Nitric oxide synthase type I and type III gene expression are developmentally regulated in rat lung

North, Amy J.; Star, Robert A.; Brannon, Timothy S.; Ujiie, Kazutomo; Wells, Lieselotte B.; Lowenstein, Charles J.; Snyder, Solomon H.; Shaul, Philip W.

doi:10.1152/ajplung.1994.266.6.l635

Cited by 101 publications

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“…In the developing lung, there is an increase in eNOS mRNA and protein in late gestation, reaching a maximal level at 20 d gestation, followed by a decrease in expression following birth (8). It has been proposed that maximizing pulmonary eNOS expression at birth may serve to optimize the capacity for NO-mediated pulmonary vasodilation during transition (17).…”

Section: Discussionmentioning

confidence: 99%

“…The latter is under the control of eNOS. Expression of eNOS in the lung is highest at the time of birth, possibly serving to optimize the capacity for pulmonary vasodilation during transition (5,8). Hepatic blood flow also changes significantly postnatally.…”

mentioning

confidence: 99%

“…eNOS plays a role in control of vascular tone in most vascular beds (6). eNOS participates in the control of vascular tone during the transition from fetal circulation to postnatal circulation in the ductus arteriosus (7) and lung (8). The role of eNOS in control of the ductus arteriosus is age dependent.…”

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confidence: 99%

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Developmental Expression of Endothelial Nitric Oxide Synthase (eNOS) in the Rat Liver

et al. 2003

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Transition from fetal to postnatal life requires significant changes in cardiac, pulmonary, and hepatic blood flow. As such, there must be changes in vascular control in these vascular systems. Vascular resistance, a major contributor to blood flow, is mediated in the ductus arteriosus and pulmonary vasculature by endothelial nitric oxide synthase (eNOS). This study was conducted to determine the ontogeny of hepatic eNOS expression and activity. Additionally, the expression and activity of inducible nitric oxide synthase (iNOS) was measured to determine whether perinatal hypoxia resulted in detectable levels. NOS mRNA and proteins were determined by reverse transcription PCR assay and semiquantitative Western blot analysis, respectively. NOS activity was measured by the formation of [ 14 C]-citrulline from [14 C]-arginine. Localization of eNOS within the liver was determined by immunohistochemistry. eNOS mRNA was detectable at low levels at 18-d gestation and increased after birth, reaching a maximum level (4.5-fold increase) at 20 d of life. Parallel patterns for eNOS protein and activity were seen, with 6.9-fold and 16.1-fold increases, respectively. In the prenatal rat, eNOS was localized to areas of extramedullary hematopoiesis, with little signal in the sinusoids. Postnatally, there was a decrease in staining in the hematopoietic cells and a gradual increase in the staining of the endothelium of the sinusoids and central veins. iNOS mRNA and protein could not be detected at any age. eNOS expression and activity are developmentally regulated, increasing after birth coincident with an initial relative hypoxia and an increase in shear forces upon closure of the ductus venosus. NO is a short-lived free radical that influences physiologic processes in essentially every organ and tissue. Some of the roles of NO include neuromodulator, prevention of clotting, mediation of bactericidal and tumoricidal activity of macrophages, and regulation of blood pressure. NO is enzymatically synthesized from L-arginine by three known NOS isoforms: constitutively expressed eNOS (or NOS-3), nNOS (or NOS-1), iNOS (or NOS-2) (1-3). NO production by eNOS is primarily regulated by fluctuations in intracellular calcium levels. In the liver under normal conditions, only eNOS is present, produced by the sinusoidal endothelial cells (4, 5). The resulting low level of NO production is a major contributor of the basal vascular tone in the normal liver (4, 5).eNOS plays a role in control of vascular tone in most vascular beds (6). eNOS participates in the control of vascular tone during the transition from fetal circulation to postnatal circulation in the ductus arteriosus (7) and lung (8). The role of eNOS in control of the ductus arteriosus is age dependent. The effects of eNOS are more pronounced in determining vascular tone of the ductus arteriosus in the preterm animal than in the near-term or adult animal (7, 9). During the transition period, blood flow to the lungs is increased by a number of factors, including closure of the ductus ...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Developmental Expression of Endothelial Nitric Oxide Synthase (eNOS) in the Rat Liver

et al. 2003

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“…The ecNOS and iNOS content of crude lung homogenates from groups N and H (both n=3) was determined by Western blot analysis as proposed by NORTH et al [15]. Lung tissue was homogenised on ice in 50 mM tris(hydroxymethyl)aminomethane (Tris)-HCl (pH 8.5).…”

Section: Western Blot Analysis For Nitric Oxide Synthase Proteins In mentioning

confidence: 99%

NOS and COX isoforms and abnormal microvessel responses to CO2 and H+ in hyperoxia-injured lungs

Naoki¹,

Kudo²,

Suzuki³

et al. 2002

European Respiratory Journal

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The aim of the present study was to compare microvessel responses to hypercapnic and isocapnic acidosis in hyperoxia-injured lungs and to assess the role of constitutive and inducible forms of nitric oxide synthase (NOS) and cyclo-oxygenase (COX).Real-time confocal luminescence microscopy was used to measure changes in the diameter of acinar arterioles, venules and capillaries in response to stimulation with hypercapnic and isocapnic acidosis in isolated rat lungs injured by 90% oxygen exposure for 48 h. Observations were made with and without inhibition of constitutive (endothelial constitutive NOS (ecNOS) and COX-1) and inducible isoforms (iNOS and COX-2) of NOS and COX. Upregulation of NOS was assessed by measuring enzyme levels in lung homogenates by Western blot analysis and enhancement of the COX-related pathway was judged from perfusate concentrations of 6-ketoprostaglandin F 1a .ecNOS and COX-1, but not iNOS and COX-2, were upregulated in hyperoxiainjured lungs. The nitric oxide produced by ecNOS attenuated COX-1 activity in injured arterioles and venules, but carbon dioxide enhanced it, leading to paradoxical dilatation of these microvessels under hypercapnic conditions with ecNOS inhibition. Although a high hydrogen ion concentration was unnecessary for excitation of COX-1, venule constriction in response to H z was enhanced by COX-1 inhibition. Constitutive, but not inducible, isoforms of cyclo-oxygenase and nitric oxide synthase play an important role in abnormal microvessel responses to carbon dioxide and hydrogen ions in hyperoxia-injured lungs. Eur Respir J 2002; 20: 43-51.

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“…nNOS expression was found to be subject to regulation by estrogen (11), and was induced after axotomy, in parallel with an increased expression of the transcription factors jun and krox (12,13). Furthermore, transient changes in levels of expression of nNOS have been observed in the developing rat nervous system and lung (14,15). Likewise, the onset of nNOS expression in the developing tectum in chicken coincides with the onset of innervation by axons from retinal ganglion cells (16).…”

Section: Introductionmentioning

confidence: 99%

Tissue- and development-specific expression of multiple alternatively spliced transcripts of rat neuronal nitric oxide synthase.

Lee

Cai²,

Hübner³

et al. 1997

J. Clin. Invest.

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Nitric oxide (NO) functions as an intercellular messenger and mediates numerous biological functions. Among the three isoforms of NO synthase that produce NO, the ubiquitously expressed neuronal NO synthase (nNOS) is responsible for a large part of NO production, yet its regulation is poorly understood. Recent reports of two alternative spliceforms of nNOS in the mouse and in man have raised the possibility of spatial and temporal modulation of expression. This study demonstrates the existence of at least three transcripts of the rat nNOS gene designated nNOSa, nNOSb, and nNOSc, respectively, with distinct 5 Ј untranslated first exons that arise from alternative splicing to a common second exon. Expression of the alternative transcripts occurs with a high degree of tissue and developmental specificity, as demonstrated by RNase protection assays on multiple tissues from both fetal and adult rats.

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Nitric oxide synthase type I and type III gene expression are developmentally regulated in rat lung

Cited by 101 publications

References 0 publications

Developmental Expression of Endothelial Nitric Oxide Synthase (eNOS) in the Rat Liver

Developmental Expression of Endothelial Nitric Oxide Synthase (eNOS) in the Rat Liver

NOS and COX isoforms and abnormal microvessel responses to CO2 and H+ in hyperoxia-injured lungs

Tissue- and development-specific expression of multiple alternatively spliced transcripts of rat neuronal nitric oxide synthase.

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