The role of insulin-like growth factor-I and growth factor-associated signal transduction pathways in estradiol and progesterone facilitation of female reproductive behaviors

Etgen, Anne M.; González‐Flores, Oscar; Todd, Brigitte J.

doi:10.1016/j.yfrne.2006.06.001

Cited by 49 publications

(42 citation statements)

References 141 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is wellestablished that IGF-1 and sex steroids are interconnected in the brain. Cross-talk between those compounds have been described in reproductive tissues and the CNS (Etgen et al, 2006;Quesada et al, 2008). Most importantly, such mutual reactions have been shown to play a critical role in the inhibition of damaging processes and neuroprotection in the brain (Garcia-Segura et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

17β‐estradiol and progesterone prevent cuprizone provoked demyelination of corpus callosum in male mice

Ács

Kipp

Norkutė

et al. 2008

Glia

177

134

View full text Add to dashboard Cite

Sex hormones, for example, estrogen and progesterone, are thought to affect and delay progression of multiple sclerosis (MS) in pregnant women. Although both steroid hormones are neuroprotective in the brain and elevated during pregnancy, only estrogen was tested in clinical trials. To evaluate the role of 17beta-estradiol (E) and progesterone (P) in prevention demyelination, young adult male mice were fed with cuprizone for a defined time interval and simultaneously treated with steroids by repeated injections into the neck region. The status of myelination was analyzed by magnetic resonance imaging and conventional histological staining. The individual application of E and P resulted only in a moderate prevention of demyelination in the corpus callosum (CC). The combined treatment with both steroid hormones counteracted the process of demyelination. Expression of the mature (PLP and MBP) and premature (PDGF-alpha-R) oligodendrocyte markers were significantly increased after hormone application in the affected CC. In addition, both hormones stimulated astrogliosis and the expression of IGF-1. Microglial invasion in demyelinated CC was pronounced and additionally localized in the midline of CC after hormone treatment. These data show that sex steroids can protect the brain from demyelination and stimulate remyelination. It appears that only the administration of both hormones is fully effective. The beneficial steroid effect requires interactions with oligodendrocytes possibly by preventing their degeneration or recruitment from precursor cells which are stimulated to remyelinated fibers. The positive hormonal influence on myelination in the CNS may be a future therapeutically strategy for the treatment of MS.

show abstract

Section: Discussionmentioning

confidence: 99%

17β‐estradiol and progesterone prevent cuprizone provoked demyelination of corpus callosum in male mice

Ács

Kipp

Norkutė

et al. 2008

Glia

177

134

View full text Add to dashboard Cite

show abstract

“…My laboratory and others have shown that IGF-1 regulates GnRH release and gene expression, and that this is subject to developmental regulation [74,75,37]. The IGF-1 system is also steroid sensitive [75,48,101]. Moreover, GnRH neurons co-express both IGF-1 and IGF-1 receptors [37,38] suggesting the possibility of autocrine regulation of cells co-expressing GnRH and IGF-1 via the IGF-1 receptor.…”

Section: Other Hypothalamic Neurotransmitter and Neurotrophic Factor mentioning

confidence: 99%

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Gore¹

2008

Frontiers in Neuroendocrinology

231

122

View full text Add to dashboard Cite

The ability of a species to reproduce successfully requires the careful orchestration of developmental processes during critical time points, particularly the late embryonic and early postnatal periods. This article begins with a brief presentation of the evidence for how gonadal steroid hormones exert these imprinting effects upon the morphology of sexually differentiated hypothalamic brain regions, the mechanisms underlying these effects, and their implications in adulthood. Then, I review the evidence that aberrant exposure to hormonally-active substances such as exogenous endocrine-disrupting chemicals (EDCs), may result in improper hypothalamic programming, thereby decreasing reproductive success in adulthood. The field of endocrine disruption has shed new light on the discipline of basic reproductive neuroendocrinology through studies on how early life exposures to EDCs may alter gene expression via non-genomic, epigenetic mechanisms, including DNA methylation and histone acetylation. Importantly, these effects may be transmitted to future generations if the germline is affected via transgenerational, epigenetic actions. By understanding the mechanisms by which natural hormones and xenobiotics affect reproductive neuroendocrine systems, we will gain a better understanding of normal developmental processes, as well as to develop the potential ability to intervene when development is disrupted.

show abstract

“…In addition to be a hormonal signal that acts in the brain to control neuroendocrine secretions and reproduction (Pfaff, 1989;Etgen et al, 2006;Beyer, 2007), progesterone is a local paracrine factor synthesized by neural cells (Garcia-Segura and Melcangi, 2006). Furthermore, progesterone is metabolized in the nervous system to the neuroactive steroids dihydroprogesterone (DHP) and tetrahydroprogesterone (THP) via the enzymatic complex formed by the 5a-reductase and the 3a-hydroxysteroid dehydrogenase (Melcangi et al, 2008).…”

mentioning

confidence: 99%

“…Growth factors, including vascular endothelial growth factor (VEGF; Swiatek-De Lange et al, 2007), brain-derived neurotrophic factor (BDNF; Gonzalez et al, 2004Gonzalez et al, , 2005De Nicola et al, 2006;Gonzalez Deniselle et al, 2007;Kaur et al, 2007), and insulin/insulin-like growth factor-I (IGF-I; Dueñas et al, 1994;Jung-Testas et al, 1994;Cardona-Gómez et al, 2000;Etgen, 2003;El-Bakri et al, 2004;Etgen et al, 2006) are involved in the mechanisms of action of progesterone in the central nervous system. Progesterone regulates the function of the retina by increasing the expression of vascular endothelial growth factor (VEGF) by Muller glial cells (Swiatek-De Lange et al, 2007) and induces the expression of BDNF in ventral horn motoneurons from rats with spinal cord injury (Gonzalez et al, , 2005De Nicola et al, 2006), in motoneurons of Wobbler mouse (Gonzalez Deniselle et al, 2007), a model of motoneuron degeneration, and in organotypic explants of the cerebral cortex (Kaur et al, 2007).…”

mentioning

confidence: 99%

Regulation of the phosphoinositide‐3 kinase and mitogen‐activated protein kinase signaling pathways by progesterone and its reduced metabolites in the rat brain

Guerra‐Araiza

Amorim

Pinto‐Almazán

et al. 2008

J of Neuroscience Research

View full text Add to dashboard Cite

Several growth factors, such as vascular endothelial growth factor, brain-derived neurotrophic factor, and insulin-like growth factor-I are involved in the actions of progesterone in the central nervous system. Previous studies in neuronal and glial cultures have shown that progesterone may regulate growth factor signaling, increasing the phosphorylation of extracellular-signal regulated kinase (ERK) and the phosphorylation of Akt, components of the mitogen-activated protein kinase (MAPK) and the phosphoinositide-3 kinase (PI3K) signaling pathways, respectively. In this study, we have evaluated whether progesterone and its reduced metabolites, dihydroprogesterone and tetrahydroprogesterone, regulate PI3K and MAPK signaling in the brain of ovariectomized rats in vivo. Significant increases in the phosphorylation of ERK, in the expression of the catalytic (p110) and the regulatory (p85) subunits of PI3K and in the phosphorylation of Akt were observed in the hypothalamus, the hippocampus, and the cerebellum 24 hr after progesterone administration. Progesterone metabolites partially mimicked the effect of progesterone and had a stronger effect on MAPK and PI3K signaling in the hypothalamus than in the other brain regions. These findings suggest that progesterone regulates MAPK and PI3K signaling pathways in the central nervous system in vivo by direct hormonal actions and by mechanisms involving progesterone metabolites.

show abstract

The role of insulin-like growth factor-I and growth factor-associated signal transduction pathways in estradiol and progesterone facilitation of female reproductive behaviors

Cited by 49 publications

References 141 publications

17β‐estradiol and progesterone prevent cuprizone provoked demyelination of corpus callosum in male mice

17β‐estradiol and progesterone prevent cuprizone provoked demyelination of corpus callosum in male mice

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Regulation of the phosphoinositide‐3 kinase and mitogen‐activated protein kinase signaling pathways by progesterone and its reduced metabolites in the rat brain

Contact Info

Product

Resources

About