2003
DOI: 10.1046/j.1471-4159.2003.01776.x
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Heme oxygenase‐1 and heme oxygenase‐2 have distinct roles in the proliferation and survival of olfactory receptor neurons mediated by cGMP and bilirubin, respectively

Abstract: Heme oxygenase (HO) is implicated in protection against oxidative stress, proliferation and apoptosis in many cell types, including neurons. We utilized olfactory receptor neurons (ORNs) as a model to define the roles of HO-1 and HO-2 in neuronal development and survival, and to determine the mediators of these effects. The olfactory system is a useful model as ORNs display neurogenesis post-natally and do not contain nitric oxide synthase (NOS) activity, which could confound results. HO isoforms were expresse… Show more

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Cited by 43 publications
(56 citation statements)
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“…The beneficial effect of HO-1 is in general agreement with many prior observations in neural and nonneural systems (Chen et al, 2003;Clark et al, 2000;Turner et al, 1999).…”
Section: Heme Oxygenase As Modulator Of Neural Injurysupporting
confidence: 91%
“…The beneficial effect of HO-1 is in general agreement with many prior observations in neural and nonneural systems (Chen et al, 2003;Clark et al, 2000;Turner et al, 1999).…”
Section: Heme Oxygenase As Modulator Of Neural Injurysupporting
confidence: 91%
“…In the normal brain and in cerebral vessels, HO-1 is undetectable, with the exception of few neuronal populations, mainly olfactory and hippocampal neurons [37][38][39][40][41][42]. In sharp contrast to other tissues, brain and cerebrovascular HO-1 is not readily induced by oxidative stress, with the exception of very limited array of strong pro-oxidant signals.…”
Section: Heme Oxygenase Isoforms In Cerebral Circulationmentioning
confidence: 96%
“…The cerebral infarction volume was greatly increased in HO2-KO mice as well as in WT mice with SnPP-inhibited HO-2 enzymatic activity [47]. In a model of glutathione depletion-induced oxidative injury, brain neuronal damage and olfactory neuronal death were also greatly aggravated in HO2-KO mice [37].…”
Section: Ho-2 Protection Against Oxidative Stress-related Neuronalmentioning
confidence: 97%
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“…Other studies found that TSG facilitated tetanus stimulationinduced hippocampal long-term potentiation through activation of NMDA receptor in the hippocampal CA1 region of normal mice; phosphorylation of CaMKII and activation of ERK1/2 cascades possibly mediated TSG-induced enhancement [76] . There are also investigations suggested that TSG attenuated lipopolysaccharide (LPS)-mediated induction of pro-inflammatory factors in microglia through reducing binding activity of NF-κB [57] , and attenuated LPSinduced NADPH oxidase activation and subsequent reactive oxygen species production [49] ; while microglia are believed to mediate development of AD and that neurons injury is usually secondary to microglia activation [77][78][79][80] . …”
Section: Antioxidant Effect Of Tsgmentioning
confidence: 99%