Guanylyl cyclase structure, function and regulation

Potter, Lincoln R.

doi:10.1016/j.cellsig.2011.09.001

Cited by 245 publications

(207 citation statements)

References 130 publications

(126 reference statements)

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“…The activation or stimulation of sGC results in increasing of cGMP levels in cells and finally causes relaxation in smooth muscle cells of the cardiovascular systems [8]. Soluble guanylyl cyclase activators are effective to induce relaxation in smooth muscle, therefore some of them have been used on clinical practice for pulmonary hypertension, congestive heart failure ABBREVIATIONS Acetylcholine (Ach) ( ) state or even without this grouping [12,13].…”

Section: Introductionmentioning

confidence: 99%

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

Martinelli¹,

Rodrigues²,

Moraes³

et al. 2018

J Pharm Pharm Sci

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-Purpose. In endothelial cells, investigate if the soluble guanylate cyclase (sGC) activation or stimulation is able to potentiate the relaxation in vessels. Methods. Aortic and coronary rings with and without endothelium were placed in a myograph and cumulative concentration-effect curves for DETA-NO or ataciguat were performed. Nitric oxide (NO) were measured by fluorescence or by selective electrode in human umbilical endothelial cells (HUVECs) in response to some treatments, including ataciguat, 8-BrcGMP and A23187. Results. The presence of the endothelium potentiated the relaxation induced by DETA-NO in aortic and coronary rings. In addition, in aortic rings the endothelium potentiated the relaxation induced by ataciguat. In the presence of nitric oxide synthase (NOS) inhibitor, the endothelium effect was abolished to DETA-NO or ataciguat, in both vessels. Ataciguat, 8-Br-cGMP and A23187 were able to induce NO production in HUVECs cells. In the presence of NOS inhibitor, the NO production induced by ataciguat and 8-Br-cGMP was abolished. Conclusions. Our results suggest that in aortic and coronary rings the endothelium potentiates the relaxation induced by activation or stimulation of sGC through a mechanism dependent of NOS activation.

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Section: Introductionmentioning

confidence: 99%

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

Martinelli¹,

Rodrigues²,

Moraes³

et al. 2018

J Pharm Pharm Sci

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“…136 The precise characterization of how the Akt isoforms contribute to the survival a second messenger that regulates cGMP-dependent protein kinase (PKG) activity. 119 There is evidence that PKG activation protects against apoptosis in various cell types. 101,[120][121][122] In N1E-115 neural cells, cGMP and PKG have a cytoprotective effect, in which PKG-Iα directly phosphorylates pro-apoptotic Bad at Ser155 and protects against spontaneous apoptosis.…”

Section: No Regulates Mitochondrial Permeability and Activitymentioning

confidence: 99%

Regulation of pancreatic β-cell survival by nitric oxide

Bedoya¹,

Salguero-Aranda

Cahuana

et al. 2012

Islets

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“…Guanylin and uroguanylin have been well-known key paracrine players in intestinal ion and water balance for over 20 years, acting as endogenous ligands of guanylyl cyclase (GUCY) 2C and increasing cyclic guanosine monophosphate (cGMP) production (356) . They are secreted by intestinal epithelial cells as prohormones, requiring proteolytic enzymic conversion into active hormones in the target tissue (357) .…”

Section: Uroguanylinmentioning

confidence: 99%

Peripheral signalling involved in energy homeostasis control

2012

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The alarming prevalence of obesity has led to a better understanding of the molecular mechanisms controlling energy homeostasis. Regulation of energy intake and expenditure is more complex than previously thought, being influenced by signals from many peripheral tissues. In this sense, a wide variety of peripheral signals derived from different organs contributes to the regulation of body weight and energy expenditure. Besides the well-known role of insulin and adipokines, such as leptin and adiponectin, in the regulation of energy homeostasis, signals from other tissues not previously thought to play a role in body weight regulation have emerged in recent years. The role of fibroblast growth factor 21 (FGF21), insulin-like growth factor 1 (IGF-I), and sex hormone-binding globulin (SHBG) produced by the liver in the regulation of body weight and insulin sensitivity has been recently described. Moreover, molecules expressed by skeletal muscle such as myostatin have also been involved in adipose tissue regulation. Better known is the involvement of ghrelin, cholecystokinin, glucagon-like peptide 1 (GLP-1) and PYY 3 -36 , produced by the gut, in energy homeostasis. Even the kidney, through the production of renin, appears to regulate body weight, with mice lacking this hormone exhibiting resistance to diet-induced obesity. In addition, the skeleton has recently emerged as an endocrine organ, with effects on body weight control and glucose homeostasis through the actions of bone-derived factors such as osteocalcin and osteopontin. The comprehension of these signals will help in a better understanding of the aetiopathology of obesity, contributing to the potential development of new therapeutic targets aimed at tackling excess body fat accumulation.

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Guanylyl cyclase structure, function and regulation

Cited by 245 publications

References 130 publications

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

Regulation of pancreatic β-cell survival by nitric oxide

Peripheral signalling involved in energy homeostasis control

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