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ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes.

ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes. Research Abstract Details 

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  • ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes. Abstract Text:

    haibing pengHaibing Peng,lujian tanLujian Tan,makoto osakiMakoto Osaki,yumei zhanYumei Zhan,kosei ijiriKosei Ijiri,kaneyuki tsuchimochiKaneyuki Tsuchimochi,miguel oteroMiguel Otero,hong wangHong Wang,bob k choyBob K Choy,franck t grallFranck T Grall,xuesong guXuesong Gu,towia a libermannTowia A Libermann,peter oettgenPeter Oettgen,mary b goldringMary B Goldring,

    The epithelium-specific ETS (ESE)-1 transcription factor is induced in chondrocytes by interleukin-1beta (IL-1beta). We reported previously that early activation of EGR-1 by IL-1beta results in suppression of the proximal COL2A1 promoter activity by displacement of Sp1 from GC boxes. Here we report that ESE-1 is a potent transcriptional suppressor of COL2A1 promoter activity in chondrocytes and accounts for the sustained, NF-kappaB-dependent inhibition by IL-1beta. Of the ETS factors tested, this response was specific to ESE-1, since ESE-3, which was also induced by IL-1beta, suppressed COL2A1 promoter activity only weakly. In contrast, overexpression of ETS-1 increased COL2A1 promoter activity and blocked the inhibition by IL-1beta. These responses to ESE-1 and ETS-1 were confirmed using siRNA-ESE1 and siRNA-ETS1. In transient cotransfections, the inhibitory responses to ESE-1 and IL-1beta colocalized in the -577/-132 bp promoter region, ESE-1 bound specifically to tandem ETS sites at -403/-381 bp, and IL-1-induced binding of ESE-1 to the COL2A1 promoter was confirmed in vivo by ChIP. Our results indicate that ESE-1 serves a potent repressor function by interacting with at least two sites in the COL2A1 promoter. However, the endogenous response may depend upon the balance of other ETS factors such as ETS-1, and other IL-1-induced factors, including EGR-1 at any given time. Intracellular ESE-1 staining in chondrocytes in cartilage from patients with osteoarthritis (OA), but not in normal cartilage, further suggests a fundamental role for ESE-1 in cartilage degeneration and suppression of repair.

    ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes. Publishing Authors By Initials

    h pengH Peng,l tanL Tan,m osakiM Osaki,y zhanY Zhan,k ijiriK Ijiri,k tsuchimochiK Tsuchimochi,m oteroM Otero,h wangH Wang,bk choyBK Choy,ft grallFT Grall,x guX Gu,ta libermannTA Libermann,p oettgenP Oettgen,mb goldringMB Goldring,

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    ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of cellular physiology

    VOLUME: 215

    Page Numbers: 562-73

    Journal Abbreviation: J. Cell. Physiol.

    ISSN: 1097-4652

    DAY: 27

    MONTH: May

    YEAR: 2008

    ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes. Information

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    LANGUAGE: eng

    NlmUniqueID: 50222

    ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes. Keywords Mesh Terms:

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    Grant and Affiliation Information for ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes.

    AFFILIATION: Department of Medicine, Beth Israel Deaconess Medical Center, New England Baptist Bone and Joint Institute, Boston, Massachusetts, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAMS

    GRANT: R01-AR47952

    ACRONYM: AR

    MEDLINETA: J Cell Physiol

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