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The objective of the present study was to examine the genetically determined differences in the natriuretic peptide receptor-A (NPRA) gene (Npr1) copies affecting the expression of cardiac hypertrophic markers, proinflammatory mediators, and matrix metalloproteinases (MMPs) in a gene-dose-dependent manner. We determined whether stimulation of Npr1 by all-trans retinoic acid (RA) and histone deacetylase (HDAC) inhibitor sodium butyric acid (SB) suppress the expression of cardiac disease markers. In the present study, we utilized Npr1 gene-disrupted heterozygous (Npr1(+/-), 1-copy), wild-type (Npr1(+/+), 2-copy), gene-duplicated (Npr1(++/+), 3-copy) mice, which were treated intraperitoneally with RA, SB, and a combination of RA/SB, a hybrid drug (HB) for 2 wk. Untreated 1-copy mice showed significantly increased heart weight-body weight (HW/BW) ratio, blood pressure, hypertrophic markers, including beta-myosin heavy chain (β-MHC) and proto-oncogenes (c-fos and c-jun), proinflammatory mediator nuclear factor kappa B (NF-κB), and MMPs (MMP-2, MMP-9) compared with 2-copy and 3-copy mice. The heterozygous (haplotype) 1-copy mice treated with RA, SB, or HB, exhibited significant reduction in the expression of β-MHC, c-fos, c-jun, NF-κB, MMP-2, and MMP-9. In drug-treated animals, the activity and expression levels of HDAC were significantly reduced and histone acetyltransferase activity and expression levels were increased. The drug treatments significantly increased the fractional shortening and reduced the systolic and diastolic parameters of the Npr1(+/-) mice hearts. Together, the present results demonstrate that a decreased Npr1 copy number enhanced the expression of hypertrophic markers, proinflammatory mediators, and MMPs, whereas an increased Npr1 repressed the cardiac disease markers in a gene-dose-dependent manner.

Titel:	Retinoic acid and sodium butyrate suppress the cardiac expression of hypertrophic markers and proinflammatory mediators in Npr1 gene-disrupted haplotype mice.
Autor/in / Beteiligte Person:	Subramanian, U ; Kumar, P ; Mani, I ; Chen, D ; Kessler, I ; Periyasamy, R ; Raghavaraju, G ; Pandey, KN
Link:	Full Text Finder (Volltext)
Zeitschrift:	Physiological genomics, Jg. 48 (2016-07-01), Heft 7, S. 477-90
Veröffentlichung:	Bethesda, MD : American Physiological Society, c1999-, 2016
Medientyp:	academicJournal
ISSN:	1531-2267 (electronic)
DOI:	10.1152/physiolgenomics.00073.2015
Schlagwort:	Animals Blood Pressure drug effects Cytokines metabolism Diastole drug effects Haplotypes drug effects Hypertrophy metabolism Male Mice Systole drug effects Biomarkers metabolism Butyric Acid pharmacology Heart drug effects Hypertrophy drug therapy Inflammation metabolism Receptors, Atrial Natriuretic Factor metabolism Tretinoin pharmacology
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, N.I.H., Extramural Language: English [Physiol Genomics] 2016 Jul 01; Vol. 48 (7), pp. 477-90. <i>Date of Electronic Publication: </i>2016 May 06. MeSH Terms: Biomarkers / metabolism ; Butyric Acid / pharmacology ; Heart / drug effects ; Hypertrophy / drug therapy ; Inflammation / metabolism ; Receptors, Atrial Natriuretic Factor / metabolism ; Tretinoin / *pharmacology ; Animals ; Blood Pressure / drug effects ; Cytokines / metabolism ; Diastole / drug effects ; Haplotypes / drug effects ; Hypertrophy / metabolism ; Male ; Mice ; Systole / drug effects References: J Med Chem. 2008 Jul 10;51(13):3895-904. (PMID: 18543902) ; J Biomed Biotechnol. 2011;2011:371832. (PMID: 21151613) ; Biochim Biophys Acta. 2006 Mar-Apr;1759(3-4):141-51. (PMID: 16757381) ; Physiol Genomics. 2007 Oct 22;31(2):193-202. (PMID: 17566078) ; Acta Pharmacol Sin. 2008 Sep;29(9):1035-41. 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(PMID: 16177190) Grant Information: P30 GM103337 United States GM NIGMS NIH HHS; R01 HL057531 United States HL NHLBI NIH HHS; R01 HL062147 United States HL NHLBI NIH HHS Contributed Indexing: Keywords: fibrosis; gene-disruption; histone acetyltransferase; histone deacetylase; hypertrophy; natriuretic peptide receptor-A Substance Nomenclature: 0 (Biomarkers) ; 0 (Cytokines) ; 107-92-6 (Butyric Acid) ; 5688UTC01R (Tretinoin) ; EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor) ; EC 4.6.1.2 (atrial natriuretic factor receptor A) Entry Date(s): Date Created: 20160521 Date Completed: 20180125 Latest Revision: 20181113 Update Code: 20240513 PubMed Central ID: PMC4967220

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Retinoic acid and sodium butyrate suppress the cardiac expression of hypertrophic markers and proinflammatory mediators in Npr1 gene-disrupted haplotype mice.