The Crosstalk between Melatonin and Sex Steroid Hormones.

Melatonin, an indolamine mainly released from the pineal gland, is associated with many biological functions, namely, the modulation of circadian and seasonal rhythms, sleep inducer, regulator of energy metabolism, antioxidant, and anticarcinogenic. Although several pieces of evidence also recognize the influence of melatonin in the reproductive physiology, the crosstalk between melatonin and sex hormones is not clear. Here, we review the effects of sex differences in the circulating levels of melatonin and update the current knowledge on the link between sex hormones and melatonin. Furthermore, we explore the effects of melatonin on gonadal steroidogenesis and hormonal control in females. The literature review shows that despite the strong evidence that sex differences impact on the circadian profiles of melatonin, reports are still considerably ambiguous, and these differences may arise from several factors, like the use of contraceptive pills, hormonal status, and sleep deprivation. Furthermore, there has been an inconclusive debate about the characteristics of the reciprocal relationship between melatonin and reproductive hormones. In this regard, there is evidence for the role of melatonin in gonadal steroidogenesis brought about by research that shows that melatonin affects multiple transduction pathways that modulate Sertoli cell physiology and consequently spermatogenesis, and also estrogen and progesterone production. From the outcome of our research, it is possible to conclude that understanding the correlation between melatonin and reproductive hormones is crucial for the correction of several complications occurring during pregnancy, like preeclampsia, and for the control of climacteric symptoms.

Thyroid Hormones in the Brain and Their Impact in Recovery Mechanisms After Stroke.

Thyroid hormones are of fundamental importance for brain development and essential factors to warrant brain functions throughout life. Their actions are mediated by binding to specific intracellular and membranous receptors regulating genomic and non-genomic mechanisms in neurons and populations of glial cells, respectively. Among others, mechanisms include the regulation of neuronal plasticity processes, stimulation of angiogenesis and neurogenesis as well modulating the dynamics of cytoskeletal elements and intracellular transport processes. These mechanisms overlap with those that have been identified to enhance recovery of lost neurological functions during the first weeks and months after ischemic stroke. Stimulation of thyroid hormone signaling in the postischemic brain might be a promising therapeutic strategy to foster endogenous mechanisms of repair. Several studies have pointed to a significant association between thyroid hormones and outcome after stroke. With this review, we will provide an overview on functions of thyroid hormones in the healthy brain and summarize their mechanisms of action in the developing and adult brain. Also, we compile the major thyroid-modulated molecular pathways in the pathophysiology of ischemic stroke that can enhance recovery, highlighting thyroid hormones as a potential target for therapeutic intervention.

Progesterone enhances transthyretin expression in the rat choroid plexus in vitro and in vivo via progesterone receptor.

Depletion of ovarian hormones 17ß-estradiol (E2) and progesterone (P) after menopause may contribute to the decline in cognitive performance and increases the risk of Alzheimer's disease (AD) in women, striking the importance of understanding the regulation of pivotal proteins involved in AD pathogenesis by ovarian hormones. Transthyretin (TTR) is now recognized as one of such proteins due to its ability to sequester and degrade amyloid ß (Aß) into less harmful peptides and preventing their aggregation. We have previously demonstrated that E2 enhances TTR expression. In this study, we investigate the effects of P on TTR expression in primary cultures of rat choroid plexus epithelial cells and in adult ovariectomized female rats. The results obtained demonstrate that, in vitro and in vivo, TTR is up-regulated by P. In addition, the mechanism underlying the response of TTR to P was investigated, and we provide evidence that this response is achieved through a progesterone receptor-mediated mechanism. Our results reinforce the importance of ovarian hormones on the regulation of TTR, which may reflect on the processing of Aß peptides and consequently on AD onset and progression.