Isoforms of nitric oxide synthase Characterization and purification from different cell types

Förstermann, Ulrich; Schmidt, Harald; Pollock, Jennifer S.; Sheng, Hong; Mitchell, Jane A.; Warner, Timothy D.; Nakane, Masaki; Murad, Ferid

doi:10.1016/0006-2952(91)90581-o

Cited by 801 publications

(307 citation statements)

References 54 publications

Supporting

Mentioning

286

Contrasting

Unclassified

Order By: Relevance

“…In many types of cells (21,22), citrulline can be enzymatically recycled to arginine, presumably for further NO synthesis. There are several isoforms of NOS, representing at least 3 different gene products, occupying soluble and particulate subcellular sites (23). Depending upon the source, these enzymes are active as monomers or homodimers with monomeric molecular weights of approximately 125-155 kd.…”

Section: Biosynthesis Of Nitric Oxidementioning

confidence: 99%

Nitric oxide and arthritis

Stefanović-Račić

Stadler

Evans

1993

Arthritis & Rheumatism

273

136

View full text Add to dashboard Cite

Section: Biosynthesis Of Nitric Oxidementioning

confidence: 99%

Nitric oxide and arthritis

Stefanović-Račić

Stadler

Evans

1993

Arthritis & Rheumatism

273

136

View full text Add to dashboard Cite

“…The nNOS and eNOS are constitutive forms of NOS and mainly expressed in the neuronal and endothelial cells, respectively. The iNOS is an inducible form of NOS and mainly expressed in macrophages [15].Primary function of NO is the activation of soluble guanylyl cyclase (sGC) to increase cGMP levels [1]. In the cilia of the rat sensory cells (olfactory cells), it is reported that odorant-stimulus induces the increase of cGMP levels and that specific NOS inhibitor L-N G -nitro arginine or NO scavenger hemoglobin inhibits this increase [4].…”

mentioning

confidence: 99%

Localization of eNOS in the Olfactory Epithelium of the Rat

Endo

Yamamoto

Yamaguchi-Yamada

et al. 2011

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

ABSTRACT. Nitric oxide (NO) is a free radical and produced from L-arginine by nitric oxide synthase (NOS). Since NO is recently suggested to be involved in olfactory perception, the expression of eNOS, an isoform of NOS, was examined in the rat olfactory epithelium. The activity of NADPH-diaphorase was also examined as a marker of NOS. In the dorsomedial region of the nasal cavity, intensely positive reactions for NADPH-diaphorase were observed in the entire cytoplasm of sensory cells (olfactory cells). By immunohistochemistry, intensely positive reactions for eNOS were also found in the dorsomedial region of the nasal cavity. These reactions were observed on the free border of the olfactory epithelium. By immunoelectron microscopy, positive reactions for eNOS were found in the cilia of olfactory cells. In addition, in situ hybridization analysis of the olfactory epithelium revealed the expression of eNOS mRNA in the olfactory cells. These results indicate the presence of eNOS in the olfactory cells of the rat, and differential expression of eNOS in the olfactory epithelium depending on the regions of the nasal cavity. In addition, NO produced by eNOS may be involved in olfactory perception in the cilia of olfactory cells.KEY WORDS: eNOS, NADPH-diaphorase, nitric oxide, olfactory epithelium, rat.J. Vet. Med. Sci. 73(4): 423-430, 2011 Nitric oxide (NO) is a free radical with many functions in the cardiovascular, nervous, and immune systems [2]. Biologically, NO is produced from L-arginine by nitric oxide synthase (NOS). NOS is divided into 3 types of major isoforms, i.e., neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS). The nNOS and eNOS are constitutive forms of NOS and mainly expressed in the neuronal and endothelial cells, respectively. The iNOS is an inducible form of NOS and mainly expressed in macrophages [15].Primary function of NO is the activation of soluble guanylyl cyclase (sGC) to increase cGMP levels [1]. In the cilia of the rat sensory cells (olfactory cells), it is reported that odorant-stimulus induces the increase of cGMP levels and that specific NOS inhibitor L-N G -nitro arginine or NO scavenger hemoglobin inhibits this increase [4]. These findings indicate that odorant-stimulus induces NO production in the rat olfactory cells. Schmachtenberg et al. (2000Schmachtenberg et al. ( , 2003 reported that NO-stimulus induces outward potassium currents in 30 out of 72 olfactory cells and inward potassium currents in 3 out of 54 cells by physiological study [36,37]. In the cilia of rat olfactory cells, moreover, NO-stimulus is reported to activate or inhibit olfactory cyclic nucleotidegated (CNG) channels [5,6,28,36,37]. These reports suggest that NO is produced by the olfactory cells in response to odorant-stimulus, and has inhibitory and/or weakly excitatory effects to the olfactory cells by gating of CNG channel. However, it is still unclear which type of NOS isoforms generates NO in the olfactory cells of the rat. Because it has been reported that iNOS and eNOS are expressed...

show abstract

“…The brain expresses all three identified nitric oxide synthase isoforms, and NOS activity in the brain is higher than in any other tissues [44]. Neurons produce NO by activation of nNOS [45], and glial cells (astrocytes, microglia and oligodendrocytes) synthetisize NO by iNOS activation [46].…”

Section: Cerebral No Production and Nos Expressions During Ischemia Amentioning

confidence: 99%

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Miclescu¹

2010

Acta Anaesthesiol Scand

View full text Add to dashboard Cite

Although survival rates are increasing, brain injury continues to be a leading cause of death after cardiac arrest (CA). Permanent brain damage after CA is determined by limited tolerance to ischemia from CA and cardiopulmonary resuscitation (CPR), as well as the unique cerebral response to reperfusion after return of spontaneous circulation (ROSC). A major pathway leading to neurotoxic cascade and neuronal injury after CA involves the increased presence of reactive oxygen and nitrogen species generated during ischemia and reperfusion. The magnitude of cerebral oxidative injury induced by free radicals increased with the duration of CA (Paper I). Nitric oxide (NO), a free radical responsible for the formation of reactive nitrogen species, is increased during global ischemia from CA and reperfusion (Paper IV). Hypothetically, the administration of a drug that counteracts the overproduction of NO and also acts as a scavenger of oxygen free radicals might be warranted in order to reduce the damage caused by nitrosative and oxidative stress. For these purposes we used methylene blue (MB), an old dye that has been used in medicine for almost half a century, and an experimental pig model of 20 min of ventricular fibrillation (VF) to reflect a clinical scenario of ischemia/reperfusion injury. Administration of MB added to a hypertonic-hyperoncotic solution (MBHSD) that was started during CPR and continued for 50 min after ROSC increased short-term survival by decreasing myocardial damage, as well as cerebral peroxidation and inflammatory injury (Paper II). Immunostaining of cerebral tissue collected at different time points after CA and ROSC (Paper IV) provided experimental evidence that cortical blood-brain barrier (BBB) disruption begins as early as during the initial phase of untreated as well as treated CA. The results indicated that MB administration reduced the neurologic injury and BBB disruption considerably, but did not reverse the ongoing detrimental processes. The demonstrated positive effects of MB were related to a decrease of nitrite/nitrate tissue content, and thus to a decrease of excess NO due to the MB inhibitory effects on NOS isoforms. A mixture of MB in hypertonic sodium lactate (MBL) was investigated to facilitate administration of MB in "the field." Based on findings that MBL cardio-and neuroprotective properties were similar to those of MBHSD, there is reason to believe that the use of MBL might be extended during ongoing CPR and after ROSC (Paper III). It would therefore make sense to try using MB as a pharmacological neuroprotectant during or after clinical CPR in order to expand the temporal therapeutic window before other measures for neuroprotection such as hypothermia are available. Keywords: Cardiac arrest, cardiopulmonary resuscitation, reperfusion injury, methylene blue, nitric oxide, nitric oxide synthases, blood-brain barrier

show abstract

Isoforms of nitric oxide synthase Characterization and purification from different cell types

Cited by 801 publications

References 54 publications

Nitric oxide and arthritis

Nitric oxide and arthritis

Localization of eNOS in the Olfactory Epithelium of the Rat

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Contact Info

Product

Resources

About