Role of FABP in Cellular Phospholipid Metabolism

Systemic sclerosis (SSc) is an autoimmune disease with fibrosis of the skin and/or internal organs, causing a decrease in quality of life and survival. There is no causative therapy, and the pathophysiology of the SSc remains unclear. Studies showed that lipid metabolism was relevant for autoimmune diseases, but little is known about the role of lipids in SSc. In the present study, we sought to explore the phospholipid profile of SSc by using the lipidomics approach. We also aimed to analyze lipidomics results for different clinical manifestations of SSc. Experiments were performed using high-performance liquid chromatography coupled to mass spectrometry for the lipidomic profiling of plasma samples from patients with SSc. Our study showed, for the first time, significant changes in the level of phospholipids such as plasmalogens and sphingomyelins from the plasma of SSc patients as compared to controls. Phosphatidylcholine plasmalogens species and sphingomyelins were significantly increased in SSc patients as compared to controls. Our results also demonstrated a significant association of changes in the metabolism of phospholipids (phosphatidylcholine and phosphatidylethanolamine plasmalogens species and sphingomyelins) with different clinical manifestations of SSc. Further lipidomic studies might lead to the detection of lipids as new biomarkers or therapeutic targets of SSc.

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Role of phosphatidylinositide metabolism in ras-induced Xenopus oocyte maturation

Molecular and Cellular Biology ◽

10.1128/mcb.10.3.923-929.1990 ◽

1990 ◽

Vol 10 (3) ◽

pp. 923-929

Author(s):

B T Pan ◽

G M Cooper

Keyword(s):

Xenopus Oocytes ◽

Second Messengers ◽

Phospholipid Metabolism ◽

Meiotic Maturation ◽

Ras Oncogene ◽

Ras Protein ◽

32P Incorporation ◽

Kinetics Of ◽

Oncogene Protein

Microinjection of Xenopus oocytes with ras protein (p21) was used to investigate the role of phospholipid metabolism in ras-induced meiotic maturation. Induction of meiosis by ras was compared with induction by progesterone, insulin, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). Neomycin, which specifically binds to phosphatidylinositides and inhibits their metabolism, blocked meiotic maturation induced by ras or insulin but not by progesterone or TPA. In addition, p21 and TPA, but not insulin or progesterone, stimulated the incorporation of 32Pi into oocyte lipids. ras protein specifically stimulated 32P incorporation into phosphatidylinositides, whereas both ras and TPA stimulated 32P incorporation into phosphatidylcholine and phosphatidylethanolamine. The stimulatory effect of p21 on phosphatidylinositide metabolism correlated with the dose response and kinetics of ras-induced meiotic maturation. In addition, the ras oncogene protein was more potent than the proto-oncogene protein both in inducing meiotic maturation and in stimulating phosphatidylinositide metabolism. These results indicate that phosphatidylinositide turnover is required for ras-induced meiosis and suggest that phosphatidylinositide-derived second messengers mediate the biological activity of ras in Xenopus oocytes.

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Role of the Yeast VAP Homolog, Scs2p, in INO1 Expression and Phospholipid Metabolism

The Journal of Biochemistry ◽

10.1093/jb/mvg068 ◽

2003 ◽

Vol 133 (4) ◽

pp. 515-522 ◽

Cited By ~ 32

Author(s):

S. Kagiwada

Keyword(s):

Phospholipid Metabolism

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The Agr-Like Quorum Sensing System Is Required for Pathogenesis of Necrotic Enteritis Caused by Clostridium perfringens in Poultry

Infection and Immunity ◽

10.1128/iai.00975-16 ◽

2017 ◽

Vol 85 (6) ◽

Cited By ~ 15

Author(s):

Qiang Yu ◽

Dion Lepp ◽

Iman Mehdizadeh Gohari ◽

Tao Wu ◽

Hongzhuan Zhou ◽

...

Keyword(s):

Quorum Sensing ◽

Clostridium Perfringens ◽

Global Gene Expression ◽

Toxin Production ◽

Phospholipid Metabolism ◽

Necrotic Enteritis ◽

Content Type ◽

Protein Levels ◽

Global Gene Expression Analysis

ABSTRACT Clostridium perfringens encodes at least two different quorum sensing (QS) systems, the Agr-like and LuxS, and recent studies have highlighted their importance in the regulation of toxin production and virulence. The role of QS in the pathogenesis of necrotic enteritis (NE) in poultry and the regulation of NetB, the key toxin involved, has not yet been investigated. We have generated isogenic agrB-null and complemented strains from parent strain CP1 and demonstrated that the virulence of the agrB-null mutant was strongly attenuated in a chicken NE model system and restored by complementation. The production of NetB, a key NE-associated toxin, was dramatically reduced in the agrB mutant at both the transcriptional and protein levels, though not in a luxS mutant. Transwell assays confirmed that the Agr-like QS system controls NetB production through a diffusible signal. Global gene expression analysis of the agrB mutant identified additional genes modulated by Agr-like QS, including operons related to phospholipid metabolism and adherence, which may also play a role in NE pathogenesis. This study provides the first evidence that the Agr-like QS system is critical for NE pathogenesis and identifies a number of Agr-regulated genes, most notably netB, that are potentially involved in mediating its effects. The Agr-like QS system thus may serve as a target for developing novel interventions to prevent NE in chickens.

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