Cortisol up-regulates corticotropin releasing factor gene expression in the fetal ovine brainstem at 0.70 gestation

Keiger, C. Jane; O'Steen, W. Keith; Brewer, Gary; Sorci‐Thomas, Mary G.; Zehnder, Timothy J.; Rose, James C.

doi:10.1016/0169-328x(95)00061-v

Cited by 8 publications

(3 citation statements)

References 49 publications

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“…Again, subtle differences in stress paradigms, in CRH hnRNA kinetics or in mRNA stability may account for these discrepancies. Among these, differential effects of age and stress on processing of RNA species provide an attractive mechanism: Age related changes in the rate of mRNA degradation have been noted [18]. This may occur due to differential use of the multiple stop codons in the CRH gene, or different lengths of the poly A+ tail [1,25].…”

Section: Discussionmentioning

confidence: 99%

Rapid phosphorylation of the CRE binding protein precedes stress-induced activation of the corticotropin releasing hormone gene in medial parvocellular hypothalamic neurons of the immature rat

Chen¹,

Hatalski²,

Brunson³

et al. 2001

Molecular Brain Research

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The mechanisms of the molecular and neuroendocrine responses to stress in the immature rat have been a focus of intense investigation. A principal regulator of the these responses in both mature and developing rat is the neuropeptide corticotropin releasing hormone (CRH), and levels of hypothalamic CRH mRNA are enhanced by stress. In vitro, transcription of the CRH gene is governed by binding of the phosphorylated form of cAMP responsive element binding protein (pCREB) to the promoter. Here we tested the hypothesis that rapid, stress-induced CRH transcription occurred during the first two postnatal weeks, and is associated with pCREB expression. The time-course of induction of unedited, heteronuclear CRH RNA (CRH hnRNA) was examined in hypothalamic paraventricular nucleus (PVN) of immature rats subjected to both modest and strong acute stressors using in situ hybridization; pCREB abundance was determined in individual neurons in specific PVN sub-nuclei using immunocytochemistry and unbiased quantitative analysis. CRH hnRNA signal was negligible in PVN of immature rats sacrificed under stress-free conditions, but was readily detectable within 2 min, and peaked at 15 min, in PVN of stressed animals. Enhanced pCREB immunoreactivity was evident within 2 min of stress onset, and was enhanced specifically in stress-responsive, CRH-expressing medial parvocellular neurons. These data support the notion that, already during early postnatal life, stress induces rapid CREB phosphorylation, interaction of pCREB-containing transcription complexes with the CRE element of the CRH gene promoter, and initiation of CRH hnRNA production in stress-responsive neurons of rat PVN.

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Section: Discussionmentioning

confidence: 99%

Rapid phosphorylation of the CRE binding protein precedes stress-induced activation of the corticotropin releasing hormone gene in medial parvocellular hypothalamic neurons of the immature rat

Chen¹,

Hatalski²,

Brunson³

et al. 2001

Molecular Brain Research

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“…Fetal plasma cortisol levels were chronically elevated at 70% of gestation (100 days) to physiological levels found at 90% of gestation, when glucocorticoid-induced maturational changes are known to occur in the HPA axis. Cortisol treatment increase CRF mRNA levels 3.5-fold in the medulla oblongata of fetuses, indicating that cortisol up-regulates CRF gene expression at 70% of gestation in the fetal ovine brainstem (Keiger et al, 1995). …”

Section: Functional Development Of the Fetal Brain Rasmentioning

confidence: 99%

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Mao

Shi

et al. 2009

Progress in Neurobiology

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Since the concept of fetal origins of adult diseases was introduced in 1980s, the development of the renin-angiotensin system (RAS) in normal and abnormal patterns has attracted attention. Recent studies have shown the importance of the fetal RAS in both prenatal and postnatal development. This review focuses on the functional development of the fetal brain RAS, and ontogeny of local brain RAS components in utero. The central RAS plays an important role in the control of fetal cardiovascular responses, body fluid balance, and neuroendocrine regulation. Recent progress has been made in demonstrating that altered fetal RAS development as a consequence of environmental insults may impact on "programming" of hypertension later in life. Given that the central RAS is of equal importance to the peripheral RAS in cardiovascular regulation, studies on the fetal brain RAS development in normal and abnormal patterns could shed light on "programming" mechanisms of adult cardiovascular diseases in fetal origins.

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“…Recently we reported the presence of all CRF family members in human fetal lungs during development, 31 while CRFR1 mRNA had previously been found in human fetal adrenals. 32 In animal fetal tissues, studies have reported the presence of CRF family members centrally in the rat and ovine hypothalamus, 33,34 in the ovine pituitary, 35 hippocampal-amygdala complex, frontal cerebral cortex (FCC) and brainstem 36 and in the mouse cerebellum. 37 In the periphery, the CRF family was detected in the rat fetal pancreas and GI tract 38 and in the fetal ovine 39 and sheep colon.…”

mentioning

confidence: 99%

Corticotropin-releasing factor (CRF) system localization in human fetal heart

Chouridou

Lambropoulou

Koureta

et al. 2016

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oBJectIVe: the corticotropin-releasing factor (cRf) family consists of the neuropeptides cRf, ucn I, II and III and the binding sites cRfR1, cRfR2 and cRf-BP. It regulates stress response and the homeostasis of an organism. In this study, we examined the presence of the cRf system in the human hearts of normal and pathological fetuses. desIGn: Heart tissues from 40 archival human fetuses were divided into Group A (without pathology, 'normal'), Group B (with chromosomal abnormalities) and Group c (with congenital disorders). Immunohistochemistry was used to localize the cRf system. Results correlated to gestational trimester and pathology. ResuLts: Immunoreactivity for all antigens was found in cardiac myocytes of all groups, in almost all samples, except ucn III which was present in almost half of the fetuses of Groups B and c and was not detected at all in Group A. ucn III was more often present during the earlier stage of development (<21weeks) and in fetuses with congenital disorders. In a fetus diagnosed with heart pathology, all but ucn III antigens were also present. concLusIons: we localized a complete cRf system in the human fetal heart and correlated the presence of ucn III to development and pathology. More studies are needed to verify and clarify the exact role of the cRf system in the human fetal heart.

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Cortisol up-regulates corticotropin releasing factor gene expression in the fetal ovine brainstem at 0.70 gestation

Cited by 8 publications

References 49 publications

Rapid phosphorylation of the CRE binding protein precedes stress-induced activation of the corticotropin releasing hormone gene in medial parvocellular hypothalamic neurons of the immature rat

Rapid phosphorylation of the CRE binding protein precedes stress-induced activation of the corticotropin releasing hormone gene in medial parvocellular hypothalamic neurons of the immature rat

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Corticotropin-releasing factor (CRF) system localization in human fetal heart

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