Do transient ischemic attacks have a neuroprotective effect?

Moncayo, Jorge; Freitas, Gabriel R. de; Bogousslavsky, Julien; Altieri, Marta; Melle, Guy van

doi:10.1212/wnl.54.11.2089

Cited by 262 publications

(220 citation statements)

References 27 publications

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“…Indeed, Kitagawa et al (1990) found that gerbils subjected to sublethal transient global ischemia exhibited reduced hippocampal CA1 neuronal death after a more severe ischemic insult 24 -48 hr later, and similar findings have been reported by others (for review, see Barone et al, 1998;Kirino, 2002). Ischemic tolerance also has been demonstrated in human clinical practice, because less severe strokes have been described in patients with prior ipsilateral transient ischemic attacks within a short period of time (Weih et al, 1999;Moncayo et al, 2000;Castillo et al, 2003). The remarkable protection induced by IPC makes this an attractive target for potential therapeutic development.…”

Section: Introductionsupporting

confidence: 59%

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

Romera¹,

Hurtado²,

Botella³

et al. 2004

J. Neurosci.

117

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A short ischemic event [ischemic preconditioning (IPC)] can result in a subsequent resistance to severe ischemic injury (ischemic tolerance). Although tumor necrosis factor-␣ (TNF-␣) contributes to the brain damage found after cerebral ischemia, its expression and neuroprotective role in models of IPC have also been described. Regarding the role of TNF-␣ convertase (TACE/ADAM17), we have recently shown its upregulation in rat brain after IPC induced by transient middle cerebral artery occlusion and that subsequent TNF-␣ release accounts for at least part of the neuroprotection found in this model. We have now used an in vitro model of IPC using rat cortical cultures exposed to sublethal oxygen-glucose deprivation (OGD) to investigate TACE expression and activity after IPC and the subsequent mechanisms of ischemic tolerance. OGD-induced cell death was significantly reduced in cells exposed to IPC by sublethal OGD 24 hr before, an effect that was inhibited by the TACE inhibitor BB3103 (1 M) and anti-TNF-␣ antibody (2 g/ml) and that was mimicked by TNF-␣ (10 pg/ml) preincubation. Western blot analysis showed that TACE expression is increased after IPC. IPC caused TNF-␣ release, an effect that was blocked by the selective TACE inhibitor BB-3103. In addition, IPC diminished the increase in extracellular glutamate caused by OGD and increased cellular glutamate uptake and expression of EAAT2 and EAAT3 glutamate transporters; however, only EAAT3 upregulation was mediated by increased TNF-␣. These data demonstrate that neuroprotection induced by IPC involves upregulation of glutamate uptake partly mediated by TACE overexpression.

show abstract

Section: Introductionsupporting

confidence: 59%

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

Romera¹,

Hurtado²,

Botella³

et al. 2004

J. Neurosci.

117

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“…This phenomenon has been described in several organs, especially the heart and brain. Ischemic tolerance has also been shown in human clinical practice; indeed, less severe strokes have been described in patients with prior ipsilateral transient ischemic attacks (TIA) within a short period of time (Weih et al, 1999;Moncayo et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

TNFR1 Upregulation Mediates Tolerance after Brain Ischemic Preconditioning

Pradillo

Romera

Hurtado

et al. 2005

J Cereb Blood Flow Metab

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A short ischemic event (ischemic preconditioning (IPC)) can result in subsequent resistance to severe ischemic injury (ischemic tolerance (IT)). The expression and neuroprotective role of tumor necrosis factor (TNF-a) have been described in models of IPC and we have showed the participation of its processing enzyme, the TNF-a convertase enzyme (TACE) in this process. We have now decided to explore the expression and localization of TNF receptors (TNFR) as well as other signalling mechanisms involved in IT. A period of 10 mins of temporary middle cerebral artery occlusion (tMCAO) was used for focal IPC. To evaluate the ability of IPC to produce IT, permanent MCAO was performed 48 hours after IPC. Ischemic preconditioning produced a reduction in infarct volume, as we showed previously. Ischemic preconditioning caused upregulation of neuronal TNFR1 that was reduced by the selective TACE inhibitor BB1101. Intracerebral administration of TNFR1 antisense oligodeoxynucleotide, which caused a reduction in TNFR1 expression, inhibited the IPC-induced protective effect, showing that TNFR1 upregulation is implicated in IT. Moreover, treatment with BB1101, TNFR1 antisense and lactacystin-a specific proteasome inhibitor-blocked IPC-induced NF-jB. Immunohistochemical studies showed the expression of TACE and TNFR1 in neurons. In summary, these data show that IPC produces neuronal upregulation of TACE and TNFR1, and that the pathway TACE/TNF-a/TNFR1/NF-jB is involved in IT.

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“…A recent human study showed that patients with repeated attacks of cerebral ischemia had a better neurologic outcome than patients without a previous ischemic attack (Moncayo et al, 2000). Another human study revealed that adenosine plasma levels were markedly increased and that the adenosine surge lasts days after transient ischemic attack and weeks after stroke (Pasini et al, 2000).…”

mentioning

confidence: 99%

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Yoshida

Nakakimura

Cui

et al. 2004

J Cereb Blood Flow Metab

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Summary:Involvement of adenosine and adenosine triphosphate-sensitive potassium (K ATP ) channels in the development of ischemic tolerance has been suggested in global ischemia, but has not been studied extensively in focal cerebral ischemia. This study evaluated modulating effects of adenosine A 1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) and mitochondrial K ATP channel blocker 5HD (5-hydroxydecanoate) on the development of tolerance to focal cerebral ischemia in rats. Preconditioning with 30-minute middle cerebral artery occlusion (MCAO) reduced cortical and subcortical infarct volume following 120-minute MCAO (test ischemia) given 72 hours later. The neuroprotective effect of preconditioning was attenuated by 0.1 mg/kg DPCPX given before conditioning ischemia (30-minute MCAO), but no influence was provoked when it was administered before test ischemia. DPCPX had no effect on infarct volume after conditioning or test ischemia when given alone. The preconditioning-induced neuroprotection disappeared when 30 mg/kg 5HD was administered before test ischemia. These results suggest a possible involvement of adenosine A 1 receptors during conditioning ischemia and of mitochondrial K ATP channels during subsequent severe ischemia in the development of tolerance to focal cerebral ischemia.

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Do transient ischemic attacks have a neuroprotective effect?

Abstract: This study suggests that ischemic tolerance may play a role in patients with ipsilateral TIAs before CI, allowing better recovery from a subsequent ischemic stroke.

Cited by 262 publications

References 27 publications

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

TNFR1 Upregulation Mediates Tolerance after Brain Ischemic Preconditioning

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

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Do transient ischemic attacks have a neuroprotective effect?

Abstract: This study suggests that ischemic tolerance may play a role in patients with ipsilateral TIAs before CI, allowing better recovery from a subsequent ischemic stroke.

Cited by 262 publications

References 27 publications

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

TNFR1 Upregulation Mediates Tolerance after Brain Ischemic Preconditioning

Adenosine A1 Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Contact Info

Product

Resources

About

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats