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Hormonal Control of Prostatic Differentiation and Morphogenesis: The Impact of Apoptosis and Steroid Hormone Receptor Expression

  • G. Aumüller
  • P. M. Holterhus
  • W. Eicheler
  • H. Renneberg
  • M. Bacher
  • L. Konrad
  • H. Bonkhoff
  • F. Rauch
  • H. G. Mannherz
Part of the Ernst Schering Research Foundation Workshop book series (SCHERING FOUND, volume 14)

Abstract

Apoptosis or active cell death (Bursch et al. 1992) is a process whereby cells die in response to specific physiological signals. The morphological sequence of events, as described by Kerr et al. (1972; for review, see Wyllie et al. 1980; Fesus et al. 1991; Fesus 1993) appears to be common to most epithelial cells. They require an expenditure of metabolic energy, active gene expression, and protein biosynthesis. Histologically, the process is characterized by cell shrinking to the extent that they pull away from neighboring cells and the basement membrane, undergoing both nuclear and cytoplasmic condensation. The latter results in the formation of the so-called apoptotic bodies, thought to require increased expression of tissue transglutaminase (Piacentini et al. 1991; Fukuda et al. 1993). Apoptotic bodies are sequestered either by neighboring cells or macrophages, thereby escaping access to the immune system. Chromatin condensation is thought to result from activation of an endogenous Ca2+, Mg2+-dependent endonuclease. Internucleosomal DNA is preferentially digested, resulting in a visual “ladder” of DNA fragments in multimers of 180 base pair units upon electrophoresis, which can be visualized in situ by means of the so-called terminal transferase reaction (Gavrieli et al. 1992).

Keywords

Androgen Receptor Benign Prostatic Hyperplasia Ventral Prostate Prostatic Epithelium Active Cell Death 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1995

Authors and Affiliations

  • G. Aumüller
  • P. M. Holterhus
  • W. Eicheler
  • H. Renneberg
  • M. Bacher
  • L. Konrad
  • H. Bonkhoff
  • F. Rauch
  • H. G. Mannherz

There are no affiliations available

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