55: Regulation of steroid sulfate transporters in human placenta during various pregnancy related disease states and their impact on estrogen synthesis pathway

2008 ◽  
Vol 199 (6) ◽  
pp. S25
Author(s):  
Clifford Mason ◽  
Catalin Buhimschi ◽  
Irina Buhimschi ◽  
Peter Swaan ◽  
Carl P. Weiner
2004 ◽  
Vol 89-90 ◽  
pp. 187-193 ◽  
Author(s):  
André G. Uitterlinden ◽  
Yue Fang ◽  
Joyce B.J. van Meurs ◽  
Hans van Leeuwen ◽  
Huibert A.P. Pols

Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 2012-2022 ◽  
Author(s):  
Wangsheng Wang ◽  
Jianneng Li ◽  
Yuchun Ge ◽  
Wenjiao Li ◽  
Qun Shu ◽  
...  

One of the dominant effects of glucocorticoids in triggering parturition in certain animal species is to drive the placental conversion of progesterone to estrogen. However, in the human placenta, estrogen is formed using dehydroepiandrosterone from the fetal adrenal glands rather than progesterone as precursor. Although aromatization of dehydroepiandrosterone is crucial in estrogen synthesis in human placenta, it is not known whether glucocorticoids affect aromatase expression. Human term placental syncytiotrophoblasts were used to examine the effect of cortisol on aromatase expression. The signaling pathway and transcription factors involved were identified in this study. Results showed that cortisol induced aromatase expression in a concentration-dependent manner, which was mediated indirectly by glucocorticoid receptor and required the participation of other proteins. The induction of aromatase by cortisol could be blocked by either specificity protein 1 (Sp1) antagonist mithramycin or knockdown of Sp1 expression. The induction of aromatase and Sp1 by cortisol could be prevented by inhibitors of the cAMP pathway, whereas activators of the cAMP pathway induced Sp1 and aromatase expression as well as Sp1 binding to aromatase promoter. Concomitantly, cortisol treatment and activation of the cAMP pathway led to increased acetylation and decreased methylation of histone 3 at the aromatase promoter. In conclusion, cortisol stimulates aromatase expression through the cAMP/Sp1 pathway in human placental syncytiotrophoblasts. These findings reveal a novel role of cortisol in increasing the local level of estrogen within the placenta that would help transform the myometrium to a contractile state, thereby contributing to a cascade of events leading to human parturition.


Stress ◽  
2020 ◽  
Vol 23 (6) ◽  
pp. 615-616
Author(s):  
Daniela Jezova ◽  
James P. Herman

2020 ◽  
Vol 8 ◽  
pp. 205031212093546
Author(s):  
Theresa J Barnes ◽  
Maxwell A Hockstein ◽  
Craig S Jabaley

Cardiovascular disease remains the leading cause of death in the United States, and cardiopulmonary bypass is a cornerstone in the surgical management of many related disease states. Pathophysiologic changes associated both with extracorporeal circulation and shock can beget a syndrome of low systemic vascular resistance paired with relatively preserved cardiac output, termed vasoplegia. While increased vasopressor requirements accompany vasoplegia, related pathophysiologic mechanisms may also lead to true catecholamine resistance, which is associated with further heightened mortality. The introduction of a second non-catecholamine vasopressor, angiotensin II, and non-specific nitric oxide scavengers offers potential means by which to manage this challenging phenomenon. This narrative review addresses both the definition, risk factors, and pathophysiology of vasoplegia and potential therapeutic interventions.


Author(s):  
Stanley M. Gartler ◽  
R. Scott Hansen ◽  
Vinzenz Oji ◽  
Heiko Traupe ◽  
Julia Horn ◽  
...  

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Huaping Xu ◽  
Xiaoyun Shi ◽  
Xin Li ◽  
Jiexin Zou ◽  
Chunyan Zhou ◽  
...  

AbstractThe existence of the neural control of mast cell functions has long been proposed. Mast cells (MCs) are localized in association with the peripheral nervous system (PNS) and the brain, where they are closely aligned, anatomically and functionally, with neurons and neuronal processes throughout the body. They express receptors for and are regulated by various neurotransmitters, neuropeptides, and other neuromodulators. Consequently, modulation provided by these neurotransmitters and neuromodulators allows neural control of MC functions and involvement in the pathogenesis of mast cell–related disease states. Recently, the roles of individual neurotransmitters and neuropeptides in regulating mast cell actions have been investigated extensively. This review offers a systematic review of recent advances in our understanding of the contributions of neurotransmitters and neuropeptides to mast cell activation and the pathological implications of this regulation on mast cell–related disease states, though the full extent to which such control influences health and disease is still unclear, and a complete understanding of the mechanisms underlying the control is lacking. Future validation of animal and in vitro models also is needed, which incorporates the integration of microenvironment-specific influences and the complex, multifaceted cross-talk between mast cells and various neural signals. Moreover, new biological agents directed against neurotransmitter receptors on mast cells that can be used for therapeutic intervention need to be more specific, which will reduce their ability to support inflammatory responses and enhance their potential roles in protecting against mast cell–related pathogenesis.


Author(s):  
Anne F. Bushnell ◽  
Sarah Webster ◽  
Lynn S. Perlmutter

Apoptosis, or programmed cell death, is an important mechanism in development and in diverse disease states. The morphological characteristics of apoptosis were first identified using the electron microscope. Since then, DNA laddering on agarose gels was found to correlate well with apoptotic cell death in cultured cells of dissimilar origins. Recently numerous DNA nick end labeling methods have been developed in an attempt to visualize, at the light microscopic level, the apoptotic cells responsible for DNA laddering.The present studies were designed to compare various tissue processing techniques and staining methods to assess the occurrence of apoptosis in post mortem tissue from Alzheimer's diseased (AD) and control human brains by DNA nick end labeling methods. Three tissue preparation methods and two commercial DNA nick end labeling kits were evaluated: the Apoptag kit from Oncor and the Biotin-21 dUTP 3' end labeling kit from Clontech. The detection methods of the two kits differed in that the Oncor kit used digoxigenin dUTP and anti-digoxigenin-peroxidase and the Clontech used biotinylated dUTP and avidinperoxidase. Both used 3-3' diaminobenzidine (DAB) for final color development.


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