Inhibition of poly(adenosine diphosphate-ribose) polymerase by the active form of vitamin D

Mabley, Jon G.; Wallace, Rebecca; Pacher, Pál; Murphy, Kanneganti; Szabó, Csaba

doi:10.3892/ijmm.19.6.947

Cited by 35 publications

(32 citation statements)

References 41 publications

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“…PARP1 activity has previously been shown to be regulated by various endogenous factors (including xanthines, purines, estrogen) (Virag and Szabo, 2001;Mabley et al, 2005;Geraets et al, 2006;Szabo et al, 2006;Mabley et al, 2007) and has been shown or suggested to be regulated/phosphorylated by protein kinase C, mitogen-activated protein kinase, and extracellular signal-regulated kinases 1 and 2 (Tanaka et al, 1987;Kauppinen et al, 2006;Hegedus et al, 2008). Based on the current findings, we conclude that the cAMP/PKA system represents an additional mode of the regulation of its activity via phosphorylation.…”

Section: Discussionsupporting

confidence: 70%

Regulation of Mitochondrial Poly(ADP-Ribose) Polymerase Activation by theβ-Adrenoceptor/cAMP/Protein Kinase A Axis during Oxidative Stress

et al. 2014

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We investigated the regulation of mitochondrial poly(ADP-ribose) polymerase 1 (PARP1) by the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) system during oxidative stress in U937 monocytes. Oxidative stress induced an early (10 minutes) mitochondrial DNA damage, and concomitant activation of PARP1 in the mitochondria. These early events were followed by a progressive mitochondrial oxidant production and nuclear PARP1 activation (by 6 hours). These processes led to a functional impairment of mitochondria, culminating in cell death of mixed (necrotic/apoptotic) type. b-Adrenoceptor blockade with propranolol or inhibition of its downstream cAMP/PKA signaling attenuated, while b-adrenoceptor agonists and cAMP/PKA activators enhanced, the oxidant-mediated PARP1 activation. In the presence of cAMP, recombinant PKA directly phosphorylated recombinant PARP1 on serines 465 (in the automodification domain) and 782 and 785 (both in the catalytic domain). Inhibition of the b-adrenergic receptor/cAMP/PKA axis protected against the oxidant-mediated cell injury. Propranolol also suppressed PARP1 activation in peripheral blood leukocytes during bacterial lipopolysaccharide (LPS)-induced systemic inflammation in mice. We conclude that the activation of mitochondrial PARP1 is an early, active participant in oxidant-induced cell death, which is under the control of b-adrenoceptor/cAMP/PKA axis through the regulation of PARP1 activity by PARP1 phosphorylation.

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Section: Discussionsupporting

confidence: 70%

Regulation of Mitochondrial Poly(ADP-Ribose) Polymerase Activation by theβ-Adrenoceptor/cAMP/Protein Kinase A Axis during Oxidative Stress

et al. 2014

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“…SIRT1 is downstream in ROS signaling, but can be importantly upstream in regulating cellular levels such as activation of FOXO3 (164), muscle ringfinger protein 1 (MuRF1) (8), and protein kinase B (Akt) (382). Therefore, these NAD-dependent metabolic sensors are regulating redox signaling in a wide array (222).…”

Section: Exercise and Redox Signalingmentioning

confidence: 99%

Oxygen Consumption and Usage During Physical Exercise: The Balance Between Oxidative Stress and ROS-Dependent Adaptive Signaling

Radák

Zhao

Koltai

et al. 2013

Antioxidants & Redox Signaling

509

425

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The complexity of human DNA has been affected by aerobic metabolism, including endurance exercise and oxygen toxicity. Aerobic endurance exercise could play an important role in the evolution of Homo sapiens, and oxygen was not important just for survival, but it was crucial to redox-mediated adaptation. The metabolic challenge during physical exercise results in an elevated generation of reactive oxygen species (ROS) that are important modulators of muscle contraction, antioxidant protection, and oxidative damage repair, which at moderate levels generate physiological responses. Several factors of mitochondrial biogenesis, such as peroxisome proliferator-activated receptor-c coactivator 1a (PGC-1a), mitogen-activated protein kinase, and SIRT1, are modulated by exercise-associated changes in the redox milieu. PGC-1a activation could result in decreased oxidative challenge, either by upregulation of antioxidant enzymes and/or by an increased number of mitochondria that allows lower levels of respiratory activity for the same degree of ATP generation. Endogenous thiol antioxidants glutathione and thioredoxin are modulated with high oxygen consumption and ROS generation during physical exercise, controlling cellular function through redox-sensitive signaling and proteinprotein interactions. Endurance exercise-related angiogenesis, up to a significant degree, is regulated by ROSmediated activation of hypoxia-inducible factor 1a. Moreover, the exercise-associated ROS production could be important to DNA methylation and post-translation modifications of histone residues, which create heritable adaptive conditions based on epigenetic features of chromosomes. Accumulating data indicate that exercise with moderate intensity has systemic and complex health-promoting effects, which undoubtedly involve regulation of redox homeostasis and signaling. Antioxid. Redox Signal. 18, 1208Signal. 18, -1246

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“…It is a stress protein, which can, however, promote neuronal death. In fact, there is an overexpression of PARP1 in the substantia nigra of PD patients [281]; increased levels of vitamin D down regulate PARP-1 expression, probably mediated by a diminishment of microglial activation [282]. All these aspects considered, clinical trials on vitamin D supplementation in Parkinson's disease have been carried out [283].…”

Section: Vitamin D Deficiency and Neurodegenerative Diseasesmentioning

confidence: 99%

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact

Moretti

Morelli

Caruso

2018

Preprint

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It is widely known that vitamin D receptors have been found in neurons and glial cells and their highest expression is in the hippocampus, hypothalamus, thalamus and subcortical grey nuclei, and substantia nigra. The vitamin D helps the regulation of neurotrophin, neural differentiation and maturation, through the control operation of growing factors synthesis (ie NGF and GDNF), the trafficking of the septo-hyppocampal pathway, and the control of the synthesis process of different neuromodulators (such as Ach, DA, and GABA).Based on these assumptions, we have written this review in order to summarize the potential role of vitamin D in neurological pathologies. The work could be titanic, and might result very fuzzy and even incoherent, if we would not have conjectured to taper our first intentions and devoted our interests towards three mainstreams: demyelinating pathologies, vascular syndromes and neurodegeneration.Due to the lack of effective therapeutic options, a part from the disease modifying strategies, the role of different risk factors should be investigated in neurology, as far as their correction may lead to the improvement of the cerebral conditions.We have explored the relationships between the gene-environmental influence and long term vitamin D deficiency, as a risk factor for the development of different types of neurological disorders, along with the role and the rationale of therapeutic trials with vitamin D implementation. Peer-reviewed version available at Int. J. Mol. Sci. 2018, 19, 2245 doi:10.3390/ijms19082245 3 SEARCH STRATEGY AND SELECTION CRITERIAWe searched MEDLINE using the search terms: "vitamin D central nervous system" , both "vitamin D" and "central nervous system"; "vitamin D immune system/response", both "vitamin D" and "immune system" or "immune response"; "vitamin D multiple sclerosis risk", both "vitamin D" and "multiple sclerosis risk"; "vitamin D multiple sclerosis relapse", both "vitamin D" and "multiple sclerosis relapse"; "vitamin D multiple sclerosis magnetic resonance imaging", both "vitamin D" and "multiple sclerosis magnetic resonance imaging"; "vitamin D multiple sclerosis disability", both "vitamin D" and "multiple sclerosis disability"; "vitamin D supplementation/therapy/treatment multiple sclerosis", both "vitamin D supplementation" or "vitamin D therapy" or "vitamin D treatment" and "multiple sclerosis"; "vascular dementia", both as -vascular-and -dementia-, "subcortical vascular dementia", both assubcortical-and -dementia-, "Alzheimer's disease", "pathogenesis neurodegeneration" "amyloid", "cholinergic afferents", "arteriolosclerosis", "cerebral flow regulation", "stroke". Publications were selected mostly form the past 20years, but did not exclude frequently referenced and highly regarded older publications. . Congress abstracts and isolated case reports were not considered. We searched the reference lists of articles identified by this search strategy and selected those we judged relevant. Review articles and book chapters are cited to provide with ...

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Inhibition of poly(adenosine diphosphate-ribose) polymerase by the active form of vitamin D

Cited by 35 publications

References 41 publications

Regulation of Mitochondrial Poly(ADP-Ribose) Polymerase Activation by theβ-Adrenoceptor/cAMP/Protein Kinase A Axis during Oxidative Stress

Regulation of Mitochondrial Poly(ADP-Ribose) Polymerase Activation by theβ-Adrenoceptor/cAMP/Protein Kinase A Axis during Oxidative Stress

Oxygen Consumption and Usage During Physical Exercise: The Balance Between Oxidative Stress and ROS-Dependent Adaptive Signaling

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact

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