Nicotinamide-induced apoptosis in insulin producing cells is associated with cleavage of poly(ADP-ribose) polymerase

Saldeen, Johan; Welsh, Nils

doi:10.1016/s0303-7207(98)00068-9

Cited by 46 publications

(21 citation statements)

References 40 publications

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“…Caspases, which are essential for apoptosis, cleave PARP into two characteristic fragments, 85 kDa and 25 kDa. Anti-PARP 85 has been shown to be specific for the 85-kDa fragment and, therefore, is a marker of apoptosis (6,34,36,43). We used this antibody to confirm smoke-induce apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of JNK activation prolongs survival after smoke inhalation from fires

Syrkina¹,

Quinn²,

Jung³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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Initial injury from smoke inhalation is mainly to the trachea and bronchi and is characterized by mucosal hyperemia and increased microvascular permeability, exfoliation of epithelial lining, mucous secretion, mucous plugging, and an acute inflammatory cell influx. In this study, we explore the role of the c-Jun N-terminal protein kinase (JNK) pathway in smoke inhalation lung injury using a rat model of exposure to smoke from burning cotton. Male Sprague-Dawley rats were exposed to smoke from burning cotton for 15 min, and 1 h after injury a JNK inhibitor (SP-600125) or vehicle was injected. We measured neutrophil influx, cytokine release, percent of apoptotic cells, airway plugging, and survival. Administration of a JNK inhibitor 1 h after smoke inhalation decreased airway apoptosis, mucous plugging, influx of inflammatory cells, and the release of cytokines and significantly prolonged animal survival (P < 0.05). These in vivo data show that the JNK pathway plays a critical role in smoke-induced lung injury and offer an attractive therapeutic approach for this injury.

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Section: Discussionmentioning

confidence: 99%

Inhibition of JNK activation prolongs survival after smoke inhalation from fires

Syrkina¹,

Quinn²,

Jung³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…DNA fragmentation was evaluated using the method described by Saldeen and Welsh (Saldeen and Welsh, 1998). For this purpose, HT22 cells were plated in 100 mm dishes at a density of 4 × 10 5 cell/dish in 10 ml of medium.…”

Section: Gel Electrophoresis Of Low Molecular Weight Dnamentioning

confidence: 99%

Apolipoprotein D subcellular distribution pattern in neuronal cells during oxidative stress

et al. 2015

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“…While PARP inhibitors offer remarkable protection under conditions of NAD + and ATP depletion, inhibition of PARP-1 in the presence of NAD + sensitises cells to DNA damage, and subsequent increase of cell death (Nagayama et al 2000). Furthermore, it has been reported that inhibition of PARP-1 can induce apoptosis in rapidly dividing cells (Saldeen and Welsh 1998), possibly by blocking the access of replication or repair enzymes to DNA. G2 cell-cycle arrest may be promoted followed by p53-independent apoptosis (Saldeen et al 2003), and resultant inhibition of cell proliferation.…”

Section: Parp-1 As a Target For Neuroprotectionmentioning

confidence: 99%

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

et al. 2010

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Delivery is a stressful and risky event menacing the newborn. The mother-dependent respiration has to be replaced by autonomous pulmonary breathing immediately after delivery. If delayed, it may lead to deficient oxygen supply compromising survival and development of the central nervous system. Lack of oxygen availability gives rise to depletion of NAD+ tissue stores, decrease of ATP formation, weakening of the electron transport pump and anaerobic metabolism and acidosis, leading necessarily to death if oxygenation is not promptly re-established. Re-oxygenation triggers a cascade of compensatory biochemical events to restore function, which may be accompanied by improper homeostasis and oxidative stress. Consequences may be incomplete recovery, or excess reactions that worsen the biological outcome by disturbed metabolism and/or imbalance produced by over-expression of alternative metabolic pathways. Perinatal asphyxia has been associated with severe neurological and psychiatric sequelae with delayed clinical onset. No specific treatments have yet been established. In the clinical setting, after resuscitation of an infant with birth asphyxia, the emphasis is on supportive therapy. Several interventions have been proposed to attenuate secondary neuronal injuries elicited by asphyxia, including hypothermia. Although promising, the clinical efficacy of hypothermia has not been fully demonstrated. It is evident that new approaches are warranted. The purpose of this review is to discuss the concept of sentinel proteins as targets for neuroprotection. Several sentinel proteins have been described to protect the integrity of the genome (e.g. PARP-1; XRCC1; DNA ligase IIIα; DNA polymerase β, ERCC2, DNA-dependent protein kinases). They act by eliciting metabolic cascades leading to (i) activation of cell survival and neurotrophic pathways; (ii) early and delayed programmed cell death, and (iii) promotion of cell proliferation, differentiation, neuritogenesis and synaptogenesis. It is proposed that sentinel proteins can be used as markers for characterising long-term effects of perinatal asphyxia, and as targets for novel therapeutic development and innovative strategies for neonatal care.

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Nicotinamide-induced apoptosis in insulin producing cells is associated with cleavage of poly(ADP-ribose) polymerase

Cited by 46 publications

References 40 publications

Inhibition of JNK activation prolongs survival after smoke inhalation from fires

Inhibition of JNK activation prolongs survival after smoke inhalation from fires

Apolipoprotein D subcellular distribution pattern in neuronal cells during oxidative stress

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

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