Phosphatidylinositol 3-kinase, phosphoinositide-specific phospholipase-Cγ and protein kinase-C signal myelin phagocytosis mediated by complement receptor-3 alone and combined with scavenger receptor-AI/II in macrophages

Makranz, Chen; Cohen, Goni; Baron, Ayellet; Levidor, Lital; Kodama, Tatsuhiko; Reichert, Fanny; Rotshenker, Shlomo

doi:10.1016/j.nbd.2003.11.007

Cited by 38 publications

(58 citation statements)

References 47 publications

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“…Wild-type C57BL6 and BalbC mice (Harlan, Israel), mice lacking SRAI/II (SRAI/II -/-) and mice lacking the a M /CD11b subunit of CR3/MAC-1 (CR3/MAC-1 2/2 ) Makranz et al, 2004Makranz et al, , 2006Reichert and Rotshenker, 2003). Mice were handled in accordance with the national research council's guide for the care and use of laboratory animals and the approval of the institutional committee.…”

Section: Materials and Methods Animalsmentioning

confidence: 99%

“…First, CR3/MAC-1 and SRAI/II are expressed with Galectin-3/MAC-2 in myelin phagocytosing microglia, but without Galectin-3/MAC-2 in microglia which do not phagocytose myelin Rotshenker, 1996, 1999). Second, CR3/MAC-1 and SRAI/II mediated myelin phagocytosis require signaling by PI3K Makranz et al, 2004). Third, PI3K is activated by Ras; primarily K-Ras which is stabilized in its active form, K-Ras-GTP, by Galectin-3/MAC-2 (Ashery et al, 2006;Elad-Sfadia et al, 2004;ShalomFeuerstein et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Galectin‐3/MAC‐2, Ras and PI3K activate complement receptor‐3 and scavenger receptor‐AI/II mediated myelin phagocytosis in microglia

Rotshenker

Reichert

Gitik

et al. 2008

Glia

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The removal of degenerated myelin is essential for repair in Wallerian degeneration that follows traumatic injury to axons and in autoimmune demyelinating diseases (e.g., multiple sclerosis). Microglia can remove degenerated myelin through phosphatidylinositol-3-kinase (PI3K)-dependent phagocytosis mediated by complement receptor-3 (CR3/MAC-1) and scavenger receptor-AI/II (SRAI/II). Paradoxically, these receptors are expressed in microglia after injury but myelin is not phagocytosed. Additionally, Galectin-3/MAC-2 is expressed in microglia that phagocytose but not in microglia that do not phagocytose, suggesting that Galectin-3/MAC-2 is instrumental in activating phagocytosis. S-trans, trans-farnesylthiosalicylic (FTS), which inhibits Galectin-3/MAC-2 dependent activation of PI3K through Ras, inhibited phagocytosis. K-Ras-GTP levels and PI3K activity increased during normal phagocytosis and decreased during FTS-inhibited phagocytosis. Galectin-3/MAC-2, which binds and stabilizes active Ras, coimmunoprecipitated with Ras and levels of the coimmunoprecipitate increased during normal phagocytosis. A role for Galectin-3/MAC-2 dependent activation of PI3K through Ras, mostly K-Ras, is thus suggested. An explanation may thus be offered for deficient phagocytosis by microglia that express CR3/MAC-1 and SRAI/II without Galectin-3/MAC-2 and efficient phagocytosis when CR3/MAC-1 and SRAI/II are co-expressed with Galectin-3/MAC-2.

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Section: Materials and Methods Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Galectin‐3/MAC‐2, Ras and PI3K activate complement receptor‐3 and scavenger receptor‐AI/II mediated myelin phagocytosis in microglia

Rotshenker

Reichert

Gitik

et al. 2008

Glia

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“…This multimolecular platform should be able both to trigger a downstream signal and to limit its duration by the partial degradation of the ligandreceptor complex. Indeed, because Src kinases activate PLC (116), this event might result in a signaling cascade responsible for a rapid rise in Ca 2ϩ levels, initiate neurotransmitter release and, in turn, transfer a lipid signal to the brain (FIGURE 8, 2). Ubiquitination of CD36, by inducing its progressive removal from the plasma membrane (210), might allow its subsequent partial degradation by the proteasome pathway (218), inducing a gradual decrease in the attraction for fat during the meal (122) (FIGURE 8, 3).…”

Section: Indirect Cooperation Hypothesismentioning

confidence: 99%

Taste of Fat: A Sixth Taste Modality?

Besnard

Passilly-Degrace

Khan

2016

Physiological Reviews

203

170

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An attraction for palatable foods rich in lipids is shared by rodents and humans. Over the last decade, the mechanisms responsible for this specific eating behavior have been actively studied, and compelling evidence implicates a taste component in the orosensory detection of dietary lipids [i.e., long-chain fatty acids (LCFA)], in addition to textural, olfactory, and postingestive cues. The interactions between LCFA and specific receptors in taste bud cells (TBC) elicit physiological changes that affect both food intake and digestive functions. After a short overview of the gustatory pathway, this review brings together the key findings consistent with the existence of a sixth taste modality devoted to the perception of lipids. The main steps leading to this new paradigm (i.e., chemoreception of LCFA in TBC, cell signaling cascade, transfer of lipid signals throughout the gustatory nervous pathway, and their physiological consequences) will be critically analyzed. The limitations to this concept will also be discussed in the light of our current knowledge of the sense of taste. Finally, we will analyze the recent literature on obesity-related dysfunctions in the orosensory detection of lipids ("fatty" taste?), in relation to the overconsumption of fat-rich foods and the associated health risks.

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“…Schwann cell-derived MCP-1, IL-1β and MIP-1α contribute to the macrophage recruitment, as neutralizing these factors leads to a severe reduction of phagocytic macrophages (Perrin et al, 2005). MAC-1 and MAC-2 are also crucial for the myelin phagocytosis by macrophages and SCs (Makranz et al, 2004;Makranz et al, 2006;Saada et al, 1996). In the present study, I observed that MAC-2, IL-1β and IL-6 are significantly higher expressed in GDF-15 KO nerve, furthermore, MCP-1 levels in the KO also showed a trend to surpass its expression in WT (Fig 3. A previous publication on an atherosclerosis model had shown that GDF-15 deficiency impairs the expression of CCR2, attenuates MCP-1 mediated macrophage migration, and as a consequence, leads to reduced macrophage recruitment (de Jager et al, 2011).…”

Section: Gdf-15 and Schwann Cells/fibroblasts/macrophagesmentioning

confidence: 99%

Growth/differentiation factor-15 and its role in peripheral nervous system lesion and regeneration

et al. 2015

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Phosphatidylinositol 3-kinase, phosphoinositide-specific phospholipase-Cγ and protein kinase-C signal myelin phagocytosis mediated by complement receptor-3 alone and combined with scavenger receptor-AI/II in macrophages

Cited by 38 publications

References 47 publications

Galectin‐3/MAC‐2, Ras and PI3K activate complement receptor‐3 and scavenger receptor‐AI/II mediated myelin phagocytosis in microglia

Galectin‐3/MAC‐2, Ras and PI3K activate complement receptor‐3 and scavenger receptor‐AI/II mediated myelin phagocytosis in microglia

Taste of Fat: A Sixth Taste Modality?

Growth/differentiation factor-15 and its role in peripheral nervous system lesion and regeneration

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