Platelet-activating factor in liver injury: A relational scope

Karidis, Nikolaos P.; Kouraklis, Gregory; Theocharis, Stamatios

doi:10.3748/wjg.v12.i23.3695

Cited by 15 publications

(14 citation statements)

References 71 publications

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“…PAF has been implicated in the responses to a variety of physiological and pathophysiological situations in mammals [30,31,54,55]. Synthesis of PAF has also been detected in some bacteria, protozoans, yeasts, plants, marine invertebrates, etc.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological characterization of anaphylaxis-like shock responses induced in mice by mannan and lipopolysaccharide

Funayama¹,

Huang²,

Sato³

et al. 2009

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Pharmacological characterization of anaphylaxis-like shock responses induced in mice by mannan and lipopolysaccharide

Funayama¹,

Huang²,

Sato³

et al. 2009

International Immunopharmacology

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“…Another macrophage-derived lipid inflammatory mediator implicated in tissue injury is platelet activating factor (PAF) (140, 141). PAF is thought to act in a paracrine and autocrine manner to amplify and propagate early stages of the inflammatory response.…”

Section: Macrophage-derived Proinflammatory/cytotoxic Mediators Implimentioning

confidence: 99%

Macrophages and Tissue Injury: Agents of Defense or Destruction?

Laskin

Sunil

Gardner

et al. 2011

Annu. Rev. Pharmacol. Toxicol.

519

471

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The past several years have seen the accumulation of evidence demonstrating that tissue injury induced by diverse toxicants is due not only to their direct effects on target tissues but also indirectly to the actions of resident and infiltrating macrophages. These cells release an array of mediators with cytotoxic, pro- and anti-inflammatory, angiogenic, fibrogenic, and mitogenic activity, which function to fight infections, limit tissue injury, and promote wound healing. However, following exposure to toxicants, macrophages can become hyperresponsive, resulting in uncontrolled or dysregulated release of mediators that exacerbate acute tissue injury and/or promote the development of chronic diseases such as fibrosis and cancer. Evidence suggests that the diverse activity of macrophages is mediated by distinct subpopulations that develop in response to signals within their microenvironment. Understanding the precise roles of these different macrophage populations in the pathogenic response to toxicants is key to designing effective treatments for minimizing tissue damage and chronic disease and for facilitating wound repair.

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“…Substantial evidence highlighting the crucial involvement of PAF in liver diseases, including cirrhosis, have recently been reviewed by our group [32]. In fact, alterations of blood PAF levels have been reported in cirrhotic patients [33][34][35].…”

Section: Introductionmentioning

confidence: 99%

Platelet-Activating Factor Involvement in Thioacetamide-Induced Experimental Liver Fibrosis and Cirrhosis

et al. 2009

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Platelet-activating factor (PAF) is a potent lipid inflammatory mediator acting on cells through its specific receptor. Plasma PAF-acetylhydrolase (PAF-AH) is the main enzyme that inactivates PAF in blood, participating in its homeostasis. The objective of this study was to investigate the involvement of PAF in the liver fibrotic process using an experimental animal model. Liver fibrosis was induced in adult male Wistar rats by administration of thioacetamide (TAA) in drinking water (300 mg/l) for three months. The animals were sacrificed at time 0 (control group) and after 1, 2, and 3 months. PAF levels in liver and blood and PAF-AH activity in plasma were determined. Liver histopathological examination was also performed. TAA administration resulted in progressively increased liver fibrosis, leading finally to the formation of cirrhotic nodules in the liver. Throughout the experiment PAF levels in liver tissue remained stable. "Total" ("free" plus "bound") PAF levels in blood decreased, reaching statistically significant differences in the first and third months compared with the control group (P < 0.05). "Free" PAF levels in blood were higher at one month (P < 0.05) and decreased gradually thereafter. In all treated groups, "bound" PAF levels in blood decreased whereas plasma PAF-AH activity increased (P < 0.05) compared with the control group. Our data indicated alterations of PAF levels in blood and PAF-AH activity during fibrosis induction, implicating participation of PAF in the liver fibrotic process.

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Platelet-activating factor in liver injury: A relational scope

Cited by 15 publications

References 71 publications

Pharmacological characterization of anaphylaxis-like shock responses induced in mice by mannan and lipopolysaccharide

Pharmacological characterization of anaphylaxis-like shock responses induced in mice by mannan and lipopolysaccharide

Macrophages and Tissue Injury: Agents of Defense or Destruction?

Platelet-Activating Factor Involvement in Thioacetamide-Induced Experimental Liver Fibrosis and Cirrhosis

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