Genomic and non-genomic actions of sex steroids in the growth plate

Abstract

Sex steroids, and particularly estrogens, are important regulators of bone growth and bone mass accrual. For a long time, it was thought that these effects were mainly caused by their modulatory effects on the somatotrophic axis. Data gathered in the past years have challenged this view and it is now widely accepted that many of the effects of sex steroids on growth and bone mass accrual are caused by direct effects on target cells in the growth plate and bone. This review summarizes and discusses some of our latest findings on the expression of sex steroid receptors in the growth plate, the source of the ligands activating these receptors, and their putatitive mechanism of action predominantly focusing on observations in the rat.

Bone and the Kidney: A Systems Biology Approach to the Molecular Mechanisms of Renal Osteodystrophy

“…Some of the paracrine effectors such as osteoprotegerin (OPG) and osteoprotegerin ligand (OPGL, or RANKL for receptor activator of NF-κB ligand) also act in a systemic manner [13], which has led to the hope that systemic OPG may be used as a therapy against bone loss [14,15]. The effects of hormones such as thyroid hormones, sex steroids and parathyroid hormone (PTH), have been well documented since the 1970s (see [16][17][18][19] for recent reviews). The current understanding is that systemic and local regulation act in a synergistic manner [20].…”

Leptin regulates estrogen receptor gene expression in ATDC5 cells through the extracellular signal regulated kinase signaling pathway

“…Estrogen plays a crucial role in the regulation of longitudinal bone growth. In humans, estrogen is responsible for the initiation of the pubertal growth spurt and closure of the growth plate in both sexes [Karperien et al, 2005; Perry et al, 2008]. The direct effects of estrogen are mediated through two known nuclear receptors, namely estrogen receptor‐α (ERα) and ‐β (ERβ).…”

Aspectos moleculares dos esteroides sexuais sobre a cartilagem e os ossos

“…A vitamina D e o PTH estimulam a atividade dos osteoclastos enquanto a calcitonina inibe. Os oncógenes c-fos e c-myc são expressos na proliferação dos osteoblastos 5,6 .…”

“…Apresentam várias funções, assim como os estrogênios, já que são precursores destes, como: aumentar a atividade dos osteoblastos, inibir a retirada de cálcio do organismo ao diminuir a formação e atividade dos osteoclastos, estimular o crescimento longitudinal dos ossos longos na puberdade, assim como causando a ossificação do disco epifisário. Com a diminuição da secreção desse hormônio sexual, a atividade osteoclástica é maior do que a osteoblástica, reduzindo potencialmente a formação óssea 6,7 .…”