Mannheim Classification of Nongenomically Initiated (Rapid) Steroid Action(s)

Falkenstein, Elisabeth; Norman, Anthony W.; Wehling, Martin

doi:10.1210/jcem.85.5.6516

Cited by 105 publications

(65 citation statements)

References 39 publications

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“…Circulating PIBF influenced by P secretion may be an important factor in cellular immune suppression. There are also some recent data that suggest that progesterone may act in an extranuclear (epigenetic or non-genomic) manner to suppress T cell rejection of the fetal semi-allograft [18][19][20]. Other cells, e.g., TH 17 cells, T reg cells, T helper cells, and dendritic cells, may also play a role.…”

Section: Discussionmentioning

confidence: 99%

Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Cohen

Check

Dougherty

2015

J Assist Reprod Genet

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Purpose To determine if exposure to progesterone alone is sufficient to increase the production of the immunomodulatory protein known as the progesterone induced blocking factor (PIBF). Also to determine what method of progesterone delivery or form of P best stimulates PIBF secretion. Methods Serum samples from patients with infertility and paid volunteers were evaluated for both PIBF and progesterone at various times during the follicular phase and the luteal phase in both natural cycles and cycles involving embryo transfer after endogenous and exogenous progesterone exposure and after various synthetic progestins. PIBF was measured by a non-commercial research ELISA assay. Comparisons were made of serum PIBF before and after exposure to progesterone, 17-hydroxyprogesterone, and oral contraceptives. PIBF was also measured before and after transfer of embryos.Results Progesterone alone without exposure to the fetal allogeneic stimulus was able to produce a marked increase in s e r u m P I B F. N e i t h e r a s y n t h e t i c p r o g e s t i n (19-nortestosterone derivative) nor 17-hydroxyprogesterone caused an increase in PIBF. Some PIBF is generally detected even in the follicular phase. Conclusions A previous concept considered that an allogeneic stimulus, e.g., from the fetal semi-allograft, was necessary to induce de novo progesterone receptors in gamma delta T cells, which, in turn, when exposed to a high concentration of progesterone, would secrete high levels of PIBF. These data show that exposure to an allogeneic stimulus is not needed to cause a marked rise in PIBF, merely progesterone alone is sufficient.

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Section: Discussionmentioning

confidence: 99%

Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Cohen

Check

Dougherty

2015

J Assist Reprod Genet

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“…Transcription of genes can be inhibited by GCs via direct interaction between the GCR and negative GRE's, such as the pro-opiomelanocortin, α-fetoprotein and A c c e p t e d M a n u s c r i p t 6 prolactin gene [14]. In line with this notion, is has been shown that glucocorticoids suppress transcription of inflammatory genes, including interleukin (IL)-1 and IL-2, via negative GREs [15,16] (Figure 1, mechanism II). However, the exact role of nGREs in mediating GCinduced effects in cellular systems remains largely unclear.…”

Section: The Classical Genomic Mechanism Of Glucocorticoid Action Is mentioning

confidence: 93%

“…Negative regulation by glucocorticoid/glucocorticoid receptor complexes results in reduced transcriptional activities of GCR target genes [19][20][21][22][23], leading to anti-inflammatory and immune-suppressive effects [24]. In this way glucocorticoids inhibit nuclear translocation and the function of several pro- However, some of the immunosuppressive, anti-inflammatory and anti-allergic glucocorticoid effects occur too fast to be explained by the classical, genomic mechanism of glucocorticoid action [9,15,[25][26][27]. For example, rapid clinical effects have been observed when glucocorticoids were administered intravenously or intra-articularly at high dose.…”

Section: The Classical Genomic Mechanism Of Glucocorticoid Action Is mentioning

confidence: 99%

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Molecular mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists

Stahn

Löwenberg

Hommes

et al. 2007

Molecular and Cellular Endocrinology

334

266

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To cite this version:Cindy Stahn, Mark Löwenberg, Daniel W. Hommes, Frank Buttgereit. Molecular mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists. Molecular and Cellular Endocrinology, Elsevier, 2007, 275 (1-2) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A c c e p t e d M a n u s c r i p t promising results. Here, we review the above mentioned mechanisms of glucocorticoid action and give particular attention to the development of optimized glucocorticoids and SEGRA's.

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“…These coronary vasoconstriction effects of aldosterone were categorized into AII-b according to Mannheim classifications indicating direct steroid action via nonclassical receptors. 24 …”

Section: The Possibility Of Transmembrane Receptors Of Aldosterone Inmentioning

confidence: 99%

Aldosterone Nongenomically Worsens Ischemia Via Protein Kinase C-Dependent Pathways in Hypoperfused Canine Hearts

et al. 2005

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Abstract-Rapid nongenomic actions of aldosterone independent of mineralocorticoid receptors (MRs) on vascular tone are divergent. Until now, the rapid nongenomic actions of aldosterone on vascular tone of coronary artery and cardiac function in the in vivo ischemic hearts were not still fully estimated. Furthermore, although aldosterone can modulate protein kinase C (PKC) activity, there is no clear consensus whether PKC is involved in the nongenomic actions of aldosterone on the ischemic hearts. In open chest dogs, the selective infusion of aldosterone into the left anterior descending coronary artery (LAD) reduced coronary blood flow (CBF) in the nonischemic hearts in a dose-dependent manner. Also, in the ischemic state that CBF was decreased to 33% of the baseline, the intracoronary administration of aldosterone (0.1 nmol/L) rapidly decreased CBF (37.4Ϯ3.8 to 19.3Ϯ5.2 mL/100 g/min; PϽ0.05), along with decreases in fractional shortening (FS) (8.4Ϯ0.7 to 5.4Ϯ0.4%; PϽ0.05) and lactate extraction rate (LER) (Ϫ31.7Ϯ2.9 to Ϫ41.4Ϯ3.7%; PϽ0.05). The decrease in CBF was reproduced by the infusion of bovine serum albumin-conjugated aldosterone. Notably, these aldosterone-induced deteriorations of myocardial contractile and metabolic functions were blunted by the co-administration of GF109203X, an inhibitor of PKC, but not spironolactone. In addition, aldosterone activated vascular PKC. These results indicate that aldosterone nongenomically induces vasoconstriction via PKCdependent pathways possibly through membrane receptors, which leads to the worsening of the cardiac contractile and metabolic functions in the ischemic hearts. Elevation of plasma or cardiac aldosterone levels may be deleterious to ischemic heart disease through its nongenomic effects. Key Words: aldosterone Ⅲ ischemia Ⅲ protein kinases A ldosterone modulates cardiovascular function in addition to the crucial role in sodium and potassium homeostasis through binding to the intracellular mineralocorticoid receptors (MRs). 1 These receptor-mediated effects with transcriptional modulation of target genes are termed genomic effects. 2 Recently, another pathway possibly mediated by the specific membrane receptors through which aldosterone acts, ie, nongenomic effects of aldosterone, has been investigated. [2][3][4] Although this nongenomic action of aldosterone was shown in a variety of tissues such as vascular smooth muscle cells or cardiomyocytes, the effects of aldosterone on vascular tone are divergent. 4 -9 Aldosterone increased systemic vascular resistance in humans, as shown in the first report on the nongenomic effects of aldosterone, whereas aldosterone inhibits vasoconstriction in renal afferent arterioles. 7-9 Until now, the rapid nongenomic effects of aldosterone on vascular tone of coronary artery and cardiac functions in vivo under ischemia are not still fully estimated. Moreover, several rapid aldosterone-induced changes of the concentration of intracellular second messengers have been described. 6,10,11 Aldosterone is reported to activate pro...

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Mannheim Classification of Nongenomically Initiated (Rapid) Steroid Action(s)

Cited by 105 publications

References 39 publications

Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Molecular mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists

Aldosterone Nongenomically Worsens Ischemia Via Protein Kinase C-Dependent Pathways in Hypoperfused Canine Hearts

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