A connection between extracellular matrix and hormonal signals during the development of the human fetal adrenal gland

Abstract

The human adrenal cortex, involved in adaptive responses to stress, body homeostasis and secondary sexual characters, emerges from a tightly regulated development of a zone-specific secretion pattern during fetal life. Its development during fetal life is critical for the well being of pregnancy, the initiation of delivery, and even for an adequate adaptation to extra-uterine life. As early as from the sixth week of pregnancy, the fetal adrenal gland is characterized by a highly proliferative zone at the periphery, a concentric migration accompanied by cell differentiation (cortisol secretion) and apoptosis in the central androgen-secreting fetal zone. After birth, a strong reorganization occurs in the adrenal gland so that it better fulfills the newborn's needs, with aldosterone production in the external zona glomerulosa, cortisol secretion in the zona fasciculata and androgens in the central zona reticularis. In addition to the major hormonal stimuli provided by angiotensin II and adrenocorticotropin, we have tested for some years the hypotheses that such plasticity may be under the control of the extracellular matrix. A growing number of data have been harvested during the last years, in particular about extracellular matrix expression and its putative role in the development of the human adrenal cortex. Laminin, collagen and fibronectin have been shown to play important roles not only in the plasticity of the adrenal cortex, but also in cell responsiveness to hormones, thus clarifying some of the unexplained observations that used to feed controversies.

Testosterone–cortisol dissociation in children exposed to prenatal maternal stress, and relationship with aggression: Project Ice Storm

“…The sensitivity analyses testing potential timing effects suggest that although the effects of maternal subjective distress on the vulnerability of the HPA and HPG axes and at least one behavioral consequence span the entire prenatal period, the second and third trimesters may be particularly vulnerable periods. The second trimester may be a particularly vulnerable period for PNMS to disrupt the relationship between basal testosterone and cortisol response (since the model is weakened without the second trimester exposed), being the time in adrenal gland development when the production of cortisol begins (Chamoux, Otis, & Gallo-Payet, 2005). In contrast, the behavioral consequences in relation to these hormones may be particularly vulnerable to third-trimester exposure, potentially due to changes in neurodevelopment.…”

Genetic Landscape of Sporadic Unilateral Adrenocortical Adenomas Without PRKACA p.Leu206Arg Mutation

“…Interestingly, a putative role for ECM expression has been hypothesized in the development of human adrenal cortex (41). Moreover, a previous transcriptome study on ACAs identified enrichment in genes related to ECM (42).…”

Obesogenic and histopathological effect of monosodium glutamate on the adrenal gland of maternal and postnatal albino rats

“…Also it was established that when human fetal adrenal cells were cultured on collagen-coated dishes, laminin and fibronectin, Collagen IV and laminin enhanced proliferation whereas fibronectin increased cell death (34) . Moreover, another study suggested that centripedal migration of the cells of the adrenal is driven by the extracellular matrix components including collagen, and that the extracellular matrix and the signaling hormones as Angiotensin II and ACTH are noteworthy interconnected and share common pathways involved in adrenal gland activity regulation (35).…”