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Docosahexaenoic Acid Improves the Nitroso-Redox Balance and Reduces VEGF-Mediated Angiogenic Signaling in Microvascular Endothelial Cells

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Keywords
  • <Br/>Purpose
  • Disturbances To The Cellular Production Of Nitric Oxide (No) And Superoxide (O2-) Can Have Deleterio
  • Dietary Agents That Could Modulate The Production Of These Signaling Molecules From Their Likely Enz
  • Endothelial Nitric Oxide Synthase (Enos) And Nadph Oxidase
  • Would Therefore Have A Major Beneficial Effect On Retinal Vascular Disease
  • The Effect Of ?-3 Polyunsaturated Fatty Acids (Pufas) On Angiogenic Signaling And No/Superoxide Prod
  • <Br/><Br/>Methods
  • Primary Rmecs Were Treated With Docosahexaenoic Acid (Dha) Or Eicosapentaenoic Acid (Epa) For 48 Hou
  • Rmec Migration Was Determined By Scratch-Wound Assay
  • Proliferation By The Incorporation Of Brdu
  • And Angiogenic Sprouting Using A Three-Dimensional Model Of In Vitro Angiogenesis
  • No Production Was Quantified By Griess Assay
  • And Phospho-Enos Accumulation And Superoxide Were Measured Using The Fluorescent Probe Dihydroethidi
  • Enos Localization To Caveolin-Rich Microdomains Was Determined By Western Blot Analysis After Subfra
  • <Br/><Br/>Results
  • Dha Treatment Increased Nitrite And Decreased Superoxide Production
  • Which Correlated With The Displacement Of Enos From Caveolar Subdomains And Colocalization With The
  • In Addition
  • Both ?-3 Pufas Demonstrated Reduced Responsiveness To Vegf-Stimulated Superoxide And Nitrite Release
  • Proliferation
  • And Angiogenic Sprout Formation
  • <Br/><Br/>Conclusions
  • Dha Improves No Bioavailability
  • Decreases O2- Production
  • And Blunts Vegf-Mediated Angiogenic Signaling
  • These Findings Suggest A Role For ?-3 Pufas
  • Particularly Dha
  • In Maintaining Vascular Integrity While Reducing Pathologic Retinal Neovascularization
Disciplines
  • Biology

Abstract

Chapter 2 Androgen Action During Prostate Carcinogenesis Diping Wang and Donald J. Tindall Abstract Androgens are critical for normal prostate development and function, as well as prostate cancer initiation and progression. Androgens function mainly by regulating target gene expression through the androgen receptor (AR). Many studies have shown that androgen-AR signaling exerts actions on key events during prostate carcinogenesis. In this review, androgen action in distinct aspects of prostate carcinogenesis, including (i) cell proliferation, (ii) cell apoptosis, and (iii) prostate cancer metastasis will be discussed. Key words: Androgen receptor, prostate cancer, androgen metabolism, androgen signaling, castration-resistant prostate cancer. 1. Androgen Signaling Androgens are the male sex hormones, which control the differ- entiation and maturation of male reproductive organs, including the prostate gland. Testosterone is the principal androgen in cir- culation and is synthesized by Leydig cells in the testes, under the regulation of luteinizing hormone (LH), which is further regulated by gonadotropin-releasing hormone (GnRH). Adrenal glands also synthesize a small amount of androgens, such as dehy- droepiandrosterone (DHEA) and androstenedione (4-dione) (1). Testosterone enters prostate cells by passive diffusion, where it is converted enzymatically by 5-α reductases to the more potent androgen dihydrotestosterone (DHT) (2). Binding of androgens to the androgen receptor (AR), a ligand-modulated transcrip- tion factor, induces a conformational change in the AR, causing release of heat shock proteins and translocation of the AR to the F. Saatcioglu (ed.), Androgen Action, Methods in Molecular Biology 776, DOI 10.1007/978-1-61779-243-4_2, © Springer Science+Business Media, LLC 2011 25 26 Wang and Tindall nucleus, where it transcriptionally regulates the expression of tar- get genes (3). In addition to the classic genomic effects of sex steroids, accu- mulating

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