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Keywords:

  • prostate gland;
  • seminal vesicles;
  • branching morphogenesis;
  • androgens;
  • testosterone;
  • AR;
  • FGF10;
  • FGF7;
  • FGFR2;
  • SHH;
  • IHH;
  • PTC;
  • SMO;
  • TGFβ;
  • BMP4;
  • BMP7;
  • GDF7;
  • GHR;
  • GLI2;
  • HOXA10;
  • HOXA13;
  • HOXD13;
  • IGF1;
  • INHBA;
  • NKX3.1;
  • SFRP1;
  • SRD5A2

Abstract The prostate gland and seminal vesicles are the major exocrine glands in the male reproductive tracts of mammals. Although the morphology of these organs varies widely among species, epithelial branching morphogenesis is a key feature of organ development in most mammals including rodents and humans. Insight into the mechanisms that control prostatic and seminal vesicle branching morphogenesis has come from experimental embryological work as well as from the study of mice and humans harboring mutations that alter branching morphogenesis. These studies have demonstrated a requirement for androgens to initiate branching morphogenesis as well as a role for androgens in sustaining the normal rate and extent of branching. In addition, these studies have revealed a series of reciprocal paracrine signals between the developing prostatic epithelium and prostatic mesenchyme that are essential for regulating branching morphogenesis. Key growth factors that participate in these signaling events include members of the fibroblast growth factor, Hedgehog, and transforming growth factor-β families. Additional genes including several homeobox-containing transcription factors have also been implicated as key regulators of prostatic and seminal vesicle branching morphogenesis. While research in recent years has greatly enhanced our understanding of the molecular control of prostatic and seminal vesicle development, known genes cannot yet explain in molecular terms the complex biological interactions that descriptive and experimental embryological studies have elucidated in the control of branching morphogenesis in these organs.