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10.1038/s41598-017-01392-1 http://scihub22266oqcxt.onion/10.1038/s41598-017-01392-1 C5430981!5430981 !28465505     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28465505 &cmd=llinks): Failed to open stream: HTTP request failed! 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Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway |pdf=|usr=}}{{28465505 }} gab.com Text Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28465505 #FOAvip Hypertension is a dominating risk factor for cardiovascular disease. To characterize the genomic response to hypertension, we administered vehicle or angiotensin II to mice and performed gene expression analyses. AngII treatment resulted in a robust increase in blood pressure and altered expression of 235 genes in the aorta, including Gucy1a3 and Gucy1b3 which encode subunits of soluble guanylyl cyclase (sGC). Western blotting and immunohistochemistry confirmed repression of sGC associated with curtailed relaxation via sGC activation. Analysis of transcription factor binding motifs in promoters of differentially expressed genes identified enrichment of motifs for RBPJ, a component of the Notch signaling pathway, and the Notch coactivators FRYL and MAML2 were reduced. Gain and loss of function experiments demonstrated that JAG/NOTCH signaling controls sGC expression together with MAML2 and FRYL. Reduced expression of sGC, correlating with differential expression of MAML2, in stroke prone and spontaneously hypertensive rats was also seen, and RNA-Seq data demonstrated correlations between JAG1, NOTCH3, MAML2 and FRYL and the sGC subunits GUCY1A3 and GUCY1B3 in human coronary artery. Notch signaling thus provides a constitutive drive on expression of the major nitric oxide receptor (GUCY1A3/GUCY1B3) in arteries from mice, rats, and humans, and this control mechanism is disturbed in hypertension. Twit Text FOAVip Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28465505 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28465505 #FOAvip English Wikipedia <ref>{{Cite pmid|28465505 }}</ref> Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway #MMPMID28465505 Rippe C ; Zhu B ; Krawczyk KK ; Bavel EV ; Albinsson S ; Sjölund J ; Bakker ENTP ; Swärd K Sci Rep 2017[May]; 7 (1 ): 1334 PMID28465505 show ga Hypertension is a dominating risk factor for cardiovascular disease. To characterize the genomic response to hypertension, we administered vehicle or angiotensin II to mice and performed gene expression analyses. AngII treatment resulted in a robust increase in blood pressure and altered expression of 235 genes in the aorta, including Gucy1a3 and Gucy1b3 which encode subunits of soluble guanylyl cyclase (sGC). Western blotting and immunohistochemistry confirmed repression of sGC associated with curtailed relaxation via sGC activation. Analysis of transcription factor binding motifs in promoters of differentially expressed genes identified enrichment of motifs for RBPJ, a component of the Notch signaling pathway, and the Notch coactivators FRYL and MAML2 were reduced. Gain and loss of function experiments demonstrated that JAG/NOTCH signaling controls sGC expression together with MAML2 and FRYL. Reduced expression of sGC, correlating with differential expression of MAML2, in stroke prone and spontaneously hypertensive rats was also seen, and RNA-Seq data demonstrated correlations between JAG1, NOTCH3, MAML2 and FRYL and the sGC subunits GUCY1A3 and GUCY1B3 in human coronary artery. Notch signaling thus provides a constitutive drive on expression of the major nitric oxide receptor (GUCY1A3/GUCY1B3) in arteries from mice, rats, and humans, and this control mechanism is disturbed in hypertension. |Angiotensin II/administration & dosage [MESH] |Animals [MESH] |Aorta/*metabolism [MESH] |Gene Expression [MESH] |Humans [MESH] |Hypertension/chemically induced/genetics/*metabolism [MESH] |Mice, Inbred C57BL [MESH] |RNA, Messenger/metabolism [MESH] |Rats, Inbred WKY [MESH] |Receptors, Notch/*metabolism [MESH] |Signal Transduction [MESH]Hypertension reduces soluble guanylyl cyclase expression in the mouse (epmc).pdf DeepDyve Pubget Overpricing