ml) and high (5 ng/ml) concentrations of TGF for 8, 24, 48 and 72 h were significantly greater than those of control group. The c-fos gene expression levels of HSCs increased gradually with the increment of TGF concentration, and significant differences in c-fos gene expression were found between the 3TGF groups.

CONCLUSIONTGF strongly up-regulates c-fos gene expression in hepatic stellate cells.

Animals ; Cells, Cultured ; Gene Expression ; drug effects ; Genes, fos ; Hepatic Stellate Cells ; drug effects ; Proto-Oncogene Proteins c-fos ; genetics ; metabolism ; Rats ; Transforming Growth Factor beta ; pharmacology

OBJECTIVETo investigate the expression sequence and distribution characteristics of the protooncogenes c-fos, c-myc and endogenous basic fibroblast growth factor (bFGF) genes in burned tissues, and to explore the possible effects of changes in these genes' functions on wound healing.

METHODSPartial-thickness burns of 30% TBSA were established on backs of Wistar rats. In situ hybridization and histological methods were used to detect expression of c-fos, c-myc and bFGF genes in normal and burned tissue at 3 h, 6 h, 1 d, 3 d, 7 d and 14 d postburn.

RESULTSAlthough expression of c-fos and c-myc genes and bFGF gene could be found in normal skin, the expression of all three were markedly induced by burn wounds and the expression models in sequence and distribution were quite different. Expression of c-fos gene increased and peaked at 6 h. Signals were mainly localized in both nuclei of dermal fibroblasts and monocytes. The expression of bFGF gene increased at 6 h and peaked at 1 d postburn, and was distributed in the cytoplasm of fibroblasts. C-myc gene peaked 3 d postburn and was also distributed in the cytoplasm of fibroblasts.

CONCLUSIONSThese results indicated that thermal injury could induce the expression of c-fos, c-myc and bFGF at gene level, showing phasic control and regional distribution. The phasic expression of these genes suggests that there is an interaction between protooncogenes and bFGF, which may play an important role in wound healing. The different expressions of c-fos and c-myc play an inducing role in regulating bFGF, and in turn affect wound healing.

Animals ; Burns ; metabolism ; Fibroblast Growth Factor 2 ; genetics ; Gene Expression Regulation ; Genes, fos ; Genes, myc ; In Situ Hybridization ; Male ; Rats ; Rats, Wistar ; Time Factors

OBJECTIVETo study the changes of the gene expression pattern of spinal cord tissues in the early stage after injury by DNA microarray (gene chip).

METHODSThe contusion model of rat spinal cord was established according to Allen's falling strike method and the gene expression patterns of normal and injured spinal cord tissues were studied by gene chip.

RESULTSThe expression of 45 genes was significantly changed in the early stage after spinal cord injury, in which 22 genes up-regulated and 23 genes down-regulated.

CONCLUSIONSThe expression of some genes changes significantly in the early stage after spinal cord injury, which indicates the complexity of secondary spinal cord injury.

Animals ; Down-Regulation ; Female ; Gene Expression ; Genes, fos ; genetics ; Male ; Oligonucleotide Array Sequence Analysis ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries ; genetics ; Up-Regulation

OBJECTIVETo investigate the changes of proto-oncogene c-fos, c-jun mRNA expression in angiotensin II (Ang II)-induced hypertrophy and effects of tanshinone II A (Tan) in the primary culture of neonatal rat cardiomyocytes.

METHODTwelve neonatal Wistar rats aged one day old of clean grade and both sexes were selected to isolate and culture cardiomyocytes. The cardiomyocytes were divided into: normal control group, Ang II (10(-6) mol x L(-1)) group, Ang II (10(-6) mol x L(-1)) +Tan (10(-8) g x L(-1)) group, Ang II (10(-6) mol x L(-1)) + valsartan (10(-6) mol x L(-1)) group, Tan (10(-8) g x L(-1)) group, valsartan (10(-6) mol x L(-1)) group. The cardiomyocyte size was determined by phase contrast microscope, the rate of protein synthesis in cardiomyocytes was measured by 3H-leucine incorporation. The c-fos, c-jun mRNA expression of cardiomyocytes were assessed using reverse transcription polymerase chain reaction (RT-PCR).

RESULTAng II was added to the culture medium and 30 min later, the c-fos, c-jun mRNA expression of cardiomyocytes increased significantly (P < 0. 01). After Ang II took effect for 24 h, the rate of protein synthesis in Ang II group increased more prominently than that in normal control group (P < 0.01). After Ang II took effect for 7 days, the size of cardiomyocyte in Ang II group increased obviously (P < 0. 05). If tanshinone II or valsartan was added to the culture medium before Ang II, both of them could inhibit the increase of c-fos, c-jun mRNA expression (P < 0.01), cardiomyocyte protein synthesis rate (P < 0.01), and cardiomyocyte size (P < 0.05) induced by Ang II.

CONCLUSIONTanshinone II could ameliorate Ang II-induced cardiomyocytes hypertrophy by inhabiting c-fos, c-jun mRNA expression.

Angiotensin II ; biosynthesis ; pharmacology ; Animals ; Cardiomegaly ; chemically induced ; metabolism ; pathology ; Diterpenes, Abietane ; Gene Expression Regulation ; drug effects ; Genes, fos ; genetics ; Genes, jun ; genetics ; Myocytes, Cardiac ; drug effects ; metabolism ; pathology ; Phenanthrenes ; pharmacology ; Proto-Oncogene Proteins c-fos ; genetics ; Proto-Oncogene Proteins c-jun ; genetics ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Tetrazoles ; pharmacology ; Valine ; analogs & derivatives ; pharmacology ; Valsartan

The expression of the p53 protein (p53) was compared with those of several oncogenes including c-fos (Fos), c-jun (Jun), and epidermal growth factor receptor (EGFR1) using immunohistochemistry in frozen and paraffin-embedded sections of 25 basal cell carcinomas (BCCs) to find out any correlation between p53 and oncogenes in the pathogenesis of human BCC. In normal skin, positive reactions were obtained for EGFR1 and Fos, while p53 and Jun were negative in all cases. In the lesions, EGFR1 was observed in all cases and p53 was positive in 9 of 25 (36%). Fos was expressed in 21 of 25 (84%) and four negative cases were all p53-positive; this negative correlation between p53 and Fos staining was statistically significant (P< 0.01). Jun was detected in 14 of 20 (70%) and no significant relationship was observed between the expression of Jun and Fos or p53. These data suggest the possibility of down regulation of Fos expression by high levels of p53 protein. Further work is necessary to determine the mechanism of this interaction.
Aged ; Carcinoma, Basal Cell/chemistry/*genetics ; Comparative Study ; Female ; Gene Expression ; Genes, fos ; Genes, jun ; Genes, p53 ; Human ; Immunohistochemistry ; Male ; Middle Age ; Oncogene Protein p65(gag-jun)/analysis ; Oncogene Proteins v-fos/analysis ; *Oncogenes ; Protein p53/analysis ; Receptor, Epidermal Growth Factor/analysis ; Skin Neoplasms/chemistry/*genetics

We investigated the expression of the growth-related nuclear proto-oncogenes, c-fos and c-myc, in early preneoplastic regions and tumor nodules of 3'-MeDAB induced rat hepatocarcinoma. To amplify the levels of these transcripts, we gave cycloheximide (100 mg/kg B.W. i.p.) to each group of rats. The elevated levels of the 2.2 kb c-fos and 2.4 kb c-myc transcripts appeared as early as the 2nd week after feeding on the 3'-MeDAB diet and lasted through the 4th; 6th weeks and tumor. Southern blot analysis indicated that gross amplification or rearrangements were not observed in DNA of the preneoplastic livers and hepatoma nodules. We also measured the rate of the incorporation of [3H] thymidine into hepatic DNA in order to monitor the rate of cell proliferation occurring at the early preneoplastic periods. We have found that the rate of [3H] thymidine incorporation corresponds to the elevated levels of c-fos and c-myc transcripts in the precancerous stages. This finding suggests that the elevated expressions of c-fos and c-myc may result from the continuous cell proliferative stimuli generated in the carcinogen altered cells, which is essential to the initiation and promotion of chemical hepatocarcinogenesis.
Animal ; Blotting, Southern ; DNA/biosynthesis ; Female ; *Gene Expression ; *Genes, fos ; *Genes, myc ; Liver Neoplasms, Experimental/chemically induced/*genetics ; Methyldimethylaminoazobenzene/*toxicity ; Precancerous Conditions/chemically induced/*genetics ; Rats ; Rats, Sprague-Dawley ; Support, Non-U.S. Gov't

OBJECTIVEIt was reported previously that genistein could inhibit proliferation of human ovarian carcinoma cell line SKOV(3), but mechanism was not clear. There is a close relationship between EGFR mediated signal transduction pathway and the development of ovarian tumor. This study aimed to investigate the effects of genistein on the EGFR mediated signal transduction pathway and to clarify its mechanisms of proliferation inhibition on human ovarian carcinoma cell line SKOV(3) and its xenograft in nude mice.

METHODSThe expression of c-erbB-2 protein was determined using immunocytochemistry. The expressions of c-jun and c-fos protein were determined using Western blotting. The expression of c-erbB-2, c-raf-1, c-jun and c-fos mRNA were tested by reverse transcription-polymerase chain reaction (RT-PCR).

RESULTSThe expression of c-erbB-2, c-raf-1 and its downstream gene c-jun and c-fos were decreased at mRNA level in the 20 micromol/L genistein group. The expression of c-erbB-2 protein were decreased, its average absorbency (A) were decreased after treatment of SKOV(3) with 20 micromol/L genistein for 48 h, reached at 0.42 +/- 0.02 (P < 0.05). Western blotting demonstrated that the expressions of c-jun and c-fos protein were decreased gradually after being treated with 20 micromol/L genistein for 12 - 72 h.

CONCLUSIONSGenistein could down-regulate the expression of two key genes, c-erbB-2 and c-raf-1 at mRNA and protein level in the EGFR mediated signal transduction pathway, and down-regulate the expression of its downstream nuclear transcription factors c-jun and c-fos at mRNA and protein level. It is suggested that interfering the expressions of some key signal molecules in EGFR mediated signal transduction system by genistein may account for its molecular foundation of proliferation inhibition in ovarian carcinoma.

Animals ; Antineoplastic Agents ; pharmacology ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; Genes, fos ; Genes, jun ; Genistein ; pharmacology ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Ovarian Neoplasms ; metabolism ; pathology ; Proto-Oncogene Proteins c-fos ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-jun ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-raf ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Receptor, Epidermal Growth Factor ; metabolism ; Receptor, ErbB-2 ; biosynthesis ; genetics ; Signal Transduction ; drug effects

OBJECTIVETo study the effects of extremely low frequency electromagnetic fields (ELF EMFs) on c-fos gene expression in mouse brain and liver tissues.

METHODSMice were exposed to 50 Hz sinusoidal 0.2 mT or 6.0 mT electromagnetic field for 2 weeks or 4 weeks. Competitive RT-PCR method was used to measure c-fos mRNA level.

RESULTSAfter exposure to 0.2 mT or 6.0 mT field for 2 weeks, c-fos mRNA levels in brain tissue [(0.0178 +/- 0.0076) amol/120 ng cDNA and (0.0092 +/- 0.0042) amol/120 ng cDNA respectively] were higher than that of control level [(0.0012 +/- 0.0005) amol/120 ng cDNA] (P < 0.05). In liver tissue c-fos mRNA levels [(0.0117 +/- 0.0055) amol/120 ng cDNA and (0.0148 +/- 0.0162) amol/120 ng cDNA respectively] were also higher than that of control level [(0.0005 +/- 0.0005) amol/120 ng cDNA] (P < 0.05). After exposure to 0.2 mT or 6.0 mT field for 4 weeks, c-fos mRNA levels in brain tissue [(0.0100 +/- 0.0054) amol/120 ng cDNA and (0.0198 +/- 0.0079) amol/120 ng cDNA respectively] were higher than that of control level [(0.0015 +/- 0.0008) amol/120 ng cDNA] (P < 0.05). In liver tissue the exposure induced much higher expression level [(0.0173 +/- 0.0122) amol/120 ng cDNA and (0.0133 +/- 0.0090) amol/120 ng cDNA respectively] while no expression was found in the control.

CONCLUSIONExposure to 50 Hz electromagnetic fields may induce up-regulation of c-fos transcription in mouse brain and liver tissue.

Animals ; Brain ; metabolism ; radiation effects ; Dose-Response Relationship, Radiation ; Electromagnetic Fields ; Gene Expression Regulation ; radiation effects ; Genes, fos ; genetics ; Liver ; metabolism ; radiation effects ; Male ; Mice ; RNA, Messenger ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors

OBJECTIVETo study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes.

METHODSSodium selenite at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis (or comet assay). Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP nick end labelling) and flow cytometry. C-myc, c-fos, and c-jun expression in rat hepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method.

RESULTSAt the doses of 5, 10, and 20 micromol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite (r=0.9501, P<0.01). Sodium selenite at the doses of 5, 10, and 20 micromol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates (%) of selenium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (3.72 +/- 1.76), (5.82 +/- 1.42), and (11.76 +/- 1.87) respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite (r=0.9897, P<0.01), these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P<0.01.

CONCLUSIONSelenium at 5-20 micromol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.

Animals ; Apoptosis ; drug effects ; Blotting, Northern ; Comet Assay ; DNA Damage ; Dose-Response Relationship, Drug ; Genes, fos ; drug effects ; genetics ; Genes, jun ; drug effects ; genetics ; Genes, myc ; drug effects ; genetics ; Hepatocytes ; drug effects ; pathology ; Male ; Nucleic Acid Hybridization ; Rats ; Rats, Sprague-Dawley ; Selenium ; pharmacology ; Sodium Selenite ; pharmacology