An ATF/CREB-binding site is essential for cell-specific and inducible transcription of the murine MIP-1β cytokine gene

Proffitt, J L; Crabtree, Gerald R.; Grove, M; Daubersies, Pierre; Bailleul, Bernard; Wright, Esmond; Plumb, Mark

doi:10.1016/0378-1119(94)00701-s

Cited by 34 publications

(32 citation statements)

References 18 publications

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“…Therefore, the demonstration of transient degradation of total IB is a marker for activation of NF-B. The proximal promoters of the MIP-1␣ and MIP-1␤ genes exhibit consensus sequences for NF-B, C/EBP, and ATF/ CBP, which confer cell-specific and inducible expression of these chemokines (19,41). Consistent with this, our data show that MIP-1␣ production by opsonized C. neoformans in microglia was dependent on NF-B.…”

Section: Discussionsupporting

confidence: 84%

Fcγ Receptor I- and III-Mediated Macrophage Inflammatory Protein 1α Induction in Primary Human and Murine Microglia

Song¹,

Shapiro²,

Goldman

et al. 2002

Infect Immun

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Microglial cell phagocytic receptors may play important roles in the pathogenesis and treatment of several neurological diseases. We studied microglial Fc receptor (FcR) activation with respect to the specific Fc␥R types involved and the downstream signaling events by using monoclonal antibody (MAb)-coated Cryptococcus neoformans immune complexes as the stimuli and macrophage inflammatory protein 1␣ (MIP-1␣) production as the final outcome. C. neoformans complexed with murine immunoglobulin G (IgG) of ␥1, ␥2a, and ␥3, but not ␥2b isotype, was effective in inducing MIP-1␣ in human microglia. Since murine ␥2b binds to human Fc␥RII (but not Fc␥RI or Fc␥RIII), these results indicate that Fc␥RI and/or Fc␥RIII is involved in MIP-1␣ production. Consistent with this, an antibody that blocks Fc␥RII (IV.3) failed to inhibit MIP-1␣ production, while an antibody that blocks Fc␥RIII (3G8) did. An anti-C. neoformans MAb, 18B7 (IgG1), but not its F(ab) 2 , induced extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase kinase phosphorylation, and MIP-1␣ release was suppressed by the ERK inhibitor U0126. C. neoformans plus 18B7 also induced degradation of I-B␣, and MIP-1␣ release was suppressed by the antioxidant NF-B inhibitor pyrrolidine dithiocarbamate. To confirm the role of FcR more directly, we isolated microglia from wild-type and various FcR-deficient mice and then challenged them with C. neoformans plus 18B7. While Fc␥RII-deficient microglia showed little difference from the wild-type microglia, both Fc␥RI ␣-chain-and Fc␥RIII ␣-chain-deficient microglia produced less MIP-1␣, and the common Fc ␥-chain-deficient microglia showed no MIP-1␣ release. Taken together, our results demonstrate a definitive role for Fc␥RI and Fc␥RIII in microglial chemokine induction and implicate ERK and NF-B as the signaling components leading to MIP-1␣ expression. Our results delineate a new mechanism for microglial activation and may have implications for central nervous system inflammatory diseases.

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Section: Discussionsupporting

confidence: 84%

Fcγ Receptor I- and III-Mediated Macrophage Inflammatory Protein 1α Induction in Primary Human and Murine Microglia

Song¹,

Shapiro²,

Goldman

et al. 2002

Infect Immun

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“…Yet, it remains to be determined whether in addition to c-Fos and JunD other AP-1 subunits are involved in TF expression. Finally, an ATF/CREBbinding site in the macrophage in¯ammatory protein 1 beta (MIP-1 beta) seems to control cell type-and LPSinduced expression of this gene in macrophages (Pro tt et al, 1995).…”

Section: Role Of Ap-1 In Wound Healingmentioning

confidence: 99%

Function and regulation of AP-1 subunits in skin physiology and pathology

2001

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The mouse skin has become the model of choice to study the regulation and function of AP-1 subunits in many physiological and pathological processes in vivo and in vitro. Genetically modi®ed mice, in vitro reconstituted skin equivalents and epidermal cell lines were established, in which AP-1-regulated genetic programs of cell proliferation, di erentiation and tumorigenesis can be analysed. Since the epidermis, as our interface with the environment, is subjected to radiation and injury, signal transduction pathways and critical AP-1 members regulating the mammalian stress response could be identi®ed. Regulated expression of important components of the cytokine network, cell surface receptors and proteases, which orchestrate the process of wound healing has been found to rely on AP-1 activity. Here we review our current knowledge on the function of AP-1 subunits and AP-1 target genes in these fascinating ®elds of skin physiology and pathology. Oncogene (2001) 20, 2413 ± 2423.

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“…CREs have been found to contribute to the induction of serum-responsive genes (39,40). Two such elements within the cytochrome c promoter bind the transcription factor CREB and account for cAMP induction of cytochrome c mRNA (19).…”

Section: Functional Recognition Sites For Creb and Nrf-1 Mediate The mentioning

confidence: 99%

“…CREs are known to mediate a serum response that is independent of cAMP signaling (39,40). Moreover, serum growth factors, including nerve growth factor, fibroblast growth factor, epidermal growth factor, and insulin, can signal through RAS and the family of mitogen activated protein kinases (46 -49).…”

Section: Table II Serum Stimulation Of Cytochrome C Promoter Constructsmentioning

confidence: 99%

Sequential Serum-dependent Activation of CREB and NRF-1 Leads to Enhanced Mitochondrial Respiration through the Induction of Cytochrome c

Herzig¹,

Scacco²,

Scarpulla³

2000

Journal of Biological Chemistry

173

158

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Progression through the cell cycle requires ATP for protein synthesis, cytoskeletal rearrangement, chromatin remodeling, and protein degradation. The mechanisms by which mammalian cells increase respiratory capacity and ATP production in preparation for cell division are largely unexplored. Here, we demonstrate that serum induction of cytochrome c mRNA and processed protein in quiescent BALB/3T3 fibroblasts is associated with a marked increase in mitochondrial respiration. Cytochrome c was induced in the absence of any increase in citrate synthase activity or in subunit IV of the cytochrome c oxidase complex mRNA or protein, indicating that the enhanced respiratory rate did not require a general increase in mitochondrial biogenesis or respiratory chain expression. Transfections with a series of cytochrome c promoter mutants showed that both nuclear respiratory factor 1 (NRF-1) and cAMPresponse element-binding protein (CREB) binding sites contributed equally to induced expression by serum. Moreover, CREB and NRF-1 were phosphorylated sequentially in response to serum, and the NRF-1 phosphorylation was accompanied by an increase in its ability to trans-activate target gene expression. The results demonstrate that the differential transcriptional expression of cytochrome c, through sequential transcription factor phosphorylations, leads to enhanced mitochondrial respiratory capacity upon serum-induced entry to the cell cycle.Entry into the cell cycle requires energy in the form of ATP for the execution of a number of regulatory and metabolic events. Protein synthesis consumes large amounts of cellular energy and is required for entry into S phase (1). In quiescent 3T3 fibroblasts, cellular protein content increases within 4 -5 h of serum stimulation and precedes DNA replication by several hours (2). Nontoxic inhibition of mitochondrial respiratory function inhibits progression to G1 in parallel with a reduction in cellular ATP (3). Protein synthesis (1) and degradation (4) as well as the depolymerization of the microtubular network during interphase (5) all depend upon the intracellular ATP concentration. ATP has also been implicated in the regulation of cyclin-dependent kinases, which in turn control cell proliferation (6).

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An ATF/CREB-binding site is essential for cell-specific and inducible transcription of the murine MIP-1β cytokine gene

Cited by 34 publications

References 18 publications

Fcγ Receptor I- and III-Mediated Macrophage Inflammatory Protein 1α Induction in Primary Human and Murine Microglia

Fcγ Receptor I- and III-Mediated Macrophage Inflammatory Protein 1α Induction in Primary Human and Murine Microglia

Function and regulation of AP-1 subunits in skin physiology and pathology

Sequential Serum-dependent Activation of CREB and NRF-1 Leads to Enhanced Mitochondrial Respiration through the Induction of Cytochrome c

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