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Suppression of matrix metalloproteinase-9 transcription by transforming growth factor-β is mediated by a nuclear factor-κB site

OGAWA, Kenji, CHEN, Feifei, KUANG, Chenzhong, CHEN, Yan·2004·Biochemical Journal
DOI 10.1042/bj20040058
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Abstract

TGF-β (transforming growth factor-β) plays a critical role in modulating the inflammatory response and other biological processes through its regulation of the production of MMPs (matrix metalloproteinases). In both Mono-Mac-6 and RAW264.7 monocyte/macrophage cells, TGF-β abrogated lipopolysaccharide-induced increases in the enzymic activity and mRNA level of MMP-9. A fragment of the human MMP-9 promoter was used to characterize its regulation by TGF-β signalling. In RAW264.7 cells, TGF-β or its downstream signalling protein, Smad3 (Sma- and Mad-related protein 3), inhibited lipopolysaccharide-stimulated promoter activity. The suppressive activity of TGF-β on the MMP-9 promoter was abrogated by an inhibitory Smad, Smad7. The MMP-9 promoter contains a putative TIE (TGF-β inhibitory element). However, neither mutation nor deletion of the TIE had any effect on the inhibitory activity of TGF-β on MMP-9 transcription, indicating that the consensus TIE is not required for this effect of TGF-β. Analysis using a series of deletion mutants of the MMP-9 promoter revealed that a region containing a consensus NF-κB (nuclear factor-κB) site is required for the basal activity and TGF-β-mediated suppression of the promoter. Mutation of the putative NF-κB site not only markedly reduced the basal transcriptional activity of the promoter, but also abrogated the responsiveness of the promoter to TGF-β. In addition, a minimal promoter containing one copy of the NF-κB sequence was responsive to TGF-β treatment. Furthermore, an electrophoretic mobility shift assay was performed with the nuclear extracts from RAW264.7 cells, and it was found that TGF-β treatment did not disrupt the binding of NF-κB p50 and p65 proteins to the NF-κB sequence. Taken together, these studies indicate that the NF-κB site is indispensable for the suppressive activity of TGF-β in the regulation of MMP-9 transcription.

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  • Entire pathways such as MAPK are no longer hijacked for non-canonical induction of TGF-beta, Smad1, and inflammation but instead engage in productive signaling by their cognate ligands, promoting tissue health, regeneration, and homeostatic production of cytokines and growth factors.

    “entire pathways (MAPK, for example) are no longer hijacked for non-canonical induction of TGF-beta, Smad1, and inflammation [57, 58], but instead engage in productive signaling by their cognate ligands, promoting tissue health, regeneration and homeostatic production of cytokines and growth factors [59–61] (with their own positive feed-backs), as we observe.”

    From Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin (2020) · cites this paper as [60]

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Metadata

Authors
OGAWA, K., CHEN, F., KUANG, C., & CHEN, Y.
Affiliations
Department of Medical and Molecular Genetics, Walther Oncology Center, Indiana University School of Medicine and the Walther Cancer Institute, Indianapolis, IN 46202, U.S.A.
Venue
Biochemical Journal
Publisher
Portland Press Ltd.
Published
2004-07-06
Volume
381
Issue
2
Pages
413-422
ISSN
  • 0264-6021
  • 1470-8728
DOI
10.1042/bj20040058
Cited by
116
References
2
Language
en

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