Biosynthesis of platelet-activating factor and its 1O-acyl analogue by liver fat-storing cells

Pinzani, Massimo; Carloni, Vinicio; Marra, Fabio; Riccardi, Donato; Laffi, Giacomo; Geñtilini, Paolo

doi:10.1016/0016-5085(94)90023-x

Cited by 41 publications

(16 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PAF promotes chemotaxis of neutrophils and stimulates their activation (489). Its production is increased by thrombin, LPS, and calcium ionophores (489).…”

Section: Production Of Growth Factors and Cytokinesmentioning

confidence: 99%

See 1 more Smart Citation

Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver

Friedman

2008

Physiological Reviews

2,423

2,549

View full text Add to dashboard Cite

The hepatic stellate cell has surprised and engaged physiologists, pathologists, and hepatologists for over 130 years, yet clear evidence of its role in hepatic injury and fibrosis only emerged following the refinement of methods for its isolation and characterization. The paradigm in liver injury of activation of quiescent vitamin A-rich stellate cells into proliferative, contractile, and fibrogenic myofibroblasts has launched an era of astonishing progress in understanding the mechanistic basis of hepatic fibrosis progression and regression. But this simple paradigm has now yielded to a remarkably broad appreciation of the cell's functions not only in liver injury, but also in hepatic development, regeneration, xenobiotic responses, intermediary metabolism, and immunoregulation. Among the most exciting prospects is that stellate cells are essential for hepatic progenitor cell amplification and differentiation. Equally intriguing is the remarkable plasticity of stellate cells, not only in their variable intermediate filament phenotype, but also in their functions. Stellate cells can be viewed as the nexus in a complex sinusoidal milieu that requires tightly regulated autocrine and paracrine cross-talk, rapid responses to evolving extracellular matrix content, and exquisite responsiveness to the metabolic needs imposed by liver growth and repair. Moreover, roles vital to systemic homeostasis include their storage and mobilization of retinoids, their emerging capacity for antigen presentation and induction of tolerance, as well as their emerging relationship to bone marrow-derived cells. As interest in this cell type intensifies, more surprises and mysteries are sure to unfold that will ultimately benefit our understanding of liver physiology and the diagnosis and treatment of liver disease.

show abstract

“…PAF promotes chemotaxis of neutrophils and stimulates their activation (489). Its production is increased by thrombin, LPS, and calcium ionophores (489).…”

Section: Production Of Growth Factors and Cytokinesmentioning

confidence: 99%

“…PAF promotes chemotaxis of neutrophils and stimulates their activation (489). Its production is increased by thrombin, LPS, and calcium ionophores (489). PAF and its receptors are induced on stellate cells during experimental fibrosis (712).…”

Section: Production Of Growth Factors and Cytokinesmentioning

confidence: 99%

Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver

Friedman

2008

Physiological Reviews

2,423

2,549

View full text Add to dashboard Cite

show abstract

“…5,39 Previous work from our group has revealed that thrombin exerts multiple actions on HSC, including stimulation of calcium influx and contractility, and secretion of platelet-activating factor. 40,41 More recently, we have reported that thrombin stimulates proliferation of cultured HSC and secretion of monocyte chemotactic protein-1, a potent chemoattractant for inflammatory cells, through activation of TR. 6 Here we show that activated HSC express the TR during liver injury in vivo.…”

Section: Discussionmentioning

confidence: 99%

Expression of the thrombin receptor in human liver: Up-regulation during acute and chronic injury

et al. 1998

Self Cite

View full text Add to dashboard Cite

Thrombin is generated during tissue damage in several organs, including the liver, and participates in the process of tissue repair through proteolytic activation of a specific thrombin receptor (TR). The aim of this study was to investigate TR expression in human liver by immunohistochemistry and in situ hybridization. In normal liver, immunostaining for TR was present in the endothelial lining of the hepatic sinusoids. During chronic hepatitis, several cells expressing the TR were detected in the inflammatory infiltrate of portal tracts. In cirrhosis with chronic active hepatitis, expression of the TR was also present in mesenchymal cells of fibrous septa. TR expression was markedly up-regulated during fulminant hepatitis, with the highest expression in mesenchymal cells in areas of regeneration. Up-regulation of TR expression was associated with increased levels of TR messenger RNA (mRNA), as assessed by in situ hybridization and RNAse protection assay of liver RNA. Immunostaining of serial sections using specific cellular markers showed that different nonparenchymal cells contribute to TR expression during liver injury. TR expression was also shown in cultured human hepatic stellate cells, with increasing signal comparing activated versus quiescent cells. Because thrombin is rapidly generated after tissue damage, regulated TR expression may be involved in tissue remodeling and/or scarring during liver damage. (HEPATOLOGY 1998;27:462-471.)

show abstract

“…In DMN-induced liver fibrosis, IFN-g did not seem to act as a nonspecific anti- leasing soluble factors that promote recruitment, pro-kines affect only isolated features of HSC activation, 24 IFN-g appears unique in its ability to coordinately inliferation, and differentiation of mononuclear phagocytes. [60][61] terfere with HSC transformation. Reduced HSC activation determined a decreased acTo assess the mechanism involved in the protection against fibrosis, we paid special attention to the process cumulation of extracellular matrix proteins in DMN / IFN-g-treated animals compared with DMN alone, as of activation of HSC, characterized by a modulation toward a myofibroblast-like phenotype.…”

Section: Procollagen I Laminin and Fibronectin Mrna Ex-mentioning

confidence: 99%

Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis

et al. 1996

View full text Add to dashboard Cite

Hepatic fibrosis is a common response to chronic liver early response to cell injury. Rats were killed after 1 or injury of variable origin (viral, metabolic, or toxic). Re-3 weeks of treatment with DMN, IFN-g, DMN / IFN-g, gardless of the etiologic factor, liver fibrosis is characor saline. Immunohistochemistry was used to iden-terized by increased production of extracellular matrix tify proliferating (desmin-positive/bromodeoxyuridine components that form the hepatic scars and consists of factor is the most potent proliferative cytokine forFrom the

show abstract

Biosynthesis of platelet-activating factor and its 1O-acyl analogue by liver fat-storing cells

Cited by 41 publications

References 49 publications

Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver

Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver

Expression of the thrombin receptor in human liver: Up-regulation during acute and chronic injury

Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis

Contact Info

Product

Resources

About