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Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides
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| Zeitschriftentitel: | American Journal of Physiology-Lung Cellular and Molecular Physiology |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | American Journal of Physiology-Lung Cellular and Molecular Physiology, 284, 2003, 2, S. L386-L394 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Ye, Jianping Wang, Liying Zhang, Xiaoying Tantishaiyakul, Vimon Rojanasakul, Yon Ye, Jianping Wang, Liying Zhang, Xiaoying Tantishaiyakul, Vimon Rojanasakul, Yon |
|---|---|
| author |
Ye, Jianping Wang, Liying Zhang, Xiaoying Tantishaiyakul, Vimon Rojanasakul, Yon |
| spellingShingle |
Ye, Jianping Wang, Liying Zhang, Xiaoying Tantishaiyakul, Vimon Rojanasakul, Yon American Journal of Physiology-Lung Cellular and Molecular Physiology Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology |
| author_sort |
ye, jianping |
| spelling |
Ye, Jianping Wang, Liying Zhang, Xiaoying Tantishaiyakul, Vimon Rojanasakul, Yon 1040-0605 1522-1504 American Physiological Society Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology http://dx.doi.org/10.1152/ajplung.00134.2002 <jats:p>The present study investigated transcriptional inactivation of TNF-α gene by nuclear factor-binding oligonucleotides (ON) and their effects on pulmonary inflammatory responses in mice. PCR-based gene mutation and gel shift assays were used to identify specific cis-acting elements necessary for nuclear factor binding and transactivation of TNF-α gene by lipopolysaccharide (LPS). LPS inducibility of TNF-α was shown to require transcriptional activation by NF-κB at multiple binding sites, including the −850 (κ1), −655 (κ2), and −510 (κ3) sites, whereas the −210 (κ4) site had no effect. Maximum inducibility was associated with the activation of κ3 site. The sequence-specific, double-stranded ON targeting this site was most effective in inhibiting TNF-α activity induced by LPS. The inhibitory effect of ON on TNF-α bioactivity was also investigated using a murine lung inflammation model. Pretreatment of mice with ON, but not its mutated sequence, inhibited LPS-induced inflammatory neutrophil influx and TNF-α production by lung cells. Effective inhibition by ON in this model was shown to require a liposomal agent for efficient cellular delivery of the ON. Together, our results indicate that transcriptional inactivation of TNF-α gene can be achieved by using ON that compete for nuclear factor binding to TNF-α gene promoter. This gene inhibition approach may be used as a research tool or as potential therapeutic modality for diseases with etiology dependent on aberrant gene expression.</jats:p> Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides American Journal of Physiology-Lung Cellular and Molecular Physiology |
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American Journal of Physiology-Lung Cellular and Molecular Physiology |
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| title |
Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_unstemmed |
Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_full |
Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_fullStr |
Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_full_unstemmed |
Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_short |
Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_sort |
inhibition of tnf-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| topic |
Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology |
| url |
http://dx.doi.org/10.1152/ajplung.00134.2002 |
| publishDate |
2003 |
| physical |
L386-L394 |
| description |
<jats:p>The present study investigated transcriptional inactivation of TNF-α gene by nuclear factor-binding oligonucleotides (ON) and their effects on pulmonary inflammatory responses in mice. PCR-based gene mutation and gel shift assays were used to identify specific cis-acting elements necessary for nuclear factor binding and transactivation of TNF-α gene by lipopolysaccharide (LPS). LPS inducibility of TNF-α was shown to require transcriptional activation by NF-κB at multiple binding sites, including the −850 (κ1), −655 (κ2), and −510 (κ3) sites, whereas the −210 (κ4) site had no effect. Maximum inducibility was associated with the activation of κ3 site. The sequence-specific, double-stranded ON targeting this site was most effective in inhibiting TNF-α activity induced by LPS. The inhibitory effect of ON on TNF-α bioactivity was also investigated using a murine lung inflammation model. Pretreatment of mice with ON, but not its mutated sequence, inhibited LPS-induced inflammatory neutrophil influx and TNF-α production by lung cells. Effective inhibition by ON in this model was shown to require a liposomal agent for efficient cellular delivery of the ON. Together, our results indicate that transcriptional inactivation of TNF-α gene can be achieved by using ON that compete for nuclear factor binding to TNF-α gene promoter. This gene inhibition approach may be used as a research tool or as potential therapeutic modality for diseases with etiology dependent on aberrant gene expression.</jats:p> |
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| author | Ye, Jianping, Wang, Liying, Zhang, Xiaoying, Tantishaiyakul, Vimon, Rojanasakul, Yon |
| author_facet | Ye, Jianping, Wang, Liying, Zhang, Xiaoying, Tantishaiyakul, Vimon, Rojanasakul, Yon, Ye, Jianping, Wang, Liying, Zhang, Xiaoying, Tantishaiyakul, Vimon, Rojanasakul, Yon |
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| description | <jats:p>The present study investigated transcriptional inactivation of TNF-α gene by nuclear factor-binding oligonucleotides (ON) and their effects on pulmonary inflammatory responses in mice. PCR-based gene mutation and gel shift assays were used to identify specific cis-acting elements necessary for nuclear factor binding and transactivation of TNF-α gene by lipopolysaccharide (LPS). LPS inducibility of TNF-α was shown to require transcriptional activation by NF-κB at multiple binding sites, including the −850 (κ1), −655 (κ2), and −510 (κ3) sites, whereas the −210 (κ4) site had no effect. Maximum inducibility was associated with the activation of κ3 site. The sequence-specific, double-stranded ON targeting this site was most effective in inhibiting TNF-α activity induced by LPS. The inhibitory effect of ON on TNF-α bioactivity was also investigated using a murine lung inflammation model. Pretreatment of mice with ON, but not its mutated sequence, inhibited LPS-induced inflammatory neutrophil influx and TNF-α production by lung cells. Effective inhibition by ON in this model was shown to require a liposomal agent for efficient cellular delivery of the ON. Together, our results indicate that transcriptional inactivation of TNF-α gene can be achieved by using ON that compete for nuclear factor binding to TNF-α gene promoter. This gene inhibition approach may be used as a research tool or as potential therapeutic modality for diseases with etiology dependent on aberrant gene expression.</jats:p> |
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| imprint | American Physiological Society, 2003 |
| imprint_str_mv | American Physiological Society, 2003 |
| institution | DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229 |
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| physical | L386-L394 |
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| series | American Journal of Physiology-Lung Cellular and Molecular Physiology |
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| spelling | Ye, Jianping Wang, Liying Zhang, Xiaoying Tantishaiyakul, Vimon Rojanasakul, Yon 1040-0605 1522-1504 American Physiological Society Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology http://dx.doi.org/10.1152/ajplung.00134.2002 <jats:p>The present study investigated transcriptional inactivation of TNF-α gene by nuclear factor-binding oligonucleotides (ON) and their effects on pulmonary inflammatory responses in mice. PCR-based gene mutation and gel shift assays were used to identify specific cis-acting elements necessary for nuclear factor binding and transactivation of TNF-α gene by lipopolysaccharide (LPS). LPS inducibility of TNF-α was shown to require transcriptional activation by NF-κB at multiple binding sites, including the −850 (κ1), −655 (κ2), and −510 (κ3) sites, whereas the −210 (κ4) site had no effect. Maximum inducibility was associated with the activation of κ3 site. The sequence-specific, double-stranded ON targeting this site was most effective in inhibiting TNF-α activity induced by LPS. The inhibitory effect of ON on TNF-α bioactivity was also investigated using a murine lung inflammation model. Pretreatment of mice with ON, but not its mutated sequence, inhibited LPS-induced inflammatory neutrophil influx and TNF-α production by lung cells. Effective inhibition by ON in this model was shown to require a liposomal agent for efficient cellular delivery of the ON. Together, our results indicate that transcriptional inactivation of TNF-α gene can be achieved by using ON that compete for nuclear factor binding to TNF-α gene promoter. This gene inhibition approach may be used as a research tool or as potential therapeutic modality for diseases with etiology dependent on aberrant gene expression.</jats:p> Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides American Journal of Physiology-Lung Cellular and Molecular Physiology |
| spellingShingle | Ye, Jianping, Wang, Liying, Zhang, Xiaoying, Tantishaiyakul, Vimon, Rojanasakul, Yon, American Journal of Physiology-Lung Cellular and Molecular Physiology, Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides, Cell Biology, Physiology (medical), Pulmonary and Respiratory Medicine, Physiology |
| title | Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_full | Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_fullStr | Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_full_unstemmed | Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_short | Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_sort | inhibition of tnf-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| title_unstemmed | Inhibition of TNF-α gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides |
| topic | Cell Biology, Physiology (medical), Pulmonary and Respiratory Medicine, Physiology |
| url | http://dx.doi.org/10.1152/ajplung.00134.2002 |