| http://purl.uniprot.org/citations/28566502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28566502 | http://www.w3.org/2000/01/rdf-schema#comment | "Guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) plays a critical role in the regulation of blood pressure and fluid volume homeostasis. Mice lacking functional Npr1 (coding for GC-A/NPRA) exhibit hypertension and congestive heart failure. However, the underlying mechanisms remain largely less clear. The objective of the present study was to determine the physiological efficacy and impact of all-trans-retinoic acid (ATRA) and sodium butyrate (NaBu) in ameliorating the renal fibrosis, inflammation, and hypertension in Npr1 gene-disrupted haplotype (1-copy; +/-) mice (50% expression levels of NPRA). Both ATRA and NaBu, either alone or in combination, decreased the elevated levels of renal proinflammatory and profibrotic cytokines and lowered blood pressure in Npr1+/- mice compared with untreated controls. The treatment with ATRA-NaBu facilitated the dissociation of histone deacetylase (HDAC) 1 and 2 from signal transducer and activator of transcription 1 (STAT1) and enhanced its acetylation in the kidneys of Npr1+/- mice. The acetylated STAT1 formed a complex with nuclear factor-κB (NF-κB) p65, thereby inhibiting its DNA-binding activity and downstream proinflammatory and profibrotic signaling cascades. The present results demonstrate that the treatment of the haplotype Npr1+/- mice with ATRA-NaBu significantly lowered blood pressure and reduced the renal inflammation and fibrosis involving the interactive roles of HDAC, NF-κB (p65), and STAT1. The current findings will help in developing the molecular therapeutic targets and new treatment strategies for hypertension and renal dysfunction in humans."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajprenal.00166.2017"xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/author | "Kumar P."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/author | "Pandey K.N."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/author | "Periasamy R."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/author | "Raghavaraju G."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/author | "Subramanian U."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/author | "Gogulamudi V.R."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/name | "Am J Physiol Renal Physiol"xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/pages | "F781-F795"xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/title | "Inhibition of HDAC enhances STAT acetylation, blocks NF-kappaB, and suppresses the renal inflammation and fibrosis in pii>Npr1pi/i> haplotype male mice."xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://purl.uniprot.org/core/volume | "313"xsd:string |
| http://purl.uniprot.org/citations/28566502 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28566502 |
| http://purl.uniprot.org/citations/28566502 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/28566502 |
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