Differential role of nitric oxide pathway and heat shock protein in preconditioning and lipopolysaccharide-induced brain ischemic tolerance

Puisieux, François; Deplanque, Dominique; Qian, Pu; Souil, Évelyne; Bastide, Michèle; Bordet, Régis

doi:10.1016/s0014-2999(99)00893-6

Cited by 85 publications

(61 citation statements)

References 26 publications

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“…A number of observations implicate nitric oxide (NO) in PC (Huang, 2004). Vascular nitric oxide synthase (NOS) expression is increased, reported for the endothelial isoform (eNOS) after LPS PC in rats (Puisieux et al, 2000), and for the inducible isoform (inducible nitric oxide synthase (iNOS)) after ischemic PC in mice (Cho et al, 2005). A temporally associated increase in vasodilatory tone, showed in rat aorta after LPS treatment (Pu et al, 1999), might be a functional correlate of increased NOS expression.…”

Section: Perfusion Changes and Ischemic Preconditioningmentioning

confidence: 99%

“…A temporally associated increase in vasodilatory tone, showed in rat aorta after LPS treatment (Pu et al, 1999), might be a functional correlate of increased NOS expression. Available pharmacologic evidence is even more indicative of NO involvement in the initial mechanisms that trigger PC, with model-specific effects of various inhibitors to eliminate PC when given during the priming insult (Cho et al, 2005;Gidday et al, 1999;Puisieux et al, 2000). Failure to observe acute PC in both neuronal NOS and eNOS knockout mice (Atochin et al, 2003) or delayed protection in iNOS knockout mice (Cho et al, 2005) could reflect effects on both the development and the expression of PC.…”

Section: Perfusion Changes and Ischemic Preconditioningmentioning

confidence: 99%

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CBF Changes Associated with Focal Ischemic Preconditioning in the Spontaneously Hypertensive Rat

Zhao

Nowak

2006

J Cereb Blood Flow Metab

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Experimental stroke models exhibit robust protection after prior preconditioning (PC) insults. This study comprehensively examined cerebral blood flow (CBF) responses to permanent middle cerebral artery (MCA) occlusion in spontaneously hypertensive rats preconditioned by noninjurious transient focal ischemia, using [ 14 C]iodoantipyrine autoradiography at varied occlusion intervals. Preconditioning was produced by 10-min occlusion of the MCA and ipsilateral common carotid artery under halothane anesthesia. These vessels were permanently coagulated 24 h later in naïve, PC, and sham-operated rats. Infarct volumes were determined from hematoxylin-eosin-stained frozen sections after 1 or 3 days. Edema-corrected infarct volume was reduced from 127621 in naïve rats to 101631 and 52628 mm 3 in sham and PC groups, respectively, at 1 day, with similar results at 3 days. All animals exhibited a consistent CBF threshold for infarction (approximately 30 mL/100 g/ min). Tissue volumes below this threshold were identical in naïve and PC groups after 15-min occlusion. However, by 3 h the volume of ischemic cortex decreased in the PC group but remained unchanged in naïve rats, predicting final infarct volumes. Cerebral blood flow recovery was confirmed in brains of individual rats evaluated by repeated laser Doppler perfusion imaging during the same 3-h interval. Modest sham protection correlated with better-maintained global perfusion, detectable also in the contralateral cortex, apparently reflecting the PC effects of prior anesthesia. These results establish that timely reperfusion of penumbra, achieved by synergistic mechanisms, is a primary determinant of PC-induced protection in experimental stroke.

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Section: Perfusion Changes and Ischemic Preconditioningmentioning

confidence: 99%

Section: Perfusion Changes and Ischemic Preconditioningmentioning

confidence: 99%

CBF Changes Associated with Focal Ischemic Preconditioning in the Spontaneously Hypertensive Rat

Zhao

Nowak

2006

J Cereb Blood Flow Metab

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“…Tolerance to experimental brain ischemia can be induced by a variety of stimuli that elicit a stress response, such as transient cerebral ischemia (Barone et al 1998), cytokines (Beltrami et al 2003) and endotoxin (Jiang et al 2007). Recent evidence indicates that Toll-like receptors (TLRs) are involved in the preconditioning-induced tolerance to ischemia Puisieux et al 2000;Dawson et al 1999;Tasaki et al 1997;Stevens et al 2008). Toll-like receptors (TLRs) are a family of signal transduction molecules that play a critical role in the induction of innate and adaptive immunity (Medzhitov et al 1997).…”

Section: Introductionmentioning

confidence: 99%

“…Toll-like receptors (TLRs) are a family of signal transduction molecules that play a critical role in the induction of innate and adaptive immunity (Medzhitov et al 1997). Preconditioning with TLR4 Puisieux et al 2000;Dawson et al 1999;Tasaki et al 1997) and TLR9 (Stevens et al 2008) ligands has been reported to induce neuroprotection against ischemic injury. By way of example, the TLR4 ligand, lipopolysaccharide (LPS), can induce protection against ischemia-induced brain injury Puisieux et al 2000;Dawson et al 1999;Tasaki et al 1997).…”

Section: Introductionmentioning

confidence: 99%

“…Preconditioning with TLR4 Puisieux et al 2000;Dawson et al 1999;Tasaki et al 1997) and TLR9 (Stevens et al 2008) ligands has been reported to induce neuroprotection against ischemic injury. By way of example, the TLR4 ligand, lipopolysaccharide (LPS), can induce protection against ischemia-induced brain injury Puisieux et al 2000;Dawson et al 1999;Tasaki et al 1997). However, whether preconditioning induced by other TLR ligands can induce neuroprotection in ischemic injury remains uninvestigated.…”

Section: Introductionmentioning

confidence: 99%

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Preconditioning with a TLR2 specific ligand increases resistance to cerebral ischemia/reperfusion injury

Fang

et al. 2008

Journal of Neuroimmunology

118

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The brain's resistance to ischemic injury can be transiently augmented by prior exposure to a sublethal stress stimulus, i.e. preconditioning. It has been reported that Toll-like receptors (TLRs) are involved in the preconditioning-induced protective effect against ischemic brain injury. In this study, we investigated the effect of preconditioning with a TLR2 specific ligand, Pam3CSK4, on focal cerebral ischemia/reperfusion (I/R) injury in mice. Pam3CSK4 was administered systemically 24 hrs before the mice were subjected to focal cerebral ischemia (1 hr) followed by reperfusion. Cerebral infarct size was determined, blood brain barrier (BBB) permeability was evaluated, and expression of tight-junction proteins were examined after focal cerebral I/R. Results showed that pre-treatment with Pam3CSK significantly reduced brain infarct size (1.9 ± 0.5% vs 9.4 ± 2.2%) compared with the untreated I/R group. Pam3CSK4 pre-treatment also significantly reduced acute mortality (4.3% vs 24.2%), preserved neurological function (8.22 ± 0.64 vs 3.91 ± 0.57), and attenuated brain edema (84.61 ± 0.08% vs 85.29 ± 0.09%) after cerebral I/R. In addition, Pam3CSK4 pre-treatment preserved BBB function as evidenced by decreased leakage of serum albumin (0.528 ± 0.026 vs 0.771 ± 0.059) and Evans Blue (9.23 ± 0.72 μg/mg vs 12.56 ± 0.65μg/mg) into brain tissue. Pam3CSK4 pretreatment also attenuated the loss of the tight junction protein occludin in response to brain I/R injury. These results suggest that TLR2 is a new target of ischemic preconditioning in the brain and preconditioning with a TLR2 specific ligand will protect the brain from I/R injury.

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Ischaemic preconditioning improves microvascular perfusion and oxygenation following reperfusion injury of the intestine

Mallick

Yang

Winslet

et al. 2005

British Journal of Surgery

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Differential role of nitric oxide pathway and heat shock protein in preconditioning and lipopolysaccharide-induced brain ischemic tolerance

Cited by 85 publications

References 26 publications

CBF Changes Associated with Focal Ischemic Preconditioning in the Spontaneously Hypertensive Rat

CBF Changes Associated with Focal Ischemic Preconditioning in the Spontaneously Hypertensive Rat

Preconditioning with a TLR2 specific ligand increases resistance to cerebral ischemia/reperfusion injury

Ischaemic preconditioning improves microvascular perfusion and oxygenation following reperfusion injury of the intestine

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