Pathways for Ischemic Cytoprotection: Role of Sirtuins in Caloric Restriction, Resveratrol, and Ischemic Preconditioning

Morris, Kahlilia C.; Lin, Hung Wen; Thompson, John W.; Pérez-Pinzón, Miguel A.

doi:10.1038/jcbfm.2010.229

Cited by 118 publications

(86 citation statements)

References 151 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SIRT1 is a member of the sirtuin family of deacetylase and ADP-ribosylase enzymes, which are involved in numerous cellular activities, including the cellular stress response, genome stability, and energy metabolism [36,37]. In contrast to ischemic neuroprotection by class I, II, and IV HDAC inhibitors (which do not inhibit sirtuins), our laboratory, and others, have demonstrated that SIRT1 activation is required for ischemic tolerance [38,39].…”

Section: Acetylationmentioning

confidence: 99%

Ischemic Preconditioning Alters the Epigenetic Profile of the Brain from Ischemic Intolerance to Ischemic Tolerance

et al. 2013

View full text Add to dashboard Cite

Ischemic preconditioning is an innate neuroprotective mechanism in which a sub-injurious ischemic exposure increases the brain's ability to withstand a subsequent, normally injurious ischemic insult. Part of ischemic preconditioning neuroprotection stems from an epigenetic reprogramming of the brain to a phenotype of ischemic tolerance, which results in a gene expression profile different from that observed in the non-injured and ischemia-injured brains. Such neuroprotective reprograming, activated by ischemic preconditioning, requires specific changes in DNA accessibility coordinated with activation of transcriptional activator and repressor proteins, which allows for expression of specific neuroprotective proteins despite a general repression of gene expression. In this review we examine the effects of injurious ischemia and ischemic preconditioning on the regulation of DNA methylation, histone post-translational modifications, and non-coding RNA expression. There is increasing interest in the role of epigenetics in disease pathobiology, and whether and how pharmacological manipulation of epigenetic processes may allow for ischemic neuroprotection. Therefore, a better understanding of the epigenomic determinants underlying the modulation of gene expression that lead to ischemic tolerance or cell death offers the promise of novel neuroprotective therapies that target global reprograming of genomic activity versus individual cellular signaling pathways.

show abstract

Section: Acetylationmentioning

confidence: 99%

Ischemic Preconditioning Alters the Epigenetic Profile of the Brain from Ischemic Intolerance to Ischemic Tolerance

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Sirtuins represent a family of nicotinamide adenine dinucleotide (NAD + )-dependent deacetylases, which couple sirtuin-dependent posttranslational modifications with cellular energy levels. 119 Caloric restriction was shown to protect against ischemic injury in the heart and brain, and increased sirtuin-1 (Sirt1) expression after prolonged caloric restriction has been linked to improved recovery after myocardial ischemia. 119 Accordingly, intermittent fasting was very recently shown to suppress ischemia-induced activation of the inflammasome in a murine model of focal transient cerebral ischemia.…”

Section: Different Organs Modulate Autoimmune Mechanisms In the Centrmentioning

confidence: 99%

“…119 Caloric restriction was shown to protect against ischemic injury in the heart and brain, and increased sirtuin-1 (Sirt1) expression after prolonged caloric restriction has been linked to improved recovery after myocardial ischemia. 119 Accordingly, intermittent fasting was very recently shown to suppress ischemia-induced activation of the inflammasome in a murine model of focal transient cerebral ischemia. 120,121 Whereas the cardioprotective action of the red wine substance resveratrol and mechanisms of ischemic preconditioning have been ascribed to the action of sirtuins, and whereas resveratrol was shown to inhibit NLRP3 inflammasome, 122 there is still debate on the exact role in ischemic injury.…”

Section: Different Organs Modulate Autoimmune Mechanisms In the Centrmentioning

confidence: 99%

“…124 This discrepancy may be because of NAD + -depleting effect of sirtuins, potentially contributing to neuronal death in models of excitotoxicity. 119 Sirt2 has been demonstrated to be a repressor of microglial activation and brain inflammation. 125 Aberrant mitochondrial homeostasis diminishes the coenzyme NAD + levels, leads to reduced Sirt2 activity, increases the level of acetylation of microtubules, and thereby causes NLRP3-inflammasome activation by a dyneinmediated transport of ASC on mitochondria to NLRP3 on the endoplasmic reticulum.…”

Section: Different Organs Modulate Autoimmune Mechanisms In the Centrmentioning

confidence: 99%

See 1 more Smart Citation

Molecular Regulation of Cell Fate in Cerebral Ischemia: Role of the Inflammasome and Connected Pathways

Trendelenburg

2014

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Analogous to Toll-like receptors, NOD-like receptors represent a class of pattern recognition receptors, which are cytosolic and constitute part of different inflammasomes. These large protein complexes are activated not only by different pathogens, but also by sterile inflammation or by specific metabolic conditions. Mutations can cause hereditary autoinflammatory systemic diseases, and inflammasome activation has been linked to many multifactorial diseases, such as diabetes or cardiovascular diseases. Increasing data also support an important role in different central nervous diseases such as stroke. Thus, the current knowledge of the functional role of this intracellular 'master switch' of inflammation is discussed with a focus on its role in ischemic stroke, neurodegeneration, and also with regard to the recent data which argues for a relevant role in other organs or biologic systems which influence stroke incidence or prognosis.

show abstract

“…Since SIRT1 has been demonstrated to enhance or restore mitochondrial activity in various tissues [62,87,91,[109][110][111] it is logical to assume that the interference between PARP-2 and SIRT1 expression [62] could be key for the protective phenotype. Indeed, in the case of doxorubicin-induced vascular damage, enhanced SIRT1 expression and consequent stabilization of the mitochondrial membrane potential was proposed to be responsible for the protection provided by the PARP-2 -/-phenotype [33] which might be a prototypical mechanism by which PARP-2 mediates oxidative stress-related pathologies.…”

Section: Parp-2 In Oxidative Stress-related Diseasesmentioning

confidence: 99%

Poly(ADP-ribose) polymerase-2: emerging transcriptional roles of a DNA-repair protein

Szántó

Brunyánszki

Kiss

et al. 2012

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Abstract:Poly(ADP-ribose) polymerase (PARP)-2 is a nuclear enzyme that belongs to the PARP family and PARP-2 is responsible for 5-15% of total cellular PARP activity. PARP-2 was originally described in connection to DNA repair and in physiological and pathophysiological processes associated with genome maintenance (e.g. centromere and telomere protection, spermiogenesis, thymopoesis, azoospermia and tumorigenesis). Recent reports identified important rearrangements in gene expression upon the knockout of PARP-2. Such rearrangements heavily impact on inflammation and metabolism. Metabolic effects are mediated through modifying PPARg and SIRT1 function. Altered gene expression gives rise to a complex phenotype characterized primarily by enhanced mitochondrial activity that results both in beneficial (loss of fat, enhanced insulin sensitivity) and in disadvantageous (pancreatic beta cell hypofunction upon high fat feeding) consequences. Enhanced mitochondrial biogenesis provides protection in oxidative stress related diseases. Hereby, we review the recent developments in PARP-2 research with special attention to the involvement of PARP-2 in transcriptional and metabolic regulation. We would like to thank the referee for his/her efforts to further improve our manuscript.1. Page 2 -the modifications here are fairly minimalistic and the abbreviations ARTD2 and ARTD1 are not even defined. Powered by Editorial Manager® and Preprint Manager® from Aries Systems Corporationand ARTD1 are not even defined.In the corresponding section we incorporated the basic information on the newly proposed nomenclature in our previous version upon the suggestion of the Reviewer. We agree with the Reviewer that the appearance of the new nomenclature in our manuscript is important. Moreover, in the current version we added ARTD-2 as a keyword to help those future readers that follow the new nomenclature. The fact that ARTD1 is the equivalent of PARP-1 is defined in the chapter "PARP superfamily" second paragraph, first row. We added the abbreviation of ARDT-2 in the last sentence in the first paragraph of the chapter "The PARP superfamily". We think that these are sufficient for the understanding of the position of PARP-2 in the PARP/ARTD superfamily.We would like to note here, that the proposed new nomenclature did not gain ground in the scientific community yet. There are only 3 relevant papers on Medline for the keyword ARTD1, ARTD2 or ARTD (since 2010, the publication of the paper by In summary, we are confident that our review sufficiently takes the new nomenclature into consideration despite of the fact that it is not yet accepted by the scientific community. Sequence homology modeling was carried out by Ame and co-workers (Ame et al. Bioessays. 26:882-893. 2004). They classified sequences as PARPs on the basis of sequence homology, therefore sequence homology does exist. However, mutation(s) in a sequence does not necessarily mean that sequence homology is lost. In the incriminated text, mutations mean rather point mutations that aff...

show abstract

Pathways for Ischemic Cytoprotection: Role of Sirtuins in Caloric Restriction, Resveratrol, and Ischemic Preconditioning

Cited by 118 publications

References 151 publications

Ischemic Preconditioning Alters the Epigenetic Profile of the Brain from Ischemic Intolerance to Ischemic Tolerance

Ischemic Preconditioning Alters the Epigenetic Profile of the Brain from Ischemic Intolerance to Ischemic Tolerance

Molecular Regulation of Cell Fate in Cerebral Ischemia: Role of the Inflammasome and Connected Pathways

Poly(ADP-ribose) polymerase-2: emerging transcriptional roles of a DNA-repair protein

Contact Info

Product

Resources

About