Injury–induced expression of endothelial nitric oxide synthase by glial and microglial cells in the leech central nervous system within minutes after injury

Shafer, Orie T.; Chen, Aileen B.; Kumar, Shreya; Muller, Kenneth J.; Sahley, Christie L.

doi:10.1098/rspb.1998.0555

Cited by 38 publications

(42 citation statements)

References 26 publications

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“…We also detected eNOS gene transcriptional expression through RT-PCR analysis, suggesting that eNOS is synthesized by umbilical cord cells. In agreement with our data, eNOS expression, typical of endothelia, has also been reported in other types of tissues and cells, such as many epithelium, fibroblasts, cardiomyocytes, osteocytes and glial cells [32][33][34][35].…”

Section: Discussion Discussion Discussion Discussionsupporting

confidence: 81%

Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS

Mauro¹,

Buscemi²,

Provenzano³

et al. 2011

Folia Histochem Cytobiol.

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Section: Discussion Discussion Discussion Discussionsupporting

confidence: 81%

Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS

Mauro¹,

Buscemi²,

Provenzano³

et al. 2011

Folia Histochem Cytobiol.

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“…In response to injury, leech connective glia and some microglia express endothelial nitric oxide synthase (eNOS) as revealed by immunolabeling. Minutes after the injury, eNOS activity could be detected as indicated by a histochemical labeling for NADPH diaphorase (822). The NO could mediate the accumulation of microglia at the lesion site in the leech: a NOS inhibitor significantly reduced microglial accumulation.…”

Section: Evolutionary Origins Of Microgliamentioning

confidence: 91%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,070

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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“…Although the role of eNOS in radiation-induced salivary gland injury remains unknown, it might be related to epithelial cell regeneration, since a marked increase in eNOS occurs in the denuded aorta and during the repair stage of inflammation (21,24).…”

Section: Measurement Of Omentioning

confidence: 99%

Peroxynitrite formation in radiation-induced salivary gland dysfunction in mice

et al. 2007

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Xerostomia frequently arises in patients with head and neck malignancies that are treated by radiation. However, the mechanisms responsible for the destruction of the salivary gland remain unknown. We previously established a xerostomia model of mice and identified the pathway through which nitric oxide (NO) affects the pathogenesis of radiation-induced salivary gland dysfunction. Although the toxicity of NO alone is modest, NO with superoxide anion (O 2•− ) rapidly forms peroxynitrite (ONOO − ), a more powerful toxic oxidant. In this study, we used the experimental model to examine: 1) when NO and O 2•− production is maximum in the salivary gland after irradiation; 2) whether peroxynitrite, as assessed by nitrotyrosine production, is responsible for salivary gland dysfunction; and 3) the effect of the iNOS selective inhibitor, aminoguanidine (AG), on nitrotyrosine formation. The increases in production of NO and O 2•− in the salivary gland peaked on day 7 after irradiation. Nitrotyrosine detected immunohistochemically was significantly reduced by AG in the salivary gland. On the basis of these results, we concluded that NO together with O 2•− forms the more reactive ONOO − , which might be an important pathogenic factor in radiation-induced salivary gland dysfunction.Radiotherapy is an established therapy for head and neck malignancies, but the treatment field might include normal several tissues and organs. As a result, xerostomia due to salivary gland dysfunction is a clinically important side effect that is often irreversible (23, 25). The actions of radiation include a direct effect of the radiation itself and the indirect DNA injury caused by the •OH radical, which induces cell death and salivary gland atrophy (3, 17). However, the actual pathogenesis of radiation-induced xerostomia is obscure, and an effective treatment has not been established.We previously established a xerostomia model using mice and identified the inflammatory pathway through which NO affects the pathogenesis of radiation-induced salivary gland dysfunction (27). NO is a radical molecule and has been identified as a vascular endothelium-derived relaxing factor (7,9,20). NO is generated by three types of nitric oxide synthase (NOS): neural NOS, endothelial NOS and inducible NOS (20). The expression of inducible NOS (iNOS) is induced by inflammatory cytokines (1,19) and that large amounts of NO are continuously released from activated macrophages through the NADPH-dependent oxidant deamination of L-arginine (9). The toxicity of NO is due both to NO itself and to NO-derived reactive oxidants (4). The modest toxicity of NO is increased by rapidly binding with NO together with O 2•− to form ONOO − , which is a more powerful, toxic oxidant (25). However, most of these reactive oxidants can not be directly detected in vivo. Thus, nitrotyrosine is used as a biomark-

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Injury–induced expression of endothelial nitric oxide synthase by glial and microglial cells in the leech central nervous system within minutes after injury

Cited by 38 publications

References 26 publications

Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS

Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS

Physiology of Microglia

Peroxynitrite formation in radiation-induced salivary gland dysfunction in mice

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