International Journal of Cell Biology
J Clin Invest We investigated DNA methylation levels at six sites across the two genes, as well as mRNA expression for each, and the relationship to infant birth weight. Footnotes Nonstandard abbreviations used: Watson B, Jr, et al. IUGR Intrauterine growth retardation.
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The top represents the putative CpG islands along the gene and the middle graph indicates the relative abundance of CpGs Percentage as a function of the base number. The most widely studied epigenetic mechanisms are DNA methylation and histone acetylation. Genetic analysis of DNA methylation and gene expression levels in whole blood of healthy human subjects. National Center for Biotechnology Information , U. Correspondence should be addressed to Gerard W.
Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2. Molecular basis of human salt sensitivity: J Clin Endocrinol Metab. In vivo 11beta-HSD-2 activity: Impaired protein stability of 11beta-hydroxysteroid dehydrogenase type 2: J Am Soc Nephrol. Chenodeoxycholic acid and deoxycholic acid inhibit 11 beta-hydroxysteroid dehydrogenase type 2 and cause cortisol-induced transcriptional activation of the mineralocorticoid receptor.
Reduced activity of 11 beta-hydroxysteroid dehydrogenase in patients with cholestasis. Hypoxia causes down-regulation of 11 beta-hydroxysteroid dehydrogenase type 2 by induction of Egr Fluid shear stress reduces 11ss-hydroxysteroid dehydrogenase type 2. Increased cortisol metabolites and reduced activity of 11beta-hydroxysteroid dehydrogenase in patients on hemodialysis.
Identification of polymorphisms in the human 11beta-hydroxysteroid dehydrogenase type 2 gene promoter: Structural analysis of the 11beta-hydroxysteroid dehydrogenase type 2 gene in end-stage renal disease.
In vivo footprinting of the human 11beta-hydroxysteroid dehydrogenase type 2 promoter: Epigenetic regulation of 11 beta-hydroxysteroid dehydrogenase type 2 expression.
The Sp1 transcription factor is crucial for the expression of 11beta-hydroxysteroid dehydrogenase type 2 in human placental trophoblasts. Reduced 11beta-hydroxysteroid dehydrogenase activity in the remaining kidney following nephrectomy. Mass spectrometry in the diagnosis of steroid-related disorders and in hypertension research. J Steroid Biochem Mol Biol. Plasma microRNAs serve as biomarkers of therapeutic efficacy and disease progression in hypertension-induced heart failure. Eur J Heart Fail.
Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster. Increased serum and urinary microRNAs in children with idiopathic nephrotic syndrome. Reduced 11beta-hydroxysteroid dehydrogenase activity in patients with the nephrotic syndrome.
Renal medullary microRNAs in Dahl salt-sensitive rats: Changes in microRNAs associated with podocytic adhesion damage under mechanical stress. J Renin Angiotensin Aldosterone Syst.
Cardiac tissue enriched factors serum response factor and GATA-4 are mutual coregulators. GATA4 expression is primarily regulated via a miRb-dependent post-transcriptional mechanism during cardiac hypertrophy. Identification of microRNA-regulated gene networks by expression analysis of target genes. MicroRNA promotes fibrosis of the kidney by silencing metabolic pathways.
Vinson C , Chatterjee R. Identification of a microRNA signature of renal ischemia reperfusion injury. Implication of microRNAs in atrial natriuretic peptide and nitric oxide signaling in vascular smooth muscle cells. Am J Physiol Cell Physiol. Novelty and Significance What Is New? Previous Article Next Article.
Frey , Bruno Vogt and Brigitte M. Share this Article Email. Thank you for your interest in spreading the word on Hypertension. Message Subject Your Name has sent you a message from Hypertension.
Message Body Your Name thought you would like to see the Hypertension web site. Share on Social Media. This adds to the growing body of evidence suggesting that HDACs may be crucial in maintaining normal fetal development.
The glucocorticoid hypothesis proposes that overexposure of the fetus to glucocorticoids may produce long lasting effects on fetal development that subsequently increase disease risk later in life [ 1 ].
The glucocorticoid hypothesis is affirmed by studies that have shown that elevated maternal cortisol is associated with heightened HPA activity [ 2 ] and alterations in brain structure [ 3 ] in affected offspring. A complex repertoire of molecular pathways have been shown to be involved in regulating placental HSD11B2 expression. The most widely studied epigenetic mechanisms are DNA methylation and histone acetylation.
HATs add acetyl groups onto the N-terminal tail of histone proteins which increases gene expression [ 18 ]. HDACs remove them, thereby repressing transcription [ 19 ]. In humans, 18 HDACs have been discovered and they are classed into four main families: Where indicated, cultures were incubated in the following primary antibodies: Cultures were counterstained with DAPI 1: Sections were dehydrated, cleared, mounted, and imaged using an Olympus AX70 Provis upright microscope.
For real-time PCR, expression levels were calculated using the 2-delta-Ct threshold method [ 22 ]. Where indicated, data was analysed as per Section 2. Values of were considered statistically significant. We utilized the BioGPS database, an online platform that enables the examination of relative levels of gene expression across multiple human tissues [ 23 ].
Using this directory, we confirmed the highest levels of HSD11B2 in the placenta, followed by the kidneys, with very little expression seen in other tissues Figure 1 a , which was confirmed by immunohistochemistry on human term placental samples Figure 1 c. We next aimed to validate the use of the human choriocarcinoma cell line, JEG-3 cells. We used the in vitro placental model JEG-3 cells, as, despite their limitations, they are a well-established cell line commonly used to mimic placental trophoblast cells [ 30 ].
HSD11B2 has previously been shown to localise in trophoblast cells, with highest expression observed in the syncytiotrophoblast [ 31 , 32 ]. To model trophoblast cells in vitro, we used the human choriocarcinoma cell line, JEG-3 cells. This is in contradiction to previous studies, where HSD11B2 expression was reported to be unchanged in JEG-3 cells following treatment with broad-spectrum class I and class II inhibitor trichostatin A [ 24 ].
HDACs play a diverse role during fetal development [ 26 ]. HDACs have also been shown to be important regulators of placental development as inhibition of class II HDACs has been shown to impair trophoblast differentiation through interactions with Hypoxia-inducible factor [ 36 ].
Iamges: epigenetic regulation of 11 beta-hydroxysteroid dehydrogenase type 2 expression
Lanz CB, et al. Pathways from BioSystems Go to the top of the page Help. However, the mechanism of the demethylating effect of the procainamide is not well defined and is possibly not confined to the S phase.
Ng HH, et al. Several dehydrogenaase factors have been found to be relevant. This section includes genomic Reference Sequences RefSeqs from all assemblies on which this gene is annotated, such as RefSeqs for chromosomes and scaffolds contigs from both reference and alternate assemblies. Arnt1 inhibited formation of the lower complex. The increased mRNA abundance and activity of HSD11B2 observed within 5 days of procainamide dosing in vivo epigenetic regulation of 11 beta-hydroxysteroid dehydrogenase type 2 expression be unexpected, as the best investigated inhibitor of DNA methyltransferase, 5-aza-CdR, acts mainly in the S phase of the cell cycle and the proliferation rate of the renal tren ace quad injection cells is generally considered to be low. Renal proximal and distal tubular cells were isolated as described
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