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Research Article Free access | 10.1172/JCI429

Inhibition of mesangial cell proliferation by E2F decoy oligodeoxynucleotide in vitro and in vivo.

Y Maeshima, N Kashihara, T Yasuda, H Sugiyama, T Sekikawa, K Okamoto, K Kanao, Y Watanabe, Y S Kanwar, and H Makino

Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

Find articles by Maeshima, Y. in: PubMed | Google Scholar

Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

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Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

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Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

Find articles by Sugiyama, H. in: PubMed | Google Scholar

Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

Find articles by Sekikawa, T. in: PubMed | Google Scholar

Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

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Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

Find articles by Kanao, K. in: PubMed | Google Scholar

Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

Find articles by Watanabe, Y. in: PubMed | Google Scholar

Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

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Department of Medicine III, Okayama University Medical School, Okayama 700, Japan.

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Published June 1, 1998 - More info

Published in Volume 101, Issue 11 on June 1, 1998
J Clin Invest. 1998;101(11):2589–2597. https://doi.org/10.1172/JCI429.
© 1998 The American Society for Clinical Investigation
Published June 1, 1998 - Version history
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Abstract

The transcription factor E2F coordinately activates several cell cycle-regulatory genes. We attempted to inhibit the proliferation of mesangial cells in vitro and in vivo by inhibiting E2F activity using a 25-bp decoy oligodeoxynucleotide that contained consensus E2F binding site sequence (E2F-decoy) as a competitive inhibitor. The decoy's effect on human mesangial cell proliferation was evaluated by [3H]thymidine incorporation. The E2F decoy inhibited proliferation in a concentration-dependent manner, whereas a mismatch control oligodeoxynucleotide had little effect. Electrophoretic mobility shift assays demonstrated that the decoy's inhibitory effect was due to the binding of the decoy oligodeoxynucleotide to E2F. The effect of the E2F decoy was then tested in a rat anti-Thy 1.1 glomerulonephritis model. The E2F decoy oligodeoxynucleotide was introduced into the left kidney 36 h after the induction of glomerulonephritis. The administration of E2F decoy suppressed the proliferation of mesangial cells by 71%. Furthermore, treatment with the E2F decoy inhibited the glomerular expression of proliferating cell nuclear antigen at the protein level as well as the mRNA level. These findings indicate that decoy oligonucleotides can suppress the activity of the transcription factor E2F, and may thus have a potential in treating glomerulonephritis.

Version history
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