Lack of association between Poly(ADP-ribose) polymerase (PARP) polymorphisms and rheumatoid arthritis in a Korean population

Lee, Kyeong-A; Bang, So-Young; Park, Byung Lae; Kim, Jeonghyun; Shin, Hyoung Doo; Bae, Sang Cheol

doi:10.1007/s00296-010-1589-9

Cited by 7 publications

(4 citation statements)

References 27 publications

(41 reference statements)

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“…Bcl-2 mRNA and protein expression in hydrogen-mediated protection on PC-12 exposed to OGD/RP (Mo et al, 2019). PARP is an enzyme involved in DNA repair and apoptosis (Lee et al, 2012). In our study, we found that OGD treatment resulted in decreased expression of Bcl-2 and PARP in cortical neuronal cells.…”

Section: Discussionsupporting

confidence: 54%

Xanomeline Protects Cortical Cells From Oxygen-Glucose Deprivation via Inhibiting Oxidative Stress and Apoptosis

Xin

Chen

et al. 2020

Front. Physiol.

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Xanomeline, a muscarinic acetylcholine receptor agonist, is one of the first compounds that was found to be effective in the treatment of schizophrenics and attenuating behavioral disturbances of patients with Alzheimer's disease (AD). However, its role in ischemia-induced injury due to oxygen and glucose deprivation (OGD) remains unclear. Primary rat neuronal cells were exposed to OGD and treated with xanomeline. The effects of xanomeline on apoptosis, cell viability, lactate dehydrogenase (LDH) levels, and reactive oxygen species (ROS) were determined using an Annexin V Apoptosis Detection Kit, a non-radioactive cell counting kit-8 (CCK-8) assay, colorimetric LDH cytotoxicity assay kit, and a dichloro-dihydro-fluorescein diacetate (DCFH-DA) assay, respectively, and the expressions of Sirtuin 1, haem oxygenase-1 (HO-1), B-cell lymphoma 2 (Bcl-2), poly ADP-ribose polymerase (PARP), and hypoxia-inducible factor α (HIF-1α) as well as the level of phosphorylated kinase B (p-Akt) were determined by Western blotting. Compared with the control, xanomeline pretreatment increased the viability of isolated cortical neurons and decreased the LDH release induced by OGD. Compared with OGD-treated cells, xanomeline inhibited apoptosis, reduced ROS production, attenuated the OGD-induced HIF-1α increase and partially reversed the reduction of HO-1, Sirtuin-1, Bcl-2, PARP, and p-Akt induced by OGD. In conclusion, xanomeline treatment protects cortical neuronal cells possibly through the inhibition of apoptosis after OGD.

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Section: Discussionsupporting

confidence: 54%

Xanomeline Protects Cortical Cells From Oxygen-Glucose Deprivation via Inhibiting Oxidative Stress and Apoptosis

Xin

Chen

et al. 2020

Front. Physiol.

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“…The role of PARP-1 in auto-reactive immune responses was shown for the first time in experimental models of rheumatoid arthritis (RA), a Th1 cell driven inflammatory autoimmune disease. In humans, an association between PARP-1 gene polymorphisms and RA was shown even if other studies reached contrasting conclusions [96,97]. A more recent study showed that a human RA-risk-associated non-coding polymorphism in the chemokine receptor CCR6 is a causal variant through which PARP-1 regulates CCR6 expression [98].…”

Section: Pathogenic Role In Non-cancer Diseasesmentioning

confidence: 99%

Multifaceted Role of PARP-1 in DNA Repair and Inflammation: Pathological and Therapeutic Implications in Cancer and Non-Cancer Diseases

Pazzaglia

Pioli

2019

Cells

146

135

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PARP-1 (poly(ADP-ribose)-polymerase 1), mainly known for its protective role in DNA repair, also regulates inflammatory processes. Notably, defects in DNA repair and chronic inflammation may both predispose to cancer development. On the other hand, inhibition of DNA repair and inflammatory responses can be beneficial in cancer therapy and PARP inhibitors are currently used for their lethal effects on tumor cells. Furthermore, excess of PARP-1 activity has been associated with many tumors and inflammation-related clinical conditions, including asthma, sepsis, arthritis, atherosclerosis, and neurodegenerative diseases, to name a few. Activation and inhibition of PARP represent, therefore, a double-edged sword that can be exploited for therapeutic purposes. In our review, we will discuss recent findings highlighting the composite multifaceted role of PARP-1 in cancer and inflammation-related diseases.

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“…Lack of association was noted between PARP polymorphisms and rheumatoid arthritis in a Korean population (Lee et al, 2012). …”

Section: Figurementioning

confidence: 99%

Therapeutic applications of PARP inhibitors: Anticancer therapy and beyond

Curtin

Szabó

2013

Molecular Aspects of Medicine

327

286

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The aim of this article is to describe the current and potential clinical translation of pharmacological inhibitors of poly(ADP-ribose) polymerase (PARP) for the therapy of various diseases. The first section of the present review summarizes the available preclinical and clinical data with PARP inhibitors in various forms of cancer. In this context, the role of PARP in single-strand DNA break repair is relevant, leading to replication-associated lesions that cannot be repaired if homologous recombination (HRR) repair is defective, and the synthetic lethality of PARP inhibitors in HRR-defective cancer. HRR defects are classically associated with BRCA1 and 2 mutations associated with familial breast and ovarian cancer, but there may be many other causes of HRR defects. Thus, PARP inhibitors may be the drugs of choice for BRCA mutant breast and ovarian cancers, and extend beyond these tumors if appropriate biomarkers can be developed to identify HRR defects. Multiple lines of preclinical data demonstrate that PARP inhibition increases cytotoxicity and tumor growth delay in combination with temozolomide, topoisomerase inhibitors and ionizing radiation. Both single agent and combination clinical trials are underway. The final part of the first section of the present review summarizes the current status of the various PARP inhibitors that are in various stages of clinical development. The second section of the present review summarizes the role of PARP in selected non-oncologic indications. In a number of severe, acute diseases (such as stroke, neurotrauma, circulatory shock and acute myocardial infarction) the clinical translatability of PARP inhibition is supported by multiple lines of preclinical data, as well as observational data demonstrating PARP activation in human tissue samples. In these disease indications, PARP overactivation due to oxidative and nitrative stress drives cell necrosis and pro-inflammatory gene expression, which contributes to disease pathology. Accordingly, multiple lines of preclinical data indicate the efficacy of PARP inhibitors to preserve viable tissue and to down-regulate inflammatory responses. As the clinical trials with PARP inhibitors in various forms of cancer progress, it is hoped that a second line of clinical investigations, aimed at testing of PARP inhibitors for various non-oncologic indications, will be initiated, as well.

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Lack of association between Poly(ADP-ribose) polymerase (PARP) polymorphisms and rheumatoid arthritis in a Korean population

Cited by 7 publications

References 27 publications

Xanomeline Protects Cortical Cells From Oxygen-Glucose Deprivation via Inhibiting Oxidative Stress and Apoptosis

Xanomeline Protects Cortical Cells From Oxygen-Glucose Deprivation via Inhibiting Oxidative Stress and Apoptosis

Multifaceted Role of PARP-1 in DNA Repair and Inflammation: Pathological and Therapeutic Implications in Cancer and Non-Cancer Diseases

Therapeutic applications of PARP inhibitors: Anticancer therapy and beyond

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