Targeting inflammatory diseases via apoptotic mechanisms

Murphy, Finbarr J; Hayes, Ian; Cotter, Thomas G.

doi:10.1016/s1471-4892(03)00072-9

Cited by 25 publications

(15 citation statements)

References 61 publications

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“…Neutrophils are short-lived cells and play a central role in development and perpetuation of LPS-induced lung injury by accumulating in the lungs and producing high levels of proinflammatory mediators, including cytokines, chemokines, and reactive oxygen species (53). Increased neutrophil apoptosis and resultant clearance from the lungs during sepsis p53 REGULATES NF-B ACTIVATION AND ACUTE LUNG INJURY has been shown to be beneficial (53,54). Thus, some of the beneficial effects of nutlin-3a and p53 activation in ALI could come from enhanced neutrophil apoptosis induced by p53.…”

Section: Discussionmentioning

confidence: 99%

p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

Liu

Park

Tsuruta

et al. 2009

The Journal of Immunology

125

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The transcriptional factor p53 has primarily been characterized for its central role in the regulation of oncogenesis. A reciprocal relationship between the activities of p53 and NF-B has been demonstrated in cancer cells, but there is little information concerning interactions between p53 and NF-B in inflammatory processes. In this study, we found that neutrophils and macrophages lacking p53, i.e., p53

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Section: Discussionmentioning

confidence: 99%

p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

Liu

Park

Tsuruta

et al. 2009

The Journal of Immunology

125

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“…Activation-induced cell death of inflammatory cells is another antiinflammatory strategy that can prevent the dissemination and perpetuation of inflammation, since inflammation can propagate through necrosis (26,27). In addition, induction of apoptosis as a therapy to control inflammation is not novel.…”

Section: Discussionmentioning

confidence: 99%

“…The effectiveness of this therapy stems from the fact that corticosteroids such as dexamethasone and hydrocortisone have been shown to markedly increase apoptosis in the portion of bronchial epithelial cells engulfing apoptotic eosinophils (26)(27)(28)(29). Although the mode of action is not fully understood, it might involve glucocorticoids binding specifically to their cognate receptor in either the membrane or the cytoplasm, resulting in translocation to the nucleus and subsequent regulation of proinflammatory genes, together with induction of apoptosis (26,28). We have reported that the preventive induction of pancreatic acinar cell apoptosis by cytoprotective substances resulted in the attenuation of cerulein-induced pancreatitis (30).…”

Section: Discussionmentioning

confidence: 99%

Preventive Effect of the Flavonoid, Wogonin, Against Ethanol-Induced Gastric Mucosal Damage in Rats

Park

Hahm

et al. 2004

Dig Dis Sci

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Whether wogonin (5,7-dihydroxy-8-methoxyflavone), a flavonoid originated from the root of Scutellaria baicalensis Georgi, which has been shown to have antiinflammatory and antitumor activities in various cell types, possesses a gastric cytoprotective effect was investigated in an ethanol-induced gastric damage model in rats. Ethanol administration alone induced evident gastric damage including gastric hemorrhages and edema, while this gastric damage was significantly attenuated by wogonin pretreatment (30 mg/kg B.W.) 1 hr before ethanol administration. As major protective mechanisms of wogonin on ethanol-induced gastric damage, we found that wogonin showed either antiinflammatory effects through dual actions on arachidonic acid metabolism, i.e., induction of prostaglandin D 2 and suppression of 5S-hydroxyeicosatetraenoic acid (5S-HETE), or preventive induction of profuse apoptosis in the stomach. Conclusively, the flavonoid wogonin could be used as a preventive agent of alcohol-induced gastropathy, whose actions were proven to be strong antiinflammation and apoptosis induction.

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“…Potential strategies include, but are not limited to small molecules that inhibit or activate specific proteins involved in the pathway, antisense oligonucleotides directed against specific genes involved in cell death, fusion proteins that can activate or block cell membrane receptors to modulate the pathway, mitochondria specific agents, or modified nanoparticles that activate apoptosis (Cho, 2014, Huang et al, 2013, Murphy et al, 2003a, Murphy et al, 2003b. Eventually, many of the potential therapeutic agents reached phase I and II clinical trial (Wong, 2011).…”

Section: G B C D E F H Amentioning

confidence: 99%

Regulated cell death in diagnostic histopathology

Skenderi¹,

Vranić²,

Damjanov³

2015

Int. J. Dev. Biol.

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Regulated cell death (RCD) is a controlled cellular process, essential for normal development, tissue integrity and homeostasis, and its dysregulation has been implicated in the pathogenesis of various conditions including developmental and immunological disorders, neurodegenerative diseases, and cancer. In this review, we briefly discuss the historical perspective and conceptual development of RCD, we overview recent classifications and some of the key players in RCD; finally we focus on current applications of RCD in diagnostic histopathology.

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Targeting inflammatory diseases via apoptotic mechanisms

Cited by 25 publications

References 61 publications

p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

Preventive Effect of the Flavonoid, Wogonin, Against Ethanol-Induced Gastric Mucosal Damage in Rats

Regulated cell death in diagnostic histopathology

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