Different expression and subcellular localization of Phosphoinositide-specific Phospholipase C enzymes in differently polarized macrophages

Raimo, Tania Di; Leopizzi, Martina; Mangino, Giorgio; Rocca, Carlo Della; Businaro, Rita; Longo, Lucia; Vasco, Vincenza Rita Lo

doi:10.1007/s12079-016-0335-9

Cited by 24 publications

(29 citation statements)

References 53 publications

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“…Previous studies indicated that PLC γ isoforms are involved in the inflammatory activation of macrophages (Di Raimo et al 2016). PLC γ subfamily is activated in the presence of AA that serves as a common link between receptor activation of Phospholipase A2 and the PI pathway (Suh et al 2008).…”

Section: Discussionmentioning

confidence: 99%

LPS, Oleuropein and Blueberry extracts affect the survival, morphology and Phosphoinositide signalling in stimulated human endothelial cells

Vasco

Leopizzi

Maio

et al. 2017

J. Cell Commun. Signal.

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Endothelial cells (EC) act as leading actors in angiogenesis. Understanding the complex network of signal transduction pathways which regulate angiogenesis might offer insights in the regulation of normal and pathological events, including tumours, vascular, inflammatory and immune diseases. The effects of olive oil and of Blueberry extracts upon the phosphoinositide (PI)-specific phospholipase C (PLC) enzymes were evaluated both in quiescent and inflammatory stimulated human umbilical vein EC (HUVEC) using molecular biology (multiliquid bioanalysis) and immunofluorescence techniques. Oleuropein significantly increased the number of surviving HUVEC compared to untreated controls, suggesting that it favours the survival and proliferation of EC. Our results suggest that Oleuropein might be useful to induce EC proliferation, an important event during angiogenesis, with special regard to wound healing. Blueberry extracts increased the number of surviving HUVEC, although the comparison to untreated controls did not result statistically significant. Lipopolysaccharide (LPS) administration significantly reduced the number of live HUVEC. LPS can also modify the expression of selected PLC genes. Adding Blueberry extracts to LPS treated HUVEC cultures did not significantly modify the variations of PLC expression induced by LPS. Oleuropein increased or reduced the expression of PLC genes, and statistically significant results were identified for selected PLC isoforms. Oleuropein also modified the effects of LPS upon PLC genes' expression. Thus, our results corroborate the hypothesis that Oleuropein owns antiinflammatory activity. The intracellular localization of PLC enzymes was modified by the different treatments we used. Podosome-like structures were observed in differently LPS treated HUVEC.

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Section: Discussionmentioning

confidence: 99%

LPS, Oleuropein and Blueberry extracts affect the survival, morphology and Phosphoinositide signalling in stimulated human endothelial cells

Vasco

Leopizzi

Maio

et al. 2017

J. Cell Commun. Signal.

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“…It has been reported that in the case of human macrophages (derived from peripheral blood mononuclear cells), PLC β 1–4, γ 1-2, δ 1, and η 1-2 are expressed in unstimulated macrophages, PLC β 1–3, γ 1-2, δ 1 and 3, and η 1-2 are expressed in M1 macrophages, and PLC β 1–3, γ 1-2, δ 3, and η 1-2 are expressed in M2 macrophages. In addition, these PLC isoforms showed different subcellular localization in differently polarized macrophages [ 46 ]. The distinct expression spectrum and subcellular localization of these PLC isoforms reflect the diverse roles that they play in the regulation of the inflammatory response.…”

Section: The Spectrum Of Expression Of Plc Isoenzymes In Macrophagmentioning

confidence: 99%

The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response

Zhu

Jones

Zhang

2018

Journal of Immunology Research

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Macrophages are crucial members of the mononuclear phagocyte system essential to protect the host from invading pathogens and are central to the inflammatory response with their ability to acquire specialized phenotypes of inflammatory (M1) and anti-inflammatory (M2) and to produce a pool of inflammatory mediators. Equipped with a broad range of receptors, such as Toll-like receptor 4 (TLR4), CD14, and Fc gamma receptors (FcγRs), macrophages can efficiently recognize and phagocytize invading pathogens and secrete cytokines by triggering various secondary signaling pathways. Phospholipase C (PLC) is a family of enzymes that hydrolyze phospholipids, the most significant of which is phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2]. Cleavage at the internal phosphate ester generates two second messengers, inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG), both of which mediate in diverse cellular functions including the inflammatory response. Recent studies have shown that some PLC isoforms are involved in multiple stages in TLR4-, CD14-, and FcγRs-mediated activation of nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and interferon regulatory factors (IRFs), all of which are associated with the regulation of the inflammatory response. Therefore, secondary signaling by PLC is implicated in the pathogenesis of numerous inflammatory diseases. This review provides an overview of our current knowledge on how PLC signaling regulates the macrophage-mediated inflammatory response.

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“…In particular, PI-PLCβ2 and PI-PLCβ3 isozymes play a crucial role in inhibiting the switch from M1 to M2 phenotype [ 24 , 25 ], and lipids generated by iPLA 2 β favor M1 polarization [ 26 ]. In addition, differently polarized macrophages were shown to own peculiar panels of expression and intracellular localization of PI-PLC enzymes, which slightly change following triggering with inflammatory stimuli [ 27 ].…”

Section: Macrophage and Phospholipase Biologymentioning

confidence: 99%

Macrophages and Phospholipases at the Intersection between Inflammation and the Pathogenesis of HIV-1 Infection

Spadaro

Cecchetti

Fantuzzi

2017

IJMS

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Persistent low grade immune activation and chronic inflammation are nowadays considered main driving forces of the progressive immunologic failure in effective antiretroviral therapy treated HIV-1 infected individuals. Among the factors contributing to this phenomenon, microbial translocation has emerged as a key driver of persistent immune activation. Indeed, the rapid depletion of gastrointestinal CD4+ T lymphocytes occurring during the early phases of infection leads to a deterioration of the gut epithelium followed by the translocation of microbial products into the systemic circulation and the subsequent activation of innate immunity. In this context, monocytes/macrophages are increasingly recognized as an important source of inflammation, linked to HIV-1 disease progression and to non-AIDS complications, such as cardiovascular disease and neurocognitive decline, which are currently main challenges in treated patients. Lipid signaling plays a central role in modulating monocyte/macrophage activation, immune functions and inflammatory responses. Phospholipase-mediated phospholipid hydrolysis leads to the production of lipid mediators or second messengers that affect signal transduction, thus regulating a variety of physiologic and pathophysiologic processes. In this review, we discuss the contribution of phospholipases to monocyte/macrophage activation in the context of HIV-1 infection, focusing on their involvement in virus-associated chronic inflammation and co-morbidities.

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Different expression and subcellular localization of Phosphoinositide-specific Phospholipase C enzymes in differently polarized macrophages

Cited by 24 publications

References 53 publications

LPS, Oleuropein and Blueberry extracts affect the survival, morphology and Phosphoinositide signalling in stimulated human endothelial cells

LPS, Oleuropein and Blueberry extracts affect the survival, morphology and Phosphoinositide signalling in stimulated human endothelial cells

The Role of Phospholipase C Signaling in Macrophage-Mediated Inflammatory Response

Macrophages and Phospholipases at the Intersection between Inflammation and the Pathogenesis of HIV-1 Infection

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