CCAAT/enhancer binding protein δ (C/EBPδ) expression and elevation in Alzheimer’s disease

Li, Rena; Strohmeyer, Ron; Liang, Zhe; Lue, Lih‐Fen; Rogers, Joseph

doi:10.1016/j.neurobiolaging.2003.10.016

Cited by 80 publications

(87 citation statements)

References 45 publications

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“…In the present study we clearly demonstrate that C/EBPd is expressed by microglial cells in vitro and that LPS upregulates C/EBPd mRNA and protein in a time-and concentration-dependent manner. We have also observed C/ EBPd expression in activated astrocytes confirming previous reports (Lee et al, 1998;Cardinaux et al, 2000;Giri et al, 2004;Li et al, 2004).…”

Section: Discussionsupporting

confidence: 92%

“…C/EBP sites are found in proinflammatory genes that are upregulated in activated microglia and are therefore potentially regulated by C/EBPd (Poli, 1998;Li et al, 2004). A direct regulation by C/EBPd has been demonstrated for the expression of COX-2 in macrophages (Wadleigh et al, 2000), NO synthase-2 (NOS-2) in C6 cells and primary astroglial cultures (Won et al, 2003), IL-1b in macrophages (Godambe et al, 1994) or IL-6 in osteoblasts (Ruddy et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…In an animal mouse model of Amyotrophic Lateral Sclerosis we have observed C/EBPd immunoreactivity in microglia which could not be observed in wild type mice, but this signal was cytoplasmic (Tarabal, Esquerda et al, unpublished observations). It is interesting to note that cytoplasmic C/EBPd immunoreactivity has also been observed in astrocytes in Alzheimer brain (Li et al, 2004) and in discrete neuronal populations in spinocerebellar ataxia type 3 (Evert et al, 2006). This is an unexpected localization for a transcription factor.…”

Section: Discussionmentioning

confidence: 99%

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CCAAT/enhancer binding protein delta in microglial activation

Ejarque-Ortíz

Gresa-Arribas

Straccia

et al. 2009

J of Neuroscience Research

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The transcription factor CCAAT/enhancer binding protein delta (C/EBP delta) regulates transcription of genes that play important roles in glial activation. Previous studies have shown the astroglial expression of C/EBP delta but the microglial expression of C/EBP delta remains virtually unexplored, with the exception of two microarray studies. In this report, using murine primary cultures and BV2 cells we clearly demonstrate that C/EBP delta is expressed by microglia and it is upregulated in microglial activation. Lipopolysaccharide upregulates C/EBP delta both in microglia and in astrocytes. This effect is time-dependent, with a maximum effect at 3 hr at mRNA level and at 4-8 hr at protein level, and concentration-dependent, with a maximum effect at 100 ng/mL. The lipopolysaccharide-induced C/EBP delta upregulation in BV2 microglia is mimicked by agonists of the toll-like receptors 2, 3 and 9 and can be prevented by an inhibitor of extracellular signal-regulated kinase activation. C/EBP delta from activated BV2 microglia binds to the cyclooxygenase-2 promoter and forms complexes with C/EBP beta isoforms. These results point to C/EBP delta as a putative key regulator of proinflammatory gene expression in microglial activation.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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CCAAT/enhancer binding protein delta in microglial activation

Ejarque-Ortíz

Gresa-Arribas

Straccia

et al. 2009

J of Neuroscience Research

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“…For example, the proinflammatory cytokines IL-1b, IL-6, and TNF-a are regulated by NF-kB and C/EBP transcription factor mechanisms. Astrocyte CEBPd is dramatically upregulated in AD cortex (Li et al 2004), and astrocyte NF-kB is activated on exposure to Ab, leading to increased expression of IL-1b and IL-6 (Bales et al 1998). NF-kB mechanisms in astrocytes also control secretion of chemokines and adhesion molecules that might permit invasion by peripheral leukocytes, further fueling the inflammatory response (Moynagh 2005).…”

Section: Inflammation In Alzheimer Diseasementioning

confidence: 99%

Inflammation in Alzheimer Disease--A Brief Review of the Basic Science and Clinical Literature

Wyss‐Coray

Rogers

2011

Cold Spring Harbor Perspectives in Medicine

846

642

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Biochemical and neuropathological studies of brains from individuals with Alzheimer disease (AD) provide clear evidence for an activation of inflammatory pathways, and longterm use of anti-inflammatory drugs is linked with reduced risk to develop the disease. As cause and effect relationships between inflammation and AD are being worked out, there is a realization that some components of this complex molecular and cellular machinery are most likely promoting pathological processes leading to AD, whereas other components serve to do the opposite. The challenge will be to find ways of fine tuning inflammation to delay, prevent, or treat AD.

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“…Acetylation of C/EBPd was proven to be important for epidermal growth factor-induced cyclooxygenase-2 gene expression [12]. C/EBPd protein is also increased in the pathologically vulnerable regions of the Alzheimers disease brain, particularly in reactive astrocytes surrounding the amyloid b peptide deposits [13]. In AIDS-associated neurological disorders, HIV-induced increase in complement factor C3 is hypothesized to contribute to the neurodegeneration, where C/EBPd is a key factor for HIVinduced C3 expression [14].…”

Section: Introductionmentioning

confidence: 99%

Role of transcriptional factors Sp1, c-Rel, and c-Jun in LPS-induced C/EBPδ gene expression of mouse macrophages

Liu

Chen

Wang

et al. 2007

Cell. Mol. Life Sci.

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Transcription factor C/EBPs are involved in the regulation of various cellular responses. Here, it was suggested that C/EBPdelta gene was activated by lipopolysaccharide (LPS) through transcription factors Sp1, c-Rel, and c-Jun. Assay of the luciferase reporter vectors containing a 5'-deletion of the C/EBPdelta gene promoter indicated that a LPS-responsive element was positioned between -345 and -35 bp of mouse C/EBPdelta gene promoter. Transcription factors Sp1, c-Rel, and c-Jun bound to this region were identified using both in vivo chromatin immunoprecipitation and in vitro DNA-protein binding assays. LPS enhanced the proteins and DNA binding capacities of c-Rel and c-Jun, and the downstream Sp1 site was essential for LPS-induced C/EBPdelta gene. Treatment of cells with ERK/JNK/p38 inhibitors or NF-kappaB inhibitor inhibited the LPS-induced C/EBPdelta gene expression by inhibiting c-Jun, c-Rel, and p300 binding to DNA. Our findings provide a better understanding of LPS-induced C/EBPdelta gene expression.

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CCAAT/enhancer binding protein δ (C/EBPδ) expression and elevation in Alzheimer’s disease

Cited by 80 publications

References 45 publications

CCAAT/enhancer binding protein delta in microglial activation

CCAAT/enhancer binding protein delta in microglial activation

Inflammation in Alzheimer Disease--A Brief Review of the Basic Science and Clinical Literature

Role of transcriptional factors Sp1, c-Rel, and c-Jun in LPS-induced C/EBPδ gene expression of mouse macrophages

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