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KLF5 and hhLIM cooperatively promote proliferation of vascular smooth muscle cells | Molecular and Cellular Biochemistry
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Krüppel-like factor 5 (KLF5) plays an important role in cellular proliferation and differentiation. In this study, we show that adenovirus-mediated overexpression of KLF5 increased neointimal formation, while human heart LIM protein (hhLIM) decreased neointimal formation following vascular injury. Interestingly, neointimal formation was significantly increased in the animals where both hhLIM and KLF5 were introduced, suggesting that KLF5 can reverse hhLIM function in cell proliferation on the coexpression with hhLIM. These results were also confirmed the cellular level. Further mechanistic studies suggested that PDGF-BB promoted the interaction between hhLIM and KLF5 through stimulating hhLIM binding to TGF-β control element (TCE) on the cyclin E promoter in a KLF5-dependent manner. Failure of KLF5 binding to the TCE, on the knockdown of KLF5 by transfecting siRNA, not only prevented the recruitment of hhLIM to the cyclin E promoter but also affected activation of the cyclin E promoter by KLF5. These data suggest that KLF5 reverses hhLIM function from anti-proliferation to pro-proliferation through its interaction with hhLIM on the cyclin E promoter.
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Keywords {🔍}
article, pubmed, cas, google, scholar, klf, vascular, smooth, muscle, cells, hhlim, zheng, factor, cell, proliferation, growth, han, biol, access, chem, physiol, privacy, cookies, content, miao, liu, neointimal, formation, protein, interaction, cyclin, promoter, expression, transcription, zhang, data, publish, search, cellular, biochemistry, heart, pdgfbb, binding, inhibits, dong, function, information, log, journal, research,
Topics {✒️}
tgf-β control element nf-kappab regulating cell cycle month download article/chapter protein kinase c-delta p15 transcription factors erk-dependent rna turn yan liu & bin zheng pro-proliferative factor klf5 pdgf-bb promoted pdgf-bb represses cell-cell adhesion cell growth autocrine growth mechanisms full article pdf related subjects signaling-mediated modification privacy choices/manage cookies tgf-beta adenovirus-mediated overexpression klf1 impair expression matrix metalloproteinase expression embryonic stem cells cell proliferation article shi klf5-dependent manner c-jun leading actin cytoskeleton remodeling hebei medical university decreased neointimal formation check access instant access european economic area oncogenic regulator set dna-binding domain cis-dna elements drosophila double-parked zhongshan east road article molecular stimulating hhlim binding conditions privacy policy sm22{alpha} promoter reverse hhlim function sui-bing miao bin zheng accepting optional cookies jin-kun wen cellular biochemistry aims mechanistic studies suggested atra activates
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headline:KLF5 and hhLIM cooperatively promote proliferation of vascular smooth muscle cells
description:Krüppel-like factor 5 (KLF5) plays an important role in cellular proliferation and differentiation. In this study, we show that adenovirus-mediated overexpression of KLF5 increased neointimal formation, while human heart LIM protein (hhLIM) decreased neointimal formation following vascular injury. Interestingly, neointimal formation was significantly increased in the animals where both hhLIM and KLF5 were introduced, suggesting that KLF5 can reverse hhLIM function in cell proliferation on the coexpression with hhLIM. These results were also confirmed the cellular level. Further mechanistic studies suggested that PDGF-BB promoted the interaction between hhLIM and KLF5 through stimulating hhLIM binding to TGF-β control element (TCE) on the cyclin E promoter in a KLF5-dependent manner. Failure of KLF5 binding to the TCE, on the knockdown of KLF5 by transfecting siRNA, not only prevented the recruitment of hhLIM to the cyclin E promoter but also affected activation of the cyclin E promoter by KLF5. These data suggest that KLF5 reverses hhLIM function from anti-proliferation to pro-proliferation through its interaction with hhLIM on the cyclin E promoter.
datePublished:2012-05-15T00:00:00Z
dateModified:2012-05-15T00:00:00Z
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KLF5
PDGF-BB
hhLIM
VSMC
TGF-β control element
Biochemistry
general
Cardiology
Cancer Research
Medical Biochemistry
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headline:KLF5 and hhLIM cooperatively promote proliferation of vascular smooth muscle cells
description:Krüppel-like factor 5 (KLF5) plays an important role in cellular proliferation and differentiation. In this study, we show that adenovirus-mediated overexpression of KLF5 increased neointimal formation, while human heart LIM protein (hhLIM) decreased neointimal formation following vascular injury. Interestingly, neointimal formation was significantly increased in the animals where both hhLIM and KLF5 were introduced, suggesting that KLF5 can reverse hhLIM function in cell proliferation on the coexpression with hhLIM. These results were also confirmed the cellular level. Further mechanistic studies suggested that PDGF-BB promoted the interaction between hhLIM and KLF5 through stimulating hhLIM binding to TGF-β control element (TCE) on the cyclin E promoter in a KLF5-dependent manner. Failure of KLF5 binding to the TCE, on the knockdown of KLF5 by transfecting siRNA, not only prevented the recruitment of hhLIM to the cyclin E promoter but also affected activation of the cyclin E promoter by KLF5. These data suggest that KLF5 reverses hhLIM function from anti-proliferation to pro-proliferation through its interaction with hhLIM on the cyclin E promoter.
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PDGF-BB
hhLIM
VSMC
TGF-β control element
Biochemistry
general
Cardiology
Cancer Research
Medical Biochemistry
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