Accepted Preprint first posted online on 3 December 2008
Journal of Molecular Endocrinology 2009;42:191.
Journal of Molecular Endocrinology (2008) In press DOI: 10.1677/JME-08-0160
© 2008 Society for Endocrinology
Mechanisms of adrenal gland growth - signal integration by ERK1/2
Andreas Hoeflich and
Max Bielohuby
A Hoeflich, Laboratory of Mouse Genetics, Research Unit Genetics and Biometry, Research Institute for the Biology of Farm Animals, FBN Dummerstorf, Dummerstorf, Germany
M Bielohuby, Neuroendocrine Unit, Medizinische Klinik Innenstadt, Ludwig Maximilians University, Munich, Germany
Correspondence: Andreas 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 (HPA) axis. This axis involves hypothalamic corticotropin releasing hormone (CRH) and pituitary adrenocorticotropic hormone (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 ERK1/2, which has been demonstrated to be controlled by 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 acts as a central integrative growth regulatory element in the adrenal gland.
Copyright © 2008 by the Society for Endocrinology.