• Made available online as an Accepted Preprint 3 December 2008
  • Accepted Preprint first posted online on 3 December 2008

Mechanisms of adrenal gland growth: signal integration by extracellular signal regulated kinases1/2

  1. Maximilian Bielohuby1
  1. Laboratory of Mouse Genetics, Research Unit Genetics and Biometry, Research Institute for the Biology of Farm Animals, FBN Dummerstorf, Wilhelm-Stahl-Allee 2, 18196 Dummerstorf, Germany1Neuroendocrine Unit, Medizinische Klinik Innenstadt, Ludwig Maximilians University, 80336 Munich, Germany
  1. (Correspondence should be addressed to A Hoeflich; Email: hoeflich{at}fbn-dummerstorf.de)

Abstract

The adrenal gland influences a multitude of processes during stress response, but also potently affects the immune system, glucose metabolism, electrolyte or water homeostasis, and cardiovascular functions. According to the present understanding, the adrenal cortex is tightly controlled by the hypothalamic–pituitary–adrenal axis. This axis involves hypothalamic CRH and pituitary ACTH which determine processes of adrenocortical growth and function. However, control of the adrenal gland comprises a plethora of additional endogenous or exogenous factors. Among those are diverse hormones, psychosocial parameters, physiological stress, secondary plant products, or even environmental pollutants. In the present review, we summarize the current view of endocrine growth control in the adrenal gland. We then discuss intracellular mechanisms of adrenal growth control and focus on extracellular signal regulated kinases 1/2 (ERK1/2), which have been demonstrated to be controlled by not only ACTH or angiotensin II, but also by a large number of additional effectors. On the basis of these multiple exogenous or endogenous factors which impact on the adrenal gland through ERK1/2 activity, we speculate on a mechanism by which ERK1/2 act as a central integrative growth regulatory elements in the adrenal gland.

  • Revision received 27 November 2008
  • Accepted 2 December 2008
| Table of Contents