Permanent focal and transient global cerebral ischemia increase glial and neuronal expression of heme oxygenase-1, but not heme oxygenase-2, protein in rat brain

Geddes, James W.; Pettigrew, L. Creed; Holtz, Mary L.; Craddock, Susan D.; Maines, Mahin D.

doi:10.1016/0304-3940(96)12703-8

Cited by 111 publications

(59 citation statements)

References 21 publications

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“…The rats were divided into seven groups and subjected to corresponding treatment. Transient cerebral ischemia induced HO-1 expression in glial and neuronal cells while no effects on HO-2 were observed (26). Probably due to its sensitivity to stress, HO-1 was also detected in the sham control.…”

Section: In Vivo Induction Of Ho-1 Expressionmentioning

confidence: 87%

Induction of heme oxygenase-1 by traditional Chinese medicine formulation ISF-1 and its ingredients as a cytoprotective mechanism against oxidative stress

Cheung¹,

Lau²,

Shen³

et al. 2008

Int J Mol Med

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Abstract. Traditional medicines are clinically used to treat post-stroke disorders in China. In search of alternative medicines for post-stroke rehabilitation, we recently identified the heme oxygenase-1 (HO-1) pathway as a key mechanism underlying the biological activities of the ischemic stroke formulation ISF-1. This study was designed to further investigate ISF-1 for HO-1 induction in cultured human cells and corresponding cytoprotective effects against oxidative injury. A rat stroke model induced by middle cerebral artery occlusion was employed to verify the activity of ISF-1 in vivo. It was found that HO-1 expression was induced by ISF-1 in a dose-and time-dependent manner. Four ingredients from ISF-1 were identified to be responsible for HO-1 induction. The appropriate combinations of these active ingredients or purified compounds resulted in synergistic induction of HO-1 expression. A minimal HO-1-inducing formulation was prepared and showed significant cytoprotection against H 2 O 2 -induced oxidative stress. Collectively, the herbal formulation ISF-1 was capable of inducing HO-1 expression, in vitro and in vivo, offering a potential mechanism for post-stroke rehabilitation. This study may shed light on the development of mechanism-defined therapies based on traditional herbal remedies.

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Section: In Vivo Induction Of Ho-1 Expressionmentioning

confidence: 87%

Induction of heme oxygenase-1 by traditional Chinese medicine formulation ISF-1 and its ingredients as a cytoprotective mechanism against oxidative stress

Cheung¹,

Lau²,

Shen³

et al. 2008

Int J Mol Med

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show abstract

“…Biliverdin is then rapidly converted by biliverdin reductase to bilirubin, a molecule with antioxidant properties, and free iron is sequestered by ferritin [65,66]. HO-1, a heat-shock protein (HSP-32), is a cytoprotective stress protein that is induced in the brain in response to permanent focal ischemia [24,25], and a hypoxia-inducible factor-1α-regulated gene [67]. The increased expression of HO-1 in ischemic brain tissue is probably of physiological consequence in the recovery of neuronal tissue following focal cerebral infarction, that leads to a beneficial outcome [26].…”

Section: Discussionmentioning

confidence: 99%

“…A growing body of evidence suggests that HO may play an important role in protection against cerebral ischemia; therefore, induction of HO-1 protein expression following cerebral ischemia can lead to a beneficial outcome [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinase Inhibitors Attenuate Neuroinflammation Following Focal Cerebral Ischemia in Mice

Park

Shin

Lee

et al. 2011

Korean J Physiol Pharmacol

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The aim of this study was to investigate whether matrix metalloproteinase (MMP) inhibitors attenuate neuroinflammation in an ischemic brain following photothrombotic cortical ischemia in mice. Male C57BL/6 mice were anesthetized, and Rose Bengal was systemically administered. Permanent focal ischemia was induced in the medial frontal and somatosensory cortices by irradiating the skull with cold white light. MMP inhibitors, such as doxycycline, minocycline, and batimastat, significantly reduced the cerebral infarct size, and the expressions of monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-α (TNF-α ), and indoleamine 2,3-dioxygenase (IDO). However, they had no effect on the expressions of heme oxygenase-1 and neuroglobin in the ischemic cortex. These results suggest that MMP inhibitors attenuate ischemic brain injury by decreasing the expression levels of MCP-1, TNF-α , and IDO, thereby providing a therapeutic benefit against cerebral ischemia.

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“…As in the case of the PD nigra, cerebral cortices and hippocampi affected by Alzheimer's disease and CNS tissues subjected to ischemidreperfusion exhibit enhanced glial HO-1 immunoreactivity, abnormal iron deposits, and mitochondrial insufficiency (Oubidar et al, 1994;Reichmann and Riederer, 1994;Schipper et al, 1995;Geddes et al, 1996;Janetzky et al, 1997). In addition, cytokines implicated in the pathogenesis of multiple sclerosis, such as tumor necrosis factor-a and interleukin-1 p, stimulate HO-1 expression in cultured astroglia followed by sequestration of non-transferrinderived iron by the mitochondrial compartment (K. Mehindate, S. Dion, and H. M. Schipper, unpublished results).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Iron Sequestration in Dopamine‐Challenged Astroglia: Role of Heme Oxygenase‐1 and the Permeability Transition Pore

Schipper

Bernier

Mehindate

et al. 1999

Journal of Neurochemistry

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Abstract:Little is currently known concerning the mechanisms responsible for the excessive deposition of redox-active iron in the substantia nigra of subjects with Parkinson's disease (PD). In the present study, we demonstrate that dopamine promotes the selective sequestration of non-transferrin-derived iron by the mitochondrial compartment of cultured rat astroglia and that the mechanism underlying this novel dopamine effect is oxidative in nature. We also provide evidence that up-regulation of the stress protein heme oxygenase-1 (HO-1) is both necessary and sufficient for mitochondrial iron trapping in dopamine-challenged astroglia. Finally, we show that opening of the mitochondrial transition pore (MTP) mediates the influx of non-transferrin-derived iron into mitochondria of dopamine-stimulated and HO-1 -transfected astroglia. Our findings provide an explanation for the pathological iron sequestration, mitochondrial insufficiency, and amplification of oxidative injury reported in the brains of PD subjects. Pharmacological blockade of transition metal trapping by "stressed" astroglial mitochondria (e.g., using HO-1 inhibitors or modulators of the MTP) may afford effective neuroprotection in patients with PD and other neurological afflictions.

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Permanent focal and transient global cerebral ischemia increase glial and neuronal expression of heme oxygenase-1, but not heme oxygenase-2, protein in rat brain

Cited by 111 publications

References 21 publications

Induction of heme oxygenase-1 by traditional Chinese medicine formulation ISF-1 and its ingredients as a cytoprotective mechanism against oxidative stress

Induction of heme oxygenase-1 by traditional Chinese medicine formulation ISF-1 and its ingredients as a cytoprotective mechanism against oxidative stress

Matrix Metalloproteinase Inhibitors Attenuate Neuroinflammation Following Focal Cerebral Ischemia in Mice

Mitochondrial Iron Sequestration in Dopamine‐Challenged Astroglia: Role of Heme Oxygenase‐1 and the Permeability Transition Pore

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