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

Umadevi, S.; Kumar, Prerna; Mani, Indra; Chen, David; Kessler, Isaac; Periyasamy, Ramu; Raghavaraju, Giri; Pandey, Kailash N.

doi:10.1152/physiolgenomics.00073.2015

Cited by 31 publications

(51 citation statements)

References 77 publications

(71 reference statements)

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“…These observations support a role for miR-205 and miR-200 family members in regulating the expression of ZEB transcription factors and EMT differentiation gene signatures in these SCC subtypes. miR-944 targets include S100PBP, implicated in adhesion; SPRY1, a modulator of EGFR signaling; and NPR1, an Inhibitor-κB homolog that attenuates NF-κB signaling (Figure 7B) (He et al, 2016; Subramanian et al, 2016). …”

Section: Resultsmentioning

confidence: 99%

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

Campbell¹,

Yau²,

Bowlby³

et al. 2018

Cell Reports

257

278

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SUMMARY This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smoking and/or human papillomavirus (HPV). SCCs harbor 3q, 5p, and other recurrent chromosomal copy-number alterations (CNAs), DNA mutations, and/or aberrant methylation of genes and microRNAs, which are correlated with the expression of multi-gene programs linked to squamous cell stemness, epithelial-to-mesenchymal differentiation, growth, genomic integrity, oxidative damage, death, and inflammation. Low-CNA SCCs tended to be HPV(+) and display hypermethylation with repression of TET1 demethylase and FANCF, previously linked to predisposition to SCC, or harbor mutations affecting CASP8, RAS-MAPK pathways, chromatin modifiers, and immunoregulatory molecules. We uncovered hypomethylation of the alternative promoter that drives expression of the ΔNp63 oncogene and embedded miR944. Co-expression of immune checkpoint, T-regulatory, and Myeloid suppressor cells signatures may explain reduced efficacy of immune therapy. These findings support possibilities for molecular classification and therapeutic approaches.

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Section: Resultsmentioning

confidence: 99%

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

Campbell¹,

Yau²,

Bowlby³

et al. 2018

Cell Reports

257

278

View full text Add to dashboard Cite

show abstract

“…Although NaB was found be beneficial to several diseases (He et al 2016, Li et al 2016, Salimi et al 2016, Subramanian et al 2016, little is known about its protection against DN. To the best of our knowledge, there has been only one study that reported NaB protection against DN (Khan & Jena 2014).…”

Section: Discussionmentioning

confidence: 99%

Sodium butyrate activates NRF2 to ameliorate diabetic nephropathy possibly via inhibition of HDAC

Dong

Jia

Liu

et al. 2017

Journal of Endocrinology

111

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Oxidative stress contributes to the pathogenesis of diabetic nephropathy (DN). Nuclear factor erythroid 2-related factor 2 (NRF2) plays a key role in cellular defense against oxidative stress. NRF2 activators have shown promising preventive effects on DN. Sodium butyrate (NaB) is a known activator of NRF2. However, it is unknown whether NRF2 is required for NaB protection against DN. Therefore, streptozotocin-induced diabetic C57BL/6 Nrf2 knockout and their wild-type mice were treated in the presence or absence of NaB for 20 weeks. Diabetic mice, but not NaB-treated diabetic mice, developed significant renal oxidative damage, inflammation, apoptosis, fibrosis, pathological changes and albuminuria. NaB inhibited histone deacetylase (HDAC) activity and elevated the expression of Nrf2 and its downstream targets heme oxygenase 1 and NAD(P)H dehydrogenase quinone 1. Notably, deletion of the Nrf2 gene completely abolished NaB activation of NRF2 signaling and protection against diabetes-induced renal injury. Interestingly, the expression of Kelch-like ECH-associated protein 1, the negative regulator of NRF2, was not altered by NaB under both diabetic and non-diabetic conditions. Moreover, NRF2 nuclear translocation was not promoted by NaB. Therefore, the present study indicates, for the first time, that NRF2 plays a key role in NaB protection against DN. Other findings suggest that NaB may activate Nrf2 at the transcriptional level, possibly by the inhibition of HDAC activity.

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“…Studies with Npr1 (encoding NPRA) gene-knockout mice have demonstrated that a deficiency in NPRA increases BP by 35–45 mmHg and causes renal, vascular, and cardiac dysfunction that leads to hypertensive heart disease in mice, much like that observed in untreated hypertensive patients [64,65,66,67,68,69]. On the other hand, increased expression (gene-duplication) of NPRA in mice significantly reduces BP and increases second-messenger cGMP corresponding to the level of Npr1 gene copy number in both male and female mice [70,71,72,73,74,75,76,77].…”

Section: Historical Perspectives and Backgroundmentioning

confidence: 99%

Genetic Ablation and Guanylyl Cyclase/Natriuretic Peptide Receptor-A: Impact on the Pathophysiology of Cardiovascular Dysfunction

Pandey

2019

IJMS

Self Cite

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Mice bearing targeted gene mutations that affect the functions of natriuretic peptides (NPs) and natriuretic peptide receptors (NPRs) have contributed important information on the pathogenesis of hypertension, kidney disease, and cardiovascular dysfunction. Studies of mice having both complete gene disruption and tissue-specific gene ablation have contributed to our understanding of hypertension and cardiovascular disorders. These phenomena are consistent with an oligogenic inheritance in which interactions among a few alleles may account for genetic susceptibility to hypertension, renal insufficiency, and congestive heart failure. In addition to gene knockouts conferring increased risks of hypertension, kidney disorders, and cardiovascular dysfunction, studies of gene duplications have identified mutations that protect against high blood pressure and cardiovascular events, thus generating the notion that certain alleles can confer resistance to hypertension and heart disease. This review focuses on the intriguing phenotypes of Npr1 gene disruption and gene duplication in mice, with emphasis on hypertension and cardiovascular events using mouse models carrying Npr1 gene knockout and/or gene duplication. It also describes how Npr1 gene targeting in mice has contributed to our knowledge of the roles of NPs and NPRs in dose-dependently regulating hypertension and cardiovascular events.

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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

Abstract: yasamy R, Raghavaraju G, Pandey KN. Retinoic acid and sodium butyrate suppress the cardiac expression of hypertrophic markers and proinflammatory mediators in Npr1 gene-disrupted haplotype mice.

Cited by 31 publications

References 77 publications

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

Sodium butyrate activates NRF2 to ameliorate diabetic nephropathy possibly via inhibition of HDAC

Genetic Ablation and Guanylyl Cyclase/Natriuretic Peptide Receptor-A: Impact on the Pathophysiology of Cardiovascular Dysfunction

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