Moloney murine leukemia virus long terminal repeat activates monocyte chemotactic protein-1 protein expression and chemotactic activity

Faller, Douglas V.; Weng, Haiqin; Graves, Dana T.; Choi, Seo‐Hyun

doi:10.1002/(sici)1097-4652(199708)172:2<240::aid-jcp11>3.0.co;2-d

Cited by 15 publications

(9 citation statements)

References 84 publications

(11 reference statements)

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“…The level of activation of the MHC class I genes was consistently much lower than what we had observed with the Mo-MuLV LTR, however. No transactivation of other promoter-reporter vectors was observed, demonstrating that transactivation by the FeLV LTR has specificity in terms of the responsive genes, just as has been reported for murine retroviral LTRs (24,25,41). Similar patterns of gene activation were seen with NIH 3T3 cells.…”

Section: Fig 4 Transcriptional Activation Of Collagenase Promoter-rsupporting

confidence: 61%

“…It has been proposed that the U3 region of the FeLV LTR plays a role in the disease pathogenesis similar to that of the MuLV LTR U3 region (30,32,48). Studies from our laboratory have shown that the U3 region of Mo-MuLV can transcriptionally upregulate the expression of certain cellular genes (24,25,41,73). We initially wished to determine if the U3 region from the FeLV-A virus has similar transactivation potential.…”

Section: Felv Ltrs Activate Collagenase Gene Expression Felv-amentioning

confidence: 99%

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Feline Leukemia Virus Long Terminal Repeat Activates Collagenase IV Gene Expression through AP-1

Ghosh

Faller

1999

J Virol

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Leukemia and lymphoma induced by feline leukemia viruses (FeLVs) are the commonest forms of illness in domestic cats. These viruses do not contain oncogenes, and the source of their pathogenic activity is not clearly understood. Mechanisms involving proto-oncogene activation subsequent to proviral integration and/or development of recombinant viruses with enhanced replication properties are thought to play an important role in their disease pathogenesis. In addition, the long terminal repeat (LTR) regions of these viruses have been shown to be important determinants for pathogenicity and tissue specificity, by virtue of their ability to interact with various transcription factors. Previously, we have shown that, in the case of Moloney murine leukemia virus, the U3 region of the LTR independently induces transcriptional activation of specific cellular genes through an LTR-generated RNA transcript (S. Y. Choi and D. V. Faller, J. Biol. Chem. 269:19691–19694, 1994; S.-Y. Choi and D. V. Faller, J. Virol. 69:7054–7060, 1995). In this report, we show that the U3 region of exogenous FeLV LTRs can induce transcription from collagenase IV (matrix metalloproteinase 9) and monocyte chemotactic protein 1 (MCP-1) promoters up to 12-fold. We also show that AP-1 DNA-binding activity and transcriptional activity are strongly induced in cells expressing FeLV LTRs and that LTR-specific RNA transcripts are generated in those cells. Activation of mitogen-activated protein kinase kinases 1 and 2 (MEK1 and -2) by the LTR is an intermediate step in the FeLV LTR-mediated induction of AP-1 activity. These findings thus suggest that the LTRs of FeLVs can independently activate transcription of specific cellular genes. This LTR-mediated cellular gene transactivation may play an important role in tumorigenesis or preleukemic states and may be a generalizable activity of leukemia-inducing retroviruses.

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Section: Fig 4 Transcriptional Activation Of Collagenase Promoter-rsupporting

confidence: 61%

Section: Felv Ltrs Activate Collagenase Gene Expression Felv-amentioning

confidence: 99%

Feline Leukemia Virus Long Terminal Repeat Activates Collagenase IV Gene Expression through AP-1

Ghosh

Faller

1999

J Virol

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“…MCP-1 expression is transcriptionally regulated. A variety of factors, which include tumor necrosis factor-␣ (TNF) 1 (11), platelet-derived growth factor (PDGF-BB) (12), interferon-␥ (13,14), stress factors (15)(16)(17), and viral infection (18), induce MCP-1 transcription. In contrast, retinoic acid, glucocorticoids, and estrogen inhibit induced MCP-1 expression in certain cell lines (19 -22).…”

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confidence: 99%

trans-Retinoic Acid Blocks Platelet-derived Growth Factor-BB-induced Expression of the Murine Monocyte Chemoattractant-1 Gene by Blocking the Assembly of a Promoter Proximal Sp1 Binding Site

Ping

Boekhoudt

Boss

1999

Journal of Biological Chemistry

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Proper regulation of the CC chemokine MCP-1 (monocyte chemoattractant protein-1) is important for normal inflammatory responses. MCP-1 is regulated by a wide variety of agents, including platelet-derived growth factor-BB (PDGF-BB) and tumor necrosis factor-␣ (TNF).Using both in vivo and in vitro assays, the elements required for expression between these two cytokines were compared. In vivo genomic footprinting showed that PDGF-BB induction occurred through the occupancy of the proximal regulatory region, and unlike TNF induction, no changes in the NF-B binding, distal regulatory region occurred. Treatment of cells with trans-retinoic acid, an inhibitor of PDGF-BB activity, resulted in a 50% reduction in PDGF-BB-mediated induction and a concomitant block in the assembly of the proximal regulatory region. trans-Retinoic acid had minimal effect on TNF induction or promoter occupancy. An inhibitor of histone deacetylation was found to stimulate expression of MCP-1 in a manner that correlated with increased accessibility to the proximal regulatory region. These results show that the mechanisms of PDGF-BB and TNF activation of MCP-1 are distinct, although they both require the proximal regulatory region Sp1 binding site. The results also suggest that part of the mechanism used by both of these cytokines involves a process that regulates transcription factor access to the regulatory regions.MCP-1 (monocyte chemoattractant protein-1), a member of the CC chemokine superfamily, functions in attracting monocytes, T lymphocytes, and basophils to sites of inflammation (1-3). The expression of MCP-1 is important for antibacterial responses, antitumor immunity, and other normal immune reactions. Aberrant expression of MCP-1 is associated with glomerular disease (4), allergic and chronic inflammatory diseases (5-7), HIV replication (8, 9), and the pathogenesis of atherosclerosis (10). MCP-1 expression is transcriptionally regulated. A variety of factors, which include tumor necrosis factor-␣ (TNF) 1 (11), platelet-derived growth factor (PDGF-BB) (12), interferon-␥ (13, 14), stress factors (15-17), and viral infection (18), induce MCP-1 transcription. In contrast, retinoic acid, glucocorticoids, and estrogen inhibit induced MCP-1 expression in certain cell lines (19 -22). Elucidating the mechanisms regulating MCP-1 expression is important for understanding the interplay between this chemokine and immune responses and for providing possible approaches to block inflammation. Toward this goal, we and others have identified several regulatory regions that are important for MCP-1 expression (11,(23)(24)(25)(26). Using in vivo genomic footprinting (IVGF) protocols to map regions of factor occupancy and changes in factor occupancy that result from TNF induction in vivo, a distal and a proximal regulatory region separated by 2.1 kilobase pairs of DNA were described (11). The distal regulatory region contains four elements: site A, B1, B2, and HS. Site A, the most 5Ј of these sites, was constitutively occupied in vivo and required for ma...

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“…atherosclerosis [32] and multiple sclerosis [33]. The expression of MCP-1 is regulated by cytokines including tumour necrosis factor (TNF) [34], platelet-derived growth factor (PDGF) [35], interferon-g (IFN-g) [36] and IL-1b [23,37], but stress factors and viral infections also cause MCP-1 expression [38,39]. Several regulatory promoter regions important for MCP-1 expression have been identified.…”

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confidence: 99%

Interference with MCP-1 gene expression by vector generated triple helix-forming RNA oligonucleotides

Kautz

Schwarz

Radeke

2005

CMLS, Cell. Mol. Life Sci.

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Triple helix-forming oligonucleotides (TFOs) that specifically bind to double-stranded DNA sequences can be rationally designed, while intracellular delivery of single stranded RNA TFOs has not yet been studied in detail. In this report, we demonstrate gene and sequence-specific inhibition of MCP-1 gene expression due to interference of intracellular-generated single-stranded RNA (CU-TFO) with an overlapping SP-1/AP-1 target. Binding of synthetic 19-nucleotide (19-nt) CU-TFO to the MCP-1 promoter duplex was verified by triplex blotting. Furthermore, we confirmed binding of a 1.1-kb fusion transcript containing the 19-nt pyrimidine CU sequence to a plasmid-encoded MCP-1 promoter target duplex at pH 7.0. In tumour necrosis factor-alpha-stimulated HEK cells, CU-TFOs inhibited MCP-1 protein release by 76 +/- 10.2% compared to intracellular-generated control oligonucleotides. Interleukin-8 as a control target gene was not affected by CU-TFO, confirming both highly specific and effective chemokine gene repression by transfectable TFO-shuttle vectors.

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Moloney murine leukemia virus long terminal repeat activates monocyte chemotactic protein-1 protein expression and chemotactic activity

Cited by 15 publications

References 84 publications

Feline Leukemia Virus Long Terminal Repeat Activates Collagenase IV Gene Expression through AP-1

Feline Leukemia Virus Long Terminal Repeat Activates Collagenase IV Gene Expression through AP-1

trans-Retinoic Acid Blocks Platelet-derived Growth Factor-BB-induced Expression of the Murine Monocyte Chemoattractant-1 Gene by Blocking the Assembly of a Promoter Proximal Sp1 Binding Site

Interference with MCP-1 gene expression by vector generated triple helix-forming RNA oligonucleotides

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