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SIRT1 mediates hypoxic preconditioning induced attenuation of neurovascular dysfunction following subarachnoid hemorrhage

Vasospasm and delayed cerebral ischemia (DCI) contribute significantly to the morbidity/mortality associated with aneurysmal subarachnoid hemorrhage (SAH). While considerable research effort has focused on preventing or reversing vasospasm, SAH-induced brain injury occurs in response to a multitude...

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Published in:Experimental neurology 2020-12, Vol.334, p.113484-113484, Article 113484
Main Authors: Vellimana, Ananth K., Aum, Diane J., Diwan, Deepti, Clarke, Julian V., Nelson, James W., Lawrence, Molly, Han, Byung Hee, Gidday, Jeffrey M., Zipfel, Gregory J.
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container_title Experimental neurology
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creator Vellimana, Ananth K.
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Zipfel, Gregory J.
description Vasospasm and delayed cerebral ischemia (DCI) contribute significantly to the morbidity/mortality associated with aneurysmal subarachnoid hemorrhage (SAH). While considerable research effort has focused on preventing or reversing vasospasm, SAH-induced brain injury occurs in response to a multitude of concomitantly acting pathophysiologic mechanisms. In this regard, the pleiotropic epigenetic responses to conditioning-based therapeutics may provide an ideal SAH therapeutic strategy. We previously documented the ability of hypoxic preconditioning (PC) to attenuate vasospasm and neurological deficits after SAH, in a manner that depends on the activity of endothelial nitric oxide synthase. The present study was undertaken to elucidate whether the NAD-dependent protein deacetylase sirtuin isoform SIRT1 is an upstream mediator of hypoxic PC-induced protection, and to assess the efficacy of the SIRT1-activating polyphenol Resveratrol as a pharmacologic preconditioning therapy. Wild-type C57BL/6J mice were utilized in the study and subjected to normoxia or hypoxic PC. Surgical procedures included induction of SAH via endovascular perforation or sham surgery. Multiple endpoints were assessed including cerebral vasospasm, neurobehavioral deficits, SIRT1 expression via quantitative real-time PCR for mRNA, and western blot for protein quantification. Pharmacological agents utilized in the study include EX-527 (SIRT1 inhibitor), and Resveratrol (SIRT1 activator). Hypoxic PC leads to rapid and sustained increase in cerebral SIRT1 mRNA and protein expression. SIRT1 inhibition blocks the protective effects of hypoxic PC on vasospasm and neurological deficits. Resveratrol pretreatment dose-dependently abrogates vasospasm and attenuates neurological deficits following SAH – beneficial effects that were similarly blocked by pharmacologic inhibition of SIRT1. SIRT1 mediates hypoxic preconditioning-induced protection against neurovascular dysfunction after SAH. Resveratrol mimics this neurovascular protection, at least in part, via SIRT1. Activation of SIRT1 is a promising, novel, pleiotropic therapeutic strategy to combat DCI after SAH. •Hypoxic preconditioning protects against deficits after subarachnoid hemorrhage.•Hypoxic preconditioning induces robust upregulation of SIRT1.•SIRT1 mediates hypoxic preconditioning induced protection in subarachnoid hemorrhage.•Resveratrol mimics preconditioning induced protection in subarachnoid hemorrhage.
doi_str_mv 10.1016/j.expneurol.2020.113484
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While considerable research effort has focused on preventing or reversing vasospasm, SAH-induced brain injury occurs in response to a multitude of concomitantly acting pathophysiologic mechanisms. In this regard, the pleiotropic epigenetic responses to conditioning-based therapeutics may provide an ideal SAH therapeutic strategy. We previously documented the ability of hypoxic preconditioning (PC) to attenuate vasospasm and neurological deficits after SAH, in a manner that depends on the activity of endothelial nitric oxide synthase. The present study was undertaken to elucidate whether the NAD-dependent protein deacetylase sirtuin isoform SIRT1 is an upstream mediator of hypoxic PC-induced protection, and to assess the efficacy of the SIRT1-activating polyphenol Resveratrol as a pharmacologic preconditioning therapy. Wild-type C57BL/6J mice were utilized in the study and subjected to normoxia or hypoxic PC. 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Activation of SIRT1 is a promising, novel, pleiotropic therapeutic strategy to combat DCI after SAH. •Hypoxic preconditioning protects against deficits after subarachnoid hemorrhage.•Hypoxic preconditioning induces robust upregulation of SIRT1.•SIRT1 mediates hypoxic preconditioning induced protection in subarachnoid hemorrhage.•Resveratrol mimics preconditioning induced protection in subarachnoid hemorrhage.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>33010255</pmid><doi>10.1016/j.expneurol.2020.113484</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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ispartof Experimental neurology, 2020-12, Vol.334, p.113484-113484, Article 113484
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source ScienceDirect Journals
subjects Animals
Antioxidants - pharmacology
Carbazoles - pharmacology
Delayed cerebral ischemia
Hypoxia-Ischemia, Brain - metabolism
Hypoxia-Ischemia, Brain - pathology
Ischemic Preconditioning - methods
Male
Mice
Mice, Inbred C57BL
Resveratrol
Resveratrol - pharmacology
SIRT1
Sirtuin
Sirtuin 1 - antagonists & inhibitors
Sirtuin 1 - metabolism
Subarachnoid hemorrhage
Subarachnoid Hemorrhage - metabolism
Subarachnoid Hemorrhage - pathology
Vasospasm
Vasospasm, Intracranial - metabolism
Vasospasm, Intracranial - pathology
Vasospasm, Intracranial - prevention & control
title SIRT1 mediates hypoxic preconditioning induced attenuation of neurovascular dysfunction following subarachnoid hemorrhage
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