Mast cells: from lipid droplets to lipid mediators

Dichlberger, Andrea; Kovanen, Petri T.; Schneider, Wolfgang J.

doi:10.1042/cs20120602

Cited by 38 publications

(22 citation statements)

References 88 publications

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“…LB in immunocytes have some commonalities in terms of protein content and lipidome with LD, but also manifest important differences [12, 13, 23-25]. Our studies suggest that even in response to an endocrine input (chronic hyperinsulinemia), the expansion in LB content in mast cells is predominantly comprised of LB that store inflammatory precursors, alongside energy substrates that may also function as precursors for bioactive lipids [13, 24]. This expansion is, unsurprisingly, linked to an elevated potency in antigen mediated de novo synthesis and release of bioactive lipids such as LTC4 [13].…”

Section: Introductionmentioning

confidence: 90%

Lipid body accumulation alters calcium signaling dynamics in immune cells

et al. 2014

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Summary There is well-established variability in the numbers of lipid bodies (LB) in macrophages, eosinophils, and neutrophils. Similarly to the steatosis observed in adipocytes and hepatocytes during hyperinsulinemia and nutrient overload, immune cell LB hyper-accumulate in response to bacterial and parasitic infection and inflammatory presentations. Recently we described that hyperinsulinemia, both in vitro and in vivo, drives steatosis and phenotypic changes in primary and transformed mast cells and basophils. LB reach high numbers in these steatotic cytosols, and here we propose that they could dramatically impact the transcytoplasmic signaling pathways. We compared calcium release and influx responses at the population and single cell level in normal and steatotic model mast cells. At the population level, all aspects of FcεRI-dependent calcium mobilization, as well as activation of calcium-dependent downstream signalling targets such as NFATC1 phosphorylation are suppressed. At the single cell level, we demonstrate that LB are both sources and sinks of calcium following FcεRI cross-linking. Unbiased analysis of the impact of the presence of LB on the rate of trans-cytoplasmic calcium signals suggest that LB enrichment accelerates calcium propagation, which may reflect a Bernoulli effect. LB abundance thus impacts this fundamental signalling pathway and its downstream targets.

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Section: Introductionmentioning

confidence: 90%

Lipid body accumulation alters calcium signaling dynamics in immune cells

et al. 2014

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“…Since the demonstration that LBs from human mast cells contain large amounts of AA [74], these organelles have been implicated in eicosanoid biology (reviewed in refs. [75,76]).…”

Section: Mast Cellsmentioning

confidence: 99%

Unraveling the complexity of lipid body organelles in human eosinophils

Melo

Weller

2014

Journal of Leukocyte Biology

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Lipid-rich organelles are common in many cell types. In cells, such as adipocytes, these organelles are termed LDs, whereas in other cells, such as leukocytes, they are called LBs. The study of leukocyte LBs has attracted attention as a result of their association with human diseases. In leukocytes, such as eosinophils, LB accumulation has been documented extensively during inflammatory conditions. In these cells, LBs are linked to the regulation of immune responses by compartmentalization of several proteins and lipids involved in the control and biosynthesis of inflammatory mediators (eicosanoids). However, it has been unclear how diverse proteins, including membrane-associated enzymes involved in eicosanoid formation, incorporate into LBs, especially if the internal content of LBs is assumed to consist solely of stores of neutral lipids, as present within adipocyte LDs. Studies of the formation, function, and ultrastructure of LBs in eosinophils have been providing insights pertinent to LBs in other leukocytes. Here, we review current knowledge of the composition and function of leukocyte LBs as provided by studies of human eosinophil LBs, including recognitions of the internal architecture of eosinophil LBs based on 3D electron tomographic analyses.

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“…One tentative possibility is that UBAC2 impacts on lipid droplet homeostasis in inflammatory cells, which utilize triacylglyceride as a precursor for the production of inflammatory lipid species called eicosanoids [83]. Clearly, the precise physiological role of UBAC2 in metabolic control (potentially ERAD-R) awaits knockout mouse studies.…”

Section: Ubac2 and Dsc2mentioning

confidence: 99%

Inactive rhomboid proteins: New mechanisms with implications in health and disease

Lemberg

Adrain

2016

Seminars in Cell & Developmental Biology

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Rhomboids, proteases containing an unusual membrane-integral serine protease active site, were first identified in Drosophila, where they fulfill an essential role in epidermal growth factor receptor signaling, by cleaving membrane-tethered growth factor precursors. It has recently become apparent that eukaryotic genomes harbor conserved catalytically inactive rhomboid protease homologs, including derlins and iRhoms. Here we highlight how loss of proteolytic activity was followed in evolution by impressive functional diversification, enabling these pseudoproteases to fulfill crucial roles within the secretory pathway, including protein degradation, trafficking regulation, and inflammatory signaling. We distil the current understanding of the roles of rhomboid pseudoproteases in development and disease.

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Mast cells: from lipid droplets to lipid mediators

Cited by 38 publications

References 88 publications

Lipid body accumulation alters calcium signaling dynamics in immune cells

Lipid body accumulation alters calcium signaling dynamics in immune cells

Unraveling the complexity of lipid body organelles in human eosinophils

Inactive rhomboid proteins: New mechanisms with implications in health and disease

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