Phylogenesis of constitutively formed nitric oxide in non-mammals

Toda, Noboru; Ayajiki, Kazuhide

doi:10.1007/112_0601

Cited by 25 publications

(16 citation statements)

References 315 publications

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“…eNOS emerged phylogenetically as fish evolved into amphibians, i.e. as respiration was transitioned from water to air (42). Thus, one of the earliest functions of eNOS may have been to enhance perfusion (through vasodilation and angiogenesis) of peripheral tissues in the setting of regional hypoxia and tissue damage.…”

Section: Discussionmentioning

confidence: 99%

De Novo Lipogenesis Maintains Vascular Homeostasis through Endothelial Nitric-oxide Synthase (eNOS) Palmitoylation*

Wei

Schneider²,

Shenouda

et al. 2011

Journal of Biological Chemistry

113

100

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Endothelial dysfunction leads to lethal vascular complications in diabetes and related metabolic disorders. Here, we demonstrate that de novo lipogenesis, an insulin-dependent process driven by the multifunctional enzyme fatty-acid synthase (FAS), maintains endothelial function by targeting endothelial nitric-oxide synthase (eNOS) to the plasma membrane. In mice with endothelial inactivation of FAS (FASTie mice), eNOS membrane content and activity were decreased. eNOS and FAS were physically associated; eNOS palmitoylation was decreased in FAS-deficient cells, and incorporation of labeled carbon into eNOS-associated palmitate was FAS-dependent. FASTie mice manifested a proinflammatory state reflected as increases in vascular permeability, endothelial inflammatory markers, leukocyte migration, and susceptibility to LPS-induced death that was reversed with an NO donor. FAS-deficient endothelial cells showed deficient migratory capacity, and angiogenesis was decreased in FASTie mice subjected to hindlimb ischemia. Insulin induced FAS in endothelial cells freshly isolated from humans, and eNOS palmitoylation was decreased in mice with insulin-deficient or insulin-resistant diabetes. Thus, disrupting eNOS bioavailability through impaired lipogenesis identifies a novel mechanism coordinating nutritional status and tissue repair that may contribute to diabetic vascular disease.Damage to blood vessels is inextricably linked with diabetes. Microvascular disease causes visual loss, renal failure, and neuropathy, and macrovascular disease (atherosclerotic coronary disease, stroke, and peripheral arterial disease) causes premature death. Macro-and microvascular complications characterize both type 1 (insulin-deficient) and type 2 (insulin-resistant with hyperinsulinemia) diabetes. Hyperglycemia is a biomarker of blood vessel disease (1), and glucose lowering delays microvascular complications (2, 3), but this therapy does not prevent progression of established microvascular (4) or macrovascular disease (5, 6). In addition to improving glycemia, optimal approaches to complications may require manipulating processes that are mostly obscure.One such process is endothelial lipid metabolism. The endothelium controls tissue access from the circulation and regulates vascular functions, including inflammation and angiogenesis. Endothelial dysfunction, largely due to defects in eNOS, 3 is characteristic of diabetes and probably promotes vascular disease (7,8). Circulating fatty acids interfere with eNOS and increase inflammation (9, 10), and insulin resistance appears to have similar effects by increasing fatty acid oxidation (11), but little is known about how fuels are partitioned inside endothelial cells. A critical pathway for fuel flow is de novo lipogenesis, the generation of fatty acids from simple sugars, which requires FAS (12, 13). One might predict that de novo lipogenesis would be irrelevant to endothelial cells, which are continually bathed in fatty acids, the product of the FAS reaction.Here, we report that endothelial...

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Section: Discussionmentioning

confidence: 99%

De Novo Lipogenesis Maintains Vascular Homeostasis through Endothelial Nitric-oxide Synthase (eNOS) Palmitoylation*

Wei

Schneider²,

Shenouda

et al. 2011

Journal of Biological Chemistry

113

100

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“…The available data suggest that NO is an evolutionarily ancient signaling molecule occurring in many invertebrate groups and that invertebrates use it in a similar manner as mammals (see for review Colasanti and Venturini, 1998;Stefano and Ottaviani, 2002;Palumbo, 2005;Toda and Ayajiki, 2006). Thus, several studies suggest involvement of NO-signaling in stress reactions in sponges exposed to heat stress (Giovine et al, 2001) and bivalve mollusks exposed to tributyltinoxide (Smith et al, 2000) and hypoxia .…”

Section: Introductionmentioning

confidence: 99%

NADPH-diaphorase activity in the central nervous system of the Gray mussel Crenomytilus grayanus (Dunker) under stress conditions: A histochemical study

Vaschenko¹,

Kotsyuba²

2008

Marine Environmental Research

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NADPH-diaphorase (NADPH-d) is a histochemical marker for nitric oxide synthase (NOS) and is widely used to identify nitric oxide (NO) producing cells in the central nervous system (CNS) of both vertebrates and invertebrates. NADPH-d histochemistry was used to quantitatively characterize putative NO-producing neurons in the CNS of the Gray mussel Crenomytilus grayanus subjected to two kinds of stress, environmental pollution and hypoxia, the latter caused by the mollusk transportation in a small volume of water. Mussels were sampled from one relatively clean (reference) and four polluted sites in Amursky and Ussuriysky Bays (Peter the Great Bay, Sea of Japan) in August, 2003. The number of NADPH-d-positive neurons was estimated and enzyme activity was determined from the optical density of the formazan precipitate in the CNS ganglia at 0, 3, and 72 h after sampling. Just after sampling, NADPH-d-positive neurons were found in the cerebropleural, visceral, and pedal ganglia. The number and staining intensity of NADPH-d-positive neurons were significantly higher in the pedal ganglia than the other two ganglia. There were significant differences in the number of NADPH-d-positive neurons and enzyme activity between the mussels from the reference and heavily polluted stations. The proportion and staining intensity of NADPH-d-positive neurons were maximum in the pedal ganglia of the mussels from the heavily polluted station in Amursky Bay. Transportation of mussels in a limited volume of water for 3h resulted in a significant increase in the proportion and staining intensity of NADPH-d-positive neurons in all ganglia. In mollusks from all stations kept in aerated aquaria for 72 h, both the proportion and staining intensity of NADPH-d-positive neurons did not differ significantly from the initial level. However, the differences in the proportion and staining intensity of NADPH-d-positive neurons between the reference and heavily polluted stations were significant. The present results suggest that NO is involved in mollusk nerve cell adaptation to environmental changes.

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“…This function is consistent with the evolutionary record. The presumed gene duplication that gave rise to TSP1 in tetrapods (2) was followed soon thereafter in amphibians and higher land-dwelling vertebrates by the gene duplication that yielded eNOS to enable local vascular control of NO production in high pressure circulatory systems (274) and the appearance of CD47, presumably by a recombination event that joined a primordial IgV domain with a presenilin transmembrane domain (208,210 -/-mice provided the first evidence that TSP1 functions as a physiological regulator of NO in the local control of tissue vascular perfusion (85). Functional imaging of blood oxygenation in the proximate hind limb muscle of mice was assessed after intestinal administration of a rapidly releasing NO donor.…”

Section: +mentioning

confidence: 99%

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

Roberts

Kaur

Isenberg

2017

Antioxidants & Redox Signaling

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Significance: In contrast to structural elements of the extracellular matrix, matricellular proteins appear transiently during development and injury responses, but their sustained expression can contribute to chronic disease. Through interactions with other matrix components and specific cell surface receptors, matricellular proteins regulate multiple signaling pathways, including those mediated by reactive oxygen and nitrogen species and H 2 S. Dysregulation of matricellular proteins contributes to the pathogenesis of vascular diseases and cancer. Defining the molecular mechanisms and receptors involved is revealing new therapeutic opportunities. Recent Advances: Thrombospondin-1 (TSP1) regulates NO, H 2 S, and superoxide production and signaling in several cell types. The TSP1 receptor CD47 plays a central role in inhibition of NO signaling, but other TSP1 receptors also modulate redox signaling. The matricellular protein CCN1 engages some of the same receptors to regulate redox signaling, and ADAMTS1 regulates NO signaling in Marfan syndrome. In addition to mediating matricellular protein signaling, redox signaling is emerging as an important pathway that controls the expression of several matricellular proteins. Critical Issues: Redox signaling remains unexplored for many matricellular proteins. Their interactions with multiple cellular receptors remains an obstacle to defining signaling mechanisms, but improved transgenic models could overcome this barrier. Future Directions: Therapeutics targeting the TSP1 receptor CD47 may have beneficial effects for treating cardiovascular disease and cancer and have recently entered clinical trials. Biomarkers are needed to assess their effects on redox signaling in patients and to evaluate how these contribute to their therapeutic efficacy and potential side effects. Antioxid. Redox Signal. 27, 874-911.

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Phylogenesis of constitutively formed nitric oxide in non-mammals

Cited by 25 publications

References 315 publications

De Novo Lipogenesis Maintains Vascular Homeostasis through Endothelial Nitric-oxide Synthase (eNOS) Palmitoylation*

De Novo Lipogenesis Maintains Vascular Homeostasis through Endothelial Nitric-oxide Synthase (eNOS) Palmitoylation*

NADPH-diaphorase activity in the central nervous system of the Gray mussel Crenomytilus grayanus (Dunker) under stress conditions: A histochemical study

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

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