Evaluation of the role of Ap1-like proteins in the enhanced apolipoprotein E gene transcription accompanying phorbol ester induced macrophage differentiation

Basheeruddin, Khaja; Rechtoris, Carol; Mazzone, Theodore

doi:10.1016/0167-4781(94)90021-3

Cited by 15 publications

(11 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As shown for apolipoproteins E and CIII [15,16], this study demonstrates that TPA modulates apo A-I gene expression at the transcriptional level in the Hep G2 cell line. TPA treatment results in partial inhibition of apo A-I gene transcription and this effect is mediated by elements located in the 5'-flanking region of the apo A-I gene between nucleotides -253 to -4 upstream of the transcription start site.…”

Section: Plasmids Cell Transfections Alkaline Phosphatase and Cat Asupporting

confidence: 73%

“…In a recent study, it was shown that apo C-Ill gene transcription was regulated by a TPA-inducible activity mediated by NFxB binding sites [15]. In another study, it was shown that transcriptional activation of the apo E gene during TPA-induced macrophage differentiation was associated with induction of AP-l-like proteins [16]. The promoter regions of several inducible genes share a conserved 8 bp motif which is known to bind the AP-1 transcription complex [17].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Transcriptional regulation of apolipoprotein A‐I expression in Hep G2 cells by phorbol ester

Vandenbrouck¹,

Lambert²,

Janvier³

et al. 1995

FEBS Letters

View full text Add to dashboard Cite

Section: Plasmids Cell Transfections Alkaline Phosphatase and Cat Asupporting

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Transcriptional regulation of apolipoprotein A‐I expression in Hep G2 cells by phorbol ester

Vandenbrouck¹,

Lambert²,

Janvier³

et al. 1995

FEBS Letters

View full text Add to dashboard Cite

“…2) and therefore could regulate the expression of NPC-1, NPC-2, CPT-1, ADRP, ACAT-1, and NCEH genes. AP-1 and NF-kB binding sites exist in the ApoE and ABCA-1 promoters (36,37), suggesting a potential mechanism of IL-33-mediated gene regulation through these signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

IL-33 Reduces Macrophage Foam Cell Formation

McLaren

Michael

Salter

et al. 2010

The Journal of Immunology

165

184

View full text Add to dashboard Cite

show abstract

“…Interestingly, one of these sites in the proximal promoter region (position Ϫ602) has already been shown to be important for the induction of apoE expression during PMA-induced differentiation of THP-1 monocytes into macrophages. 25 Indeed, TGF-␤ induces the binding of AP-1, and this was affected by inhibitors of p38 kinase, JNK, and CK2 (Figures 4 and 5). Interestingly, when the action of curcumin and SB202190 on apoE expression in macrophages was investigated, inhibition was seen of both the TGF-␤-independent expression, driven by the differentiating agent PMA, and that induced by this cytokine (supplemental Figure III).…”

Section: Discussionmentioning

confidence: 99%

“…Because c-Jun is a major component of AP-1 21 and, as an AP-1-like recognition sequence in the promoter of the apoE gene, has been implicated in its induced expression during macrophage differentiation, 25 EMSAs were also performed to evaluate the effect of TGF-␤ and the inhibitors on DNAprotein interactions. As shown in Figure 4B, 2 major DNAprotein complexes were seen with a consensus AP-1 recognition sequence.…”

Section: Singh and Ramji Regulation Of Apolipoprotein E Expression 1325mentioning

confidence: 99%

Transforming Growth Factor-β–Induced Expression of the Apolipoprotein E Gene Requires c-Jun N-Terminal Kinase, p38 Kinase, and Casein Kinase 2

Singh

Ramji

2006

ATVB

View full text Add to dashboard Cite

Objective-The cytokine transforming growth factor-␤ (TGF-␤) and apolipoprotein E (apoE) play potent antiatherogenic roles. Despite such importance, the mechanisms underlying the regulation of apoE expression by TGF-␤ have not been characterized and were therefore investigated. Methods and Results-Using THP-1 cell line as a model system, with key findings confirmed in primary cultures, we show that TGF-␤ induces the expression of apoE, and this is prevented by pharmacological inhibitors of c-Jun N-terminal kinase (JNK), p38 kinase, and casein kinase 2 (CK2). In support for an important role for these pathways, TGF-␤ activates JNK, p38 kinase, and CK2, and dominant-negative (DN) forms of these proteins inhibit the cytokine-induced apoE expression. TGF-␤ also increases the phosphorylation and expression of c-Jun, a downstream target for JNK action and a component of activator protein-1 (AP-1), and DN c-Jun inhibits the induction of apoE expression in response to the cytokine. AP-1 DNA binding was also induced by TGF-␤, and the action of p38 kinase, JNK, and CK2 converged on the activation of c-Jun/AP-1. Key Words: apolipoprotein E Ⅲ atherosclerosis Ⅲ macrophage Ⅲ TGF-␤ Ⅲ signal transduction Ⅲ gene expression A therosclerosis, the leading cause of death in Westernized societies, is a form of chronic inflammation regulated by the action of cytokines. 1 Among the cytokines, transforming growth factor-␤ (TGF-␤) plays a potent antiatherogenic role. 2 For example, TGF-␤ inhibits foam cell formation 3 and the production of NO, 4 induces the expression of tissue inhibitors of metalloproteinases, 5 and stimulates the expression of interleukin-1 receptor antagonist, 6 all of which are largely antiatherogenic actions. The cytokine also acts in an antiinflammatory manner as demonstrated by a profound inflammatory response in TGF-␤-deficient mice. 7 In addition, inhibition of TGF-␤ signaling accelerates the development of atherosclerosis in murine models of the disease. 8 Furthermore, a number of studies have found an inverse association between TGF-␤ levels and the development of atherosclerotic lesions. 2,9 Because TGF-␤ inhibits foam cell formation, it is essential that a detailed understanding is obtained of the action of the cytokine on the expression of key genes implicated in the process and the molecular mechanisms through which this is achieved. Such studies will improve our understanding of the molecular basis of foam cell formation and atherosclerosis and, in the longer term, lead to the identification of potentially novel targets for therapeutic intervention. TGF-␤ inhibits the expression of lipoprotein lipase 10 and scavenger receptors A and CD36, 11-12 implicated in the uptake of cholesterol, and induces the expression of those involved in cholesterol efflux, such as ATP-binding cassette transporters A1 and G1. 3,13 Apolipoprotein E (apoE), a major component of several classes of plasma lipoproteins, is a key stimulator of cellular cholesterol efflux and reverse cholesterol transport. 14 The apoE expressed by mo...

show abstract

Evaluation of the role of Ap1-like proteins in the enhanced apolipoprotein E gene transcription accompanying phorbol ester induced macrophage differentiation

Cited by 15 publications

References 33 publications

Transcriptional regulation of apolipoprotein A‐I expression in Hep G2 cells by phorbol ester

Transcriptional regulation of apolipoprotein A‐I expression in Hep G2 cells by phorbol ester

IL-33 Reduces Macrophage Foam Cell Formation

Transforming Growth Factor-β–Induced Expression of the Apolipoprotein E Gene Requires c-Jun N-Terminal Kinase, p38 Kinase, and Casein Kinase 2

Contact Info

Product

Resources

About