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PubMed1996

Involvement of adenosine and glutamate receptors in the induction of c-fos in the striatum by haloperidol.

The psychostimulant drugs amphetamine and cocaine induce the expression of immediate early genes, such as c-fos, in the striatum via D1 dopamine receptor activation. This occurs primarily in the striato-nigral neurons. Conversely, neuroleptic drugs, such as haloperidol, which block D2-type dopamine receptors, induce c-fos expression in striatal neurons projecting to the globus pallidus. In order to gain insight into the neurochemical substrates of neuroleptic-induced c-fos expression, we examined the effects of adenosine A2 and N-methyl-D-aspartate (NMDA) receptor antagonists as well as inhibition of nitric oxide synthase, on haloperidol-induced Fos immunoreactivity in the striatum. While blockade of D1 receptors had no effect on haloperidol-induced Fos expression, adenosine A2 receptor antagonists decreased the number of neurons in the striatum expressing haloperidol-induced Fos by half. NMDA receptor antagonists also potently blocked the induction of Fos immunoreactivity by haloperidol, while inhibition of nitric oxide synthase activity had no effect. These results indicate that in the presence of a dopamine D2 antagonist, Fos expression in striato-pallidal neurons is mediated in part through activation of A2 receptors by adenosine, and via NMDA receptor activation by glutamate.

Animals↗
PubMed1998

Interaction between the serotonergic, dopaminergic, and glutamatergic systems in fenfluramine-induced Fos expression in striatal neurons.

Fenfluramine (FE) is a halogenated amphetamine derivative used in the treatment of obesity and thought to induce serotonin (5-HT) release from nerve terminals and to reduce re-uptake. However, other pathways may also be involved. In this work, the effects of FE on the major striatal afferent systems, and the possible interactions of these systems in FE-induced striatal expression of Fos, were studied by lesion of the serotonergic and/or dopaminergic system and administration of NMDA glutamate (MK-801) or D1 dopamine (SCH-23390) receptor antagonists. Both the D1 and NMDA receptor antagonists suppressed Fos expression in response to FE almost entirely. FE-induced Fos expression was also dramatically reduced 24 h after 6-hydroxydopamine (6-OHDA) lesion of the dopaminergic system. However, the reduction was not so marked after chronic 6-OHDA lesion, probably due to compensatory changes. Chronic (5,7-dihydroxytryptamine injection, 4 weeks before) or acute (p-chlorophenylalanine injection) lesion of the serotonergic system led to a marked reduction in Fos expression in response to FE (decrease of about 50%). After simultaneous chronic lesion of both serotonergic and dopaminergic systems, a considerable number of Fos-positive nuclei were still observed (decrease of about 70% in the dorsal and dorsomedial regions). The FE-induced expression of Fos was almost totally suppressed (decrease of about 95% in the dorsal and dorsomedial regions) after simultaneous acute lesion. Our results indicate that FE-induced striatal expression of Fos is due in large measure to DA release and dopaminergic stimulation of D1 receptors. However, concurrent stimulation of NMDA glutamate receptors also appears to be essential, and 5-HT release (although not indispensable) doubles striatal Fos expression.

Animals↗
PubMed2000

Substantia nigra glutamate antagonists produce contralateral turning and basal ganglia Fos expression: interactions with D1 and D2 dopamine receptor agonists.

Experiments measuring behavior and immediate-early gene expression in the basal ganglia can reveal interactions between dopamine (DA) and glutamate neurotransmission. Nigrostriatal DA projections influence two striatal efferent pathways that, in turn, directly and indirectly influence the activity of the substantia nigra pars reticulata (SNr). This report tests the interactions between striatal DA receptors and nigral glutamate receptors on basal ganglia function by examining both contralateral turning and Fos immunoreactivity in striatum and pallidum following unilateral intranigral microinfusions of glutamate antagonists given to intact and 6-OHDA-lesioned rats. The NMDA antagonist AP5 (1 microg), or the AMPA/kainate antagonist DNQX (0.015-1.5 microg), injected into the SNr (0.5 microl) elicited contralateral turning as well as both striatal and pallidal Fos expression. Moreover, intranigral DNQX elicited more turning and greater numbers of Fos-positive striatal neurons in 6-OHDA-lesioned animals than in unlesioned controls, suggesting that the 6-OHDA injection induces functional changes in nigral glutamate transmission. In 6-OHDA-lesioned rats, systemic injections of the DA D1 receptor agonist SKF38393 (0.5 mg/kg, i.p.) increased striatal Fos expression due to intranigral DNQX. In contrast, the D2 agonist quinpirole (0.1 mg/kg, i.p.) decreased striatal Fos expression but increased the pallidal Fos arising from intranigral AP5. In additional experiments, both intact and 6-OHDA-lesioned rats were given simultaneous intranigral and intrastriatal infusions and turning and pallidal Fos expression were measured. 6-OHDA-lesioned rats given 5 microg of intrastriatal quinpirole exhibited both turning and pallidal Fos that was significantly increased by intranigral AP5. These results indicate that the opposing influences of D2 agonists and endogenous nigral glutamate transmission are mediated by striatal D2 receptors. Finally, the behavioral effects of intranigral glutamate antagonism can be dissociated from the effects on striatal or pallidal immediate-early gene expression.

Animals↗
PubMed1999

Inhibition of ultraviolet B--induced c-fos gene expression and p38 mitogen-activated protein kinase activation by (-)-epigallocatechin gallate in a human keratinocyte cell line.

(-)-Epigallocatechin gallate (EGCG), the major polyphenol isolated from green tea, is an active chemoprevention agent against cancer. However, the molecular mechanisms that underlie the inhibitory effects of EGCG are not well understood. In this study, we tested the effects of EGCG on ultraviolet (UV) B radiation-induced c-fos gene expression in a human keratinocyte cell line, HaCaT. EGCG inhibited UVB-induced steady-state message and transcriptional activation of the c-fos gene in a dose-dependent manner. Western analyses further indicated that EGCG had an inhibitory effect on UVB-induced accumulation of the c-fos protein within the same dose range. To further examine the mechanism by which EGCG inhibits UVB-induced c-fos expression, we tested the effect of EGCG on upstream activators of the c-fos gene. We found that EGCG significantly inhibited activation of p38 mitogen-activated protein kinase but not c-jun NH2-terminal kinase or extracellular signal-regulated protein kinase activation. Our previous studies have indicated that UVB-induced c-fos expression may play a key role in UVB-induced activation of the activator protein-1 transcription factor and EGCG-inhibited, UVB-induced activation of AP-1 in HaCaT cells. Because AP-1 is important for tumor promotion and c-fos is a major component of AP-1, the inhibitory effects of EGCG on c-fos expression may further explain the anti-tumor-promoting effects of EGCG.

Anticarcinogenic Agents↗
PubMed2001

Expression of Fos immunoreactivity in some catecholaminergic brainstem neurons in rats following high-altitude exposure.

This study examined the response of neurons of the cardiorespiratory centers, i.e., the nucleus tractus solitarius and the ventrolateral medulla as well as the area postrema in adult and postnatal rats subjected to high-altitude exposure at 4,000 m and 8,000 m. In adult control rats, sporadic Fos-positive neurons were detected in the above-mentioned areas. On exposure to 4,000 m altitude, the number of Fos-positive neurons was noticeably increased. At 8,000 m, the incidence of labeled cells was markedly increased, with many of them doubly labeled for tyrosine hydroxylase. In postnatal rats, Fos expression was not detected in these areas in either control rats or rats exposed to 4,000 m altitude. Fos-positive cells, however, were observed in the these areas in postnatal rats exposed to 8,000 m. In the latter, tyrosine hydroxylase labeling was observed in some Fos-positive cells in the nucleus tractus solitarius and ventrolateral medulla. In rats killed at 24 hr after exposure to high altitude, Fos expression in both the adult and the postnatal rats was comparable to that in their corresponding control rats. Present results suggest that Fos expression in various brainstem areas was induced by reduced oxygen tension in the ambient air at high altitude. Double labeling of some Fos-positive neurons with tyrosine hydroxylase indicates an increased sympathetic activation, which may be involved in the mediation of cardiorespiratory responses to hypoxia. This, however, was less evident in the postnatal animals. It is possible that the peripheral chemoreceptors or the regulation of autonomic functions is not fully developed in this age group.

Altitude Sickness↗
PubMed2002

Enhanced fos expression in the zebra finch (Taeniopygia guttata) brain following first courtship.

Young zebra finch males that court a female for the first time develop a stable preference for the females of that species. On the neuronal level, consolidation of the imprinted information takes place. Here we demonstrate that first courtship or being chased around in the cage leads to enhanced fos expression in forebrain areas implicated in learning and imprinting in zebra finch males compared with birds reared in isolation or in the aviary. Two of the forebrain areas highly active during first courtship (as demonstrated by the 14C-2-deoxyglucose technique), the imprinting locus latral neo/hyperstriatum ventrale (LNH) and the secondary visual area hyperstriatum accessorium/dorsale (HAD), demonstrate enhanced fos expression. Two other imprinting-related areas, the medial neo/hyperstriatum ventrale (MNH) and archistriatum/neostriatum caudale (ANC), do show c-fos induction; however, the areas are not congruous with those demarcated by the 2-DG autoradiographic studies. Additional telencephalic areas include the olfactory lobe, the information storage site lobus parolfactorius (LPO), the memory site hippocampus, the auditory caudomedial neostriatum implicated in the strength of song learning, and the caudolateral neostriatum, which is comparable to the mammalian prefrontal cortex. In addition, c-fos is induced by first courtship and chasing in neurosecretory cell groups of the preoptic area and hypothalamus associated with the repertoire of sexual behavior and stress or enhanced arousal. Enhanced fos expression is also observed in brainstem sources of specific (noradrenergic, catecholaminergic) and nonspecific (reticular formation) activating pathways with inputs to higher brain areas implicated in the imprinting process. Birds reared in isolation or alternatively in the aviary with social and sexual contact to conspecifics showed attenuated or no fos expression in most of the above-mentioned areas. First courtship and chasing both lead to enhanced uptake of 2-DG in the four imprinting areas, as well as subsequent changes in spine density-an anatomical manifestation of the imprinting process. fos expression in the imprinting and other telencephalic, preoptic, hypothalamic, and mesencephalic brain regions indicates processing of stimuli originating from exposure (like chasing) and the analysis of stimuli in a behaviorally relevant, sexually explicit context (like first courtship). c-fos induction in these brain areas indicates its involvement in the triggering of neural changes that accompany the learning process of imprinting, leading eventually to alterations in dendritic spine density in the zebra finch.

Animals↗
PubMed2004

Fos expression in otolith-related brainstem neurons of postnatal rats following off-vertical axis rotation.

To determine the critical time of responsiveness of developing otolith organ-related brainstem neurons and their distribution, Fos protein expression in response to off-vertical axis rotations (OVAR) was mapped in conscious Sprague Dawley rats from P5 to adulthood. OVAR was used to activate sequentially all utricular hair cells per 360 degrees revolution. We detected the coding of horizontal head positions in otolith organ-related neurons within the vestibular nucleus as early as P7. In the vestibular nuclear complex and its subgroups, the density of Fos-immunoreactive (Fos-ir) neurons increased steadily with age and reached the adult level by P21. In both labyrinthectomized rats subjected to OVAR and normal rats kept stationary, labeled neurons were found sporadically in the aforementioned brain regions in each age group, confirming that Fos labeling observed in neurons of normal experimental rats subjected to OVAR was due to otolith organ stimulation. Whereas OVAR-induced Fos-ir neurons were also first observed in vestibular-related brain areas, such as the prepositus hypoglossal nucleus, gigantocellular reticular nucleus, and locus coeruleus, of normal experimental rats at P7, those in the inferior olive were observed only from P14 onward. This indicates the unique maturation time of inferior olivary neurons in gravity-related spatial coding. In general, age-dependent increase in OVAR-induced Fos-ir neurons was observed in brain areas that received otolith inputs. The locus coeruleus was exceptional in that prominent OVAR-induced Fos-ir neuronal number did not change with maturation, and this was well above the low but significant number of Fos-ir neurons in control preparations. Taken together, our results suggest that neuronal subpopulations within the developing network of the horizontal otolith system provide an anatomical basis for the postnatal development of otolith organ-related sensorimotor functions. J. Comp. Neurol. 470:282-296, 2004.

Age Factors↗
PubMed2001

Identification of NPY-induced c-Fos expression in hypothalamic neurones projecting to the dorsal vagal complex and the lower thoracic spinal cord.

Neuropeptide Y exerts profound effects on body weight and glucose homeostasis. We have investigated the effect of centrally administered neuropeptide Y on the activity of descending neurones of the hypothalamic paraventricular nucleus by combining retrograde tract tracing with c-Fos immunocytochemistry. Male rats were injected with True Blue into the dorsal vagal complex and with FluoroGold into the intermediolateral column of the lower thoracic spinal cord. One week after the last surgical procedure, animals were injected centrally with an orexigenic dose of neuropeptide Y (5 microg) and sacrificed 60 to 240 minutes following this injection. Temporal analysis of NPY-induced c-Fos expression showed a peak at 90 minutes, which was nearly returned to basal levels between 120 and 240 minutes. Expression of c-Fos was prominent in several of the subnuclei of the paraventricular nucleus and in the adjacent perifornical nucleus. Neurones projecting to the spinal cord were prominent in the dorsal, lateral, and ventral portion of the medial parvicellular subnuclei of the PVN. About 15% of IML projecting neurones of the medial parvicellular subnucleus were Fos-positive, whereas less than 5% of IML projecting neurones from other subnuclei were Fos-positive. Hardly any PVN neurones projecting to the dorsal vagal complex were concomitantly Fos-positive. A considerably larger (>10%) proportion of perifornical neurones projecting to the nucleus of the solitary tract were c-Fos-immunopositive. In conclusion, NPY induces c-Fos in paraventricular neurones projecting to intermediolateral column of the spinal cord and in neurones of the perifornical nucleus projecting to the dorsal vagal complex.

Animals↗
PubMed1995

Basal expression of the inducible transcription factors c-Jun, JunB, JunD, c-Fos, FosB, and Krox-24 in the adult rat brain.

Jun, Fos, and Krox proteins are inducible transcription factors contributing to the control of gene expression. The elucidation of their individual expression patterns in the nervous system provides new insights into the ability of neurons to react with changes of gene expression to external stimulation under physiological or pathological conditions. The expression of c-Jun, JunB, JunD, c-Fos, FosB, and Krox-24 was investigated in the brain of untreated male Sprague-Dawley and female BDIX rats by immunocytochemistry using specific antibodies. JunD immunoreactivity (IR) labeled the highest number of neurons, being present in almost all neurons of the brain. JunD was expressed at high levels in those areas that also exhibit c-Jun, JunB, c-Fos, and FosB-IR, such as locus coeruleus, periolivary nuclei (ncl.), pontine and central gray, lateral lemniscal ncl., inferior and superior colliculi, leaflet of geniculate ncl., midline nuclei of thalamus, dorsomedial and paraventricular ncl. of hypothalamus, ncl. supraopticus, dorsolateral part of caudate putamen and lateral septal ncl. In contrast to the high number of JunD-positive neurons, c-Jun, JunB, c-Fos, and FosB proteins were detected in rather low numbers of neurons in these brain areas; the rank of the number of immunopositive neurons was c-Fos > JunB > c-Jun > FosB. Particularly high levels of expression were observed for c-Jun in medullary motoneurons, medial geniculate ncl., arcuate ncl., and dentate gyrus, and for JunB in the CA-1 area of the hippocampus and islands of Calleja. The zinc finger protein Krox-24 was expressed in many neurons of these brain areas, with only discrete Jun- and Fos-IR; additionally, many intensely labeled nuclei were present in spinal ncl. of the trigeminal ventromedial ncl. of the hypothalamus and the CA-1 area of the hippocampus. In the cerebellum, nuclear labeling was detected only for c-Jun, JunD, and Krox-24 in granule cells. JunD-IR was also found in glial cells of gray matter and fiber tracts, whereas glial c-Jun-IR was observed only in fiber tracts. Apart from a weak JunD-IR, some areas did not express Jun, Fos, and Krox proteins such as cuneate and gracile ncl., venterobasal complex of thalamus, globus pallidum, and Purkinje cells of the cerebellum. Our data indicate that inducible transcription factors of the fos, jun, and krox gene families show patterns of individual expression in untreated animals, thereby reflecting different mechanisms and/or thresholds for induction under physiological conditions.

Animals↗
PubMed1995

Noxious heat-evoked Fos-like immunoreactivity in the rat medulla, with emphasis on the catecholamine cell groups.

The objectives of the present study were 1) to utilize Fos immunohistochemistry as a marker for neuronal activity in order to examine the population of neurons in the medulla that is engaged by activation of nociceptive peripheral afferents and 2) to determine whether catecholamine-containing neurons in the medulla also express noxious heat-evoked Fos-like immunoreactivity. Noxious heating of the hindpaw evoked specific patterns of Fos-like immunoreactivity in the medulla in regions known to be involved in both nociceptive processing and cardiovascular regulation. Noxious heating of the hindpaw significantly increased the mean number of neurons expressing Fos-like immunoreactivity in the contralateral ventrolateral medulla. Increased numbers of Fos-positive neurons also were observed in both the ipsilateral and the contralateral A1 catecholamine cell groups. Similarly, in the contralateral medullary dorsal reticular fields, noxious heating of the hindpaw significantly increased the mean number of neurons expressing Fos-like immunoreactivity. In contrast, in the paramedian reticular nucleus, noxious heating of the hindpaw resulted in a significant decrease in the mean number of neurons expressing Fos-like immunoreactivity. No significant differences in the mean numbers of neurons expressing Fos-like immunoreactivity were noted in the A2, C1, or C2/C3 medullary catecholamine cell groups. These results suggest that noxious stimuli affect pools of neurons in the medulla with multiple physiological functions.

Afferent Pathways↗
PubMed1995

Fos expression in the medullary dorsal horn of the rat after chronic constriction injury to the infraorbital nerve.

Chronic constriction injury to the rat's infraorbital nerve (IoN-CCI) induces asymmetric face grooming directed to the injured nerve territory and, beginning at 7-12 days postoperative, hyperresponsiveness to mechanical stimulation in this territory (B.P. Vos, A.M. Strassman, and R.J. Maciewicz, 1994, J. Neurosci. 14:2708-2723). To examine central mechanisms involved in these behavioral alterations, changes in nonevoked and mechanical stimulation-evoked fos-like immunoreactivity (fos-LI) following IoN-CCI were quantified in the medullary dorsal horn. Following the appearance of hyperresponsiveness in IoN-CCI rats, experimental and matched sham-operated rats were anesthetized with urethane and received either no stimulation or repeated stimulation with either a 2- or 15-g von Frey hair applied to the hairy skin between vibrissae B3-4/C3-4 on the operated side. Unstimulated IoN-CCI rats had increased fos-LI in laminae I-IV of the ipsilateral medullary dorsal horn. In both groups, mechanical stimulation produced a distinct pattern of fos-LI in the ipsilateral medullary dorsal horn, the quantity of which was related to stimulus intensity. For both stimulus intensities, the total amount and the rostrocaudal spread of evoked fos-LI were significantly larger in IoN-CCI rats. In IoN-CCI rats, stimulation-evoked increases in fos-LI were proportionally larger in laminae I-II than in III-IV. This laminar effect was also present in sham-operated rats but only for 15-g stimulation. Neither condition nor stimulus intensity affected fos-LI in the contralateral medullary dorsal horn. Positive correlations were found between the behavioral parameters of increased trigeminal nociceptive activity and the total amount of fos-LI in the ipsilateral medullary dorsal horn. The results demonstrate that IoN-CCI induces significant alterations in the central processing of afferent signals, which may underlie behavioral manifestations of increased nociceptive activity.

Analysis of Variance↗
PubMed1991

Cell-specific inhibitory and stimulatory effects of Fos and Jun on transcription activation by nuclear receptors.

We investigated the effect of c-Fos and/or c-Jun co-expression on transcription activation by the progesterone (PR), glucocorticoid (GR) or androgen (AR) receptors using three different reporter genes and four different cell lines. We found that c-Fos could only inhibit, while c-Jun could either inhibit or further stimulate receptor-induced transcription. All these effects were receptor, promoter, and cell type specific, and, importantly, the steroid receptors had non-reciprocal effects on the transactivation ability of c-Jun in the presence or absence of c-Fos. Collectively, these results argue against heterodimer formation as a mechanism to explain the phenomena. Transactivation by the endogenous PR in T47D cells could be inhibited by increasing the intracellular c-Fos level with forskolin as well as by co-expressing c-Fos; no such effect was seen in MCF-7 cells. The inhibition by c-Fos of PR-induced transcription involves a competitive mechanism, which requires the presence of the intact c-Fos leucine zipper and is directed mainly at the transcription activation function (TAF) located in the PR and GR hormone binding domains (TAF-2). However, the co-expression of c-Fos did not alter the 'squelching/transcriptional interference' by the PR of estrogen receptor (ER)-induced transcription. Multiple mechanisms are discussed which may be involved in the crosstalk between the two signal transduction pathways.

Base Sequence↗
PubMed1993

c-fos transcriptional activation and repression correlate temporally with the phosphorylation status of TCF.

EGF-induction of human astrocytoma and A431 cells leads to c-fos transcriptional activation and then repression. This could be correlated with changes in the DNA binding characteristics of the c-fos regulatory protein ternary complex factor (TCF) present in nuclear extracts from these cells. Band shifts showed the appearance of induction-related slowly migrating protein-DNA complexes, detected as ternary complexes on the c-fos SRE using a truncated SRF molecule and by direct binding to the Drosophila E74 Ets-protein recognition sequence. By several criteria both types of complexes represented TCF. The appearance of the slow ternary and direct complexes correlated with c-fos transcriptional activation, and their disappearance coincided with the ensuing c-fos shut-off. Blocking c-fos transcriptional repression with the phosphatase inhibitor okadaic acid led to their continued presence. They were sensitive to protein phosphatase 2A but not 1 alpha, and similar slow complexes were formed by partially purified p62TCF phosphorylated by a copurifying kinase activity. Thus the phosphorylation state of TCF correlated strongly with c-fos promoter activity. Since ternary complex formation mediated by full-sized SRF was only slightly affected under comparable conditions, we propose a model for c-fos regulation involving modification of constitutively bound TCF.

Cell Division↗
PubMed1992

Transcriptional activation of c-fos and c-jun protooncogenes by serum growth factors in osteoblast-like MC3T3-E1 cells.

The present study was undertaken to clarify the relationship between c-fos and c-jun protooncogene expression and the differentiation and/or proliferation of osteoblasts, using osteoblast-like MC3T3-E1 (E1) cells. c-fos mRNA was barely detectable, whereas c-jun mRNA was constitutively expressed in E1 cells after serum deprivation for 24-72 h. When serum was added, a rapid and transient induction of c-fos and c-jun mRNAs was observed. The c-fos and c-jun mRNAs reached peak levels at 30 minutes, with a rapid disappearance of c-fos mRNA within 3 h and a much slower decrease in c-jun mRNA. The addition of serum together with cycloheximide, an inhibitor of protein synthesis, resulted in the superinduction of both c-fos and c-jun mRNAs. Among various growth factors, PDGF, EGF, and bFGF mimicked the serum effect, whereas IGF-I and TGF-beta failed to induce c-fos and c-jun mRNA. The effects of PDGF, EGF, and bFGF were completely abolished by pretreatment with actinomycin D, an inhibitor of RNA synthesis, suggesting a transcriptional mechanism. Nuclear runoff experiments showed that the transcription rate of c-fos and c-jun protooncogenes was increased by serum and growth factors. The effects of PDGF, EGF, and bFGF were inhibited by H-7 or staurosporine, inhibitors of protein kinase C (PKC), but not by HA1004 with a much weaker inhibitory activity, suggesting the involvement of PKC for the activation of the protooncogenes.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

c-fos reduces growth factor requirements for mitogenic stimulation of L6 rat myoblasts.

Addition of fetal calf serum (FCS) to serum-deprived L6J1 rat myoblasts increases fos-like immunoreactivity. The nuclear immunoreactivity reached a maximum 2 h after serum addition. Effects of the c-fos protein on myoblast proliferation were analyzed in L6J1 rat myoblasts transfected with the murine c-fos gene under control of a metallothionein promoter. L6J1 myoblasts with elevated expression of transfected c-fos reached higher cell densities than neo transfected control myoblasts when approaching a stationary phase in normal culture conditions (5% FCS). The differences in cell densities were even more pronounced at low serum concentrations (0.5% FCS). c-fos transfected cells also had a faster growth rate than did control cells in serum-free medium supplemented with calcium chloride, lithium chloride, sodium selenite, hydrocortisone, and insulin. The cell morphology of c-fos transfected L6J1 myoblasts was not affected compared to control myoblasts. These results suggest that c-fos protein expression in L6J1 myoblasts is activated by serum and that mitogenic stimulation of L6J1 myoblasts is facilitated by the presence of elevated amounts of c-fos protein.

Animals↗
PubMed1995

Competition between c-fos and 1,25(OH)2 vitamin D3 in the transcriptional control of type I collagen synthesis in MC3T3-E1 osteoblastic cells.

Interaction between c-fos and 1,25(OH)2 vitamin D3 (VD) on the type I collagen synthesis was studied. VD inhibited collagen synthesis and type I collagen mRNA expression in MC3T3-E1 osteoblastic cells. In contrast, VD reversed the inhibition of collagen synthesis and mRNA expression of the c-fos transfectants that overexpressed c-fos gene to a comparable level as those of the control transfectants. The gel shift assay showed the vitamin D receptor (VDR) complex binding to vitamin D responsive element (VDRE) was inhibited under constitutively expressed c-fos gene, suggesting that c-fos gene product, c-Fos, may inhibit the binding of VDR complex to VDRE by making a c-Fos-VDR complex. The result suggests the existence of a fine tuning between c-fos and VD in the bone metabolism which may be relevant to the pathogenesis of rheumatoid bone lesion.

3T3 Cells↗
PubMed2004

Role of catecholaminergic inputs to the medial prefrontal cortex in local and subcortical expression of Fos after psychological stress.

A wide variety of stressors elicit Fos expression in the medial prefrontal cortex (mPFC). No direct attempts, however, have been made to determine the role of the inputs that drive this response. We examined the effects of lesions of mPFC catecholamine terminals on local expression of Fos after exposure to air puff, a stimulus that in the rat acts as an acute psychological stressor. We also examined the effects of these lesions on Fos expression in a variety of subcortical neuronal populations implicated in the control of adrenocortical activation, one classic hallmark of the stress response. Lesions of the mPFC that were restricted to dopaminergic terminals significantly reduced numbers of Fos-immunoreactive (Fos-IR) cells seen in the mPFC after air puff, but had no significant effect on stress-induced Fos expression in the subcortical structures examined. Lesions of the mPFC that affected both dopaminergic and noradrenergic terminals also reduced numbers of Fos-IR cells observed in the mPFC after air puff. Additionally, these lesions resulted in a significant reduction in stress-induced Fos-IR in the ventral bed nucleus of the stria terminalis. These results demonstrate a role for catecholaminergic inputs to the mPFC, in the generation of both local and subcortical responses to psychological stress.

Animals↗
PubMed2005

Role of c-Fos protein on glutamate toxicity in primary neural hippocampal cells.

The hippocampus is extremely sensitive to microenvironmental signals and toxic events, including massive glutamate release. Despite the extensive literature related to the cascade of molecular events triggered in postsynaptic neurons, the distinction between proapoptotic and survival pathways is still being discussed. In this study, we have investigated the role of c-Fos in glutamate-induced toxicity in primary cultures of hippocampal neurons by using antisense oligonucleotide (ASO) technology. Exposure of cells (5 days in vitro; DIV) to glutamate 0.5 mM for 24 hr caused massive nuclear alteration. An increase in the number of caspase-3-positive cells was also observed 24 hr after glutamate treatment. The expression of c-fos and c-jun immediate-early genes was increased 30 min after glutamate exposure. The study of c-Fos and c-Jun protein expression revealed an increase in the number of cells positive for both antibodies. To investigate whether the expression of c-Fos protein after glutamate treatment was related to cell death activation or cell survival pathways, cells were exposed to 5 microM of c-fos ASO at 4 DIV, 24 hr before glutamate treatment. The presence of the ASO in the medium significantly decreased the number of altered nuclei, and this was associated with a significant reduction in the number of c-Fos-positive cells after glutamate treatment. Exposure of cells to the c-fos ASO under the conditions described above decreased caspase-3 immunostaining induced by glutamate. These results suggest that the synthesis of c-Fos protein after glutamate exposure favors cell death pathway activation in which caspase-3 is also involved.

Analysis of Variance↗