Abstract
The present review focuses primarily on the studies we made in recent years to improve the understanding of the molecular mechanisms of PGF2alpha-induced hypertrophy of Vascular Smooth Muscle Cells (VSMC). In this review, we will summarize the recent findings in the context of the PGF2alpha signaling pathway in three parts: PGF2alpha binding to its receptor, transactivation of EGF receptor, two independent signaling transduction pathways increasing the expression of NOX1 gene.
MeSH terms
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Activating Transcription Factor 1 / physiology
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Animals
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Dinoprost / metabolism
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Dinoprost / physiology*
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ErbB Receptors / genetics
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Gene Expression Regulation
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Humans
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Hypertrophy
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MADS Domain Proteins / physiology
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MEF2 Transcription Factors
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Muscle, Smooth, Vascular / cytology*
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Muscle, Smooth, Vascular / pathology*
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Myogenic Regulatory Factors / physiology
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NADPH Oxidase 1
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NADPH Oxidases / genetics
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Phosphatidylinositol 3-Kinases / physiology
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Protein Kinase C-delta / physiology
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Receptors, Prostaglandin / metabolism
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Signal Transduction / physiology*
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Superoxides / metabolism
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Transcriptional Activation
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Up-Regulation
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src-Family Kinases / physiology
Substances
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Activating Transcription Factor 1
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MADS Domain Proteins
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MEF2 Transcription Factors
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MEF2B protein, human
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Myogenic Regulatory Factors
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Receptors, Prostaglandin
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prostaglandin F2alpha receptor
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Superoxides
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Dinoprost
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NADPH Oxidase 1
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NADPH Oxidases
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NOX1 protein, human
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Phosphatidylinositol 3-Kinases
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ErbB Receptors
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src-Family Kinases
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Protein Kinase C-delta