Implication of microRNAs in atrial natriuretic peptide and nitric oxide signaling in vascular smooth muscle cells

Kotlo, Kumar; Hesabi, Bahar; Danziger, Robert S.

doi:10.1152/ajpcell.00088.2011

Cited by 32 publications

(26 citation statements)

References 69 publications

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“…29,30 Recently, miR-26b was reported to be implicated in nitric oxide and atrial natriuretic peptide signaling in vascular smooth muscle cells. 40 In conclusion, the present study provides the first evidence of 3′-UTR-directed regulation of HSD11B2 mRNA by miRNAs. Because 11β-HSD2 is specifically expressed in the CCD, but not in the PCT, the miRNA profile in these 2 matrices was established and differential expression of 53 miRNAs, including 13 predicted to bind to the 3′-UTR, identified.…”

Section: Discussionsupporting

confidence: 52%

Regulation of 11β-Hydroxysteroid Dehydrogenase Type 2 by MicroRNA

et al. 2014

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Abstract-The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is selectively expressed in aldosterone target tissues, conferring aldosterone selectivity for the mineralocorticoid receptor. A diminished activity causes salt-sensitive hypertension. The mechanism of the variable and distinct 11β-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) expression in the cortical collecting duct is poorly understood. Here, we analyzed for the first time whether the 11β-HSD2 expression is modulated by microRNAs (miRNAs). In silico analysis revealed 53 and 27 miRNAs with potential binding sites on human or rat HSD11B2 3′-untranslated region. A reporter assay demonstrated 3′-untranslated region-dependent regulation of human and rodent HSD11B2. miRNAs were profiled from cortical collecting ducts and proximal convoluted tubules. Bioinformatic analyses showed a distinct clustering for cortical collecting ducts and proximal convoluted tubules with 53 of 375 miRNAs, where 13 were predicted to bind to the rat HSD11B2 3′-untranslated region. To gain insight into potentially relevant miRNAs in vivo, we investigated 2 models with differential 11β-HSD2 activity linked with saltsensitive hypertension.(1) Comparing Sprague-Dawley with low and Wistar rats with high 11β-HSD2 activity revealed rno-miR-20a-5p, rno-miR-19b-3p, and rno-miR-190a-5p to be differentially expressed. (2) Uninephrectomy lowered 11β-HSD2 activity in the residual kidney with differentially expressed rno-miR-19b-3p, rno-miR-29b-3p, and rnomiR-26-5p. In conclusion, miRNA-dependent mechanisms seem to modulate 11β-HSD2 dosage in health and disease The online-only Data Supplement is available with this article at http://hyper.ahajournals.org/lookup/suppl

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Section: Discussionsupporting

confidence: 52%

Regulation of 11β-Hydroxysteroid Dehydrogenase Type 2 by MicroRNA

et al. 2014

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“…Their vascular effect is mediated mainly through the type A receptor (NPRA) (67) present on smooth muscle cells (109). ANP comes from the circulation and is also formed locally by endothelial cells (106). Local administration of ANP leads to increased ATBF and lipolysis to an extent similar to catecholamines and independently of them.…”

Section: Other Possible Regulators Of Atbfmentioning

confidence: 99%

Update on adipose tissue blood flow regulation

Sotorník

Brassard

Martin

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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According to Fick's principle, any metabolic or hormonal exchange through a given tissue depends on the product of the blood flow to that tissue and the arteriovenous difference. The proper function of adipose tissue relies on adequate adipose tissue blood flow (ATBF), which determines the influx and efflux of metabolites as well as regulatory endocrine signals. Adequate functioning of adipose tissue in intermediary metabolism requires finely tuned perfusion. Because metabolic and vascular processes are so tightly interconnected, any disruption in one will necessarily impact the other. Although altered ATBF is one consequence of expanding fat tissue, it may also aggravate the negative impacts of obesity on the body's metabolic milieu. This review attempts to summarize the current state of knowledge on adipose tissue vascular bed behavior under physiological conditions and the various factors that contribute to its regulation as well as the possible participation of altered ATBF in the pathophysiology of metabolic syndrome. obesity; insulin; sympathetic nervous system; nitric oxide; angiotensin II; atrial natriuretic peptide; glucagon-like peptide-1; glucose-dependent insulinotropic polypeptide OVER THE LAST DECADES, THE WORLDWIDE PANDEMIC of obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM) (188) has attracted ever-increasing attention to the role and significance of adipose tissue (AT). Originally regarded as a mere energy store with insulation and protective cushioning functions, AT is now recognized as a bona fide and highly active metabolic and endocrine organ (102). It has also become evident that the white AT is a heterogeneous tissue. From a metabolic point of view, AT can be subdivided into central (abdominal) and peripheral (hips and buttocks) depots (78). Although extra-abdominal fat accumulation does not bring upon higher metabolic and cardiovascular risk, some reports show a protective influence (124). Conversely, a negative metabolic effect has been associated with central fat (102), which in fact comprises two distinct masses (visceral and subcutaneous) with different metabolic and hormonal activities and impacts on metabolic syndrome pathogenesis (95) and blood flow rates (102).Metabolic processes in fatty tissue require adequate substrate(s) and humoral factor delivery (76). Conversely, adipocytes communicate with other metabolically active tissues through humoral factors (128) as well as through metabolic products (118) serving as energetic substrates. Humoral factors derived from AT arise not only from adipocytes themselves but also from other components of AT such as macrophages and endothelial cells. Moreover, AT is a known conversion site for several hormones or humoral factors, e.g., steroid hormones (156) or components of the renin-angiotensin-aldosterone system (RAAS). All of these functions of AT are tightly linked to the pattern of blood supply and its regulation, which largely differ from other metabolically active organs such as the liver or skeletal muscle (141).In add...

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“…and other microRNAs, thereby regulating smooth muscle cell contraction (137). Brief bursts of myocardial ischemia induced miR-1, miR-21 and miR-24; this, in turn, induced eNOS mRNA and upregulated eNOS protein, whereas no effect was seen on iNOS.…”

Section: (D) No and Micrornasmentioning

confidence: 99%

The Key Role of Nitric Oxide in Hypoxia: Hypoxic Vasodilation and Energy Supply–Demand Matching

Umbrello

Dyson²,

Feelisch³

et al. 2013

Antioxidants & Redox Signaling

108

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SIGNIFICANCE: A mismatch between energy supply and demand induces tissue hypoxia with the potential to cause cell death and organ failure. Whenever arterial oxygen concentration is reduced, increases in blood flow -'hypoxic vasodilation' -occur in an attempt to restore oxygen supply. Nitric oxide is a major signalling and effector molecule mediating the body's response to hypoxia, given its unique characteristics of vasodilation (improving blood flow and oxygen supply) and modulation of energetic metabolism (reducing oxygen consumption and promoting utilization of alternative pathways).RECENT ADVANCES: This review covers the role of oxygen in metabolism and responses to hypoxia, the hemodynamic and metabolic effects of nitric oxide, and mechanisms underlying the involvement of nitric oxide in hypoxic vasodilation. Recent insights into nitric oxide metabolism will be discussed, including the role for dietary intake of nitrate, endogenous nitrite reductases, and release of nitric oxide from storage pools. The processes through which nitric oxide levels are elevated during hypoxia are presented, namely (i) increased synthesis from nitric oxide synthases, increased reduction of nitrite to nitric oxide by heme-or pterin-based enzymes and increased release from nitric oxide stores, and (ii) reduced deactivation by mitochondrial cytochrome c oxidase.CRITICAL ISSUES: Several reviews covered modulation of energetic metabolism by nitric oxide, while here we highlight the crucial role NO plays in achieving cardiocirculatory homeostasis during acute hypoxia through both vasodilation and metabolic suppression FUTURE DIRECTIONS: We identify a key position for nitric oxide in the body's adaptation to an acute energy supply-demand mismatch.

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Implication of microRNAs in atrial natriuretic peptide and nitric oxide signaling in vascular smooth muscle cells

Cited by 32 publications

References 69 publications

Regulation of 11β-Hydroxysteroid Dehydrogenase Type 2 by MicroRNA

Regulation of 11β-Hydroxysteroid Dehydrogenase Type 2 by MicroRNA

Update on adipose tissue blood flow regulation

The Key Role of Nitric Oxide in Hypoxia: Hypoxic Vasodilation and Energy Supply–Demand Matching

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