The Experts below are selected from a list of 29352 Experts worldwide ranked by ideXlab platform
Yanxia Jia - One of the best experts on this subject based on the ideXlab platform.
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Lipid profiling demonstrates that suppressing arabidopsis phospholipase dδ retards aba promoted leaf senescence by attenuating Lipid Degradation
PLOS ONE, 2013Co-Authors: Yanxia Jia, Faqing TaoAbstract:Senescence is the last phase of the plant life cycle and has an important role in plant development. Degradation of membrane Lipids is an essential process during leaf senescence. Several studies have reported fundamental changes in membrane Lipids and phospholipase D (PLD) activity as leaves senesce. Suppression of phospholipase Dα1 (PLDα1) retards abscisic acid (ABA)-promoted senescence. However, given the absence of studies that have profiled changes in the compositions of membrane Lipid molecules during leaf senescence, there is no direct evidence that PLD affects Lipid composition during the process. Here, we show that application of n-butanol, an inhibitor of PLD, and N-Acylethanolamine (NAE) 12∶0, a specific inhibitor of PLDα1, retarded ABA-promoted senescence to different extents. Furthermore, phospholipase Dδ (PLDδ) was induced in leaves treated with ABA, and suppression of PLDδ retarded ABA-promoted senescence in Arabidopsis. Lipid profiling revealed that detachment-induced senescence had different effects on plastidic and extraplastidic Lipids. The accelerated Degradation of plastidic Lipids during ABA-induced senescence in wild-type plants was attenuated in PLDδ-knockout (PLDδ-KO) plants. Dramatic increases in phosphatidic acid (PA) and decreases in phosphatidylcholine (PC) during ABA-induced senescence were also suppressed in PLDδ-KO plants. Our results suggest that PLDδ-mediated hydrolysis of PC to PA plays a positive role in ABA-promoted senescence. The attenuation of PA formation resulting from suppression of PLDδ blocks the Degradation of membrane Lipids, which retards ABA-promoted senescence.
Faqing Tao - One of the best experts on this subject based on the ideXlab platform.
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Lipid profiling demonstrates that suppressing arabidopsis phospholipase dδ retards aba promoted leaf senescence by attenuating Lipid Degradation
PLOS ONE, 2013Co-Authors: Yanxia Jia, Faqing TaoAbstract:Senescence is the last phase of the plant life cycle and has an important role in plant development. Degradation of membrane Lipids is an essential process during leaf senescence. Several studies have reported fundamental changes in membrane Lipids and phospholipase D (PLD) activity as leaves senesce. Suppression of phospholipase Dα1 (PLDα1) retards abscisic acid (ABA)-promoted senescence. However, given the absence of studies that have profiled changes in the compositions of membrane Lipid molecules during leaf senescence, there is no direct evidence that PLD affects Lipid composition during the process. Here, we show that application of n-butanol, an inhibitor of PLD, and N-Acylethanolamine (NAE) 12∶0, a specific inhibitor of PLDα1, retarded ABA-promoted senescence to different extents. Furthermore, phospholipase Dδ (PLDδ) was induced in leaves treated with ABA, and suppression of PLDδ retarded ABA-promoted senescence in Arabidopsis. Lipid profiling revealed that detachment-induced senescence had different effects on plastidic and extraplastidic Lipids. The accelerated Degradation of plastidic Lipids during ABA-induced senescence in wild-type plants was attenuated in PLDδ-knockout (PLDδ-KO) plants. Dramatic increases in phosphatidic acid (PA) and decreases in phosphatidylcholine (PC) during ABA-induced senescence were also suppressed in PLDδ-KO plants. Our results suggest that PLDδ-mediated hydrolysis of PC to PA plays a positive role in ABA-promoted senescence. The attenuation of PA formation resulting from suppression of PLDδ blocks the Degradation of membrane Lipids, which retards ABA-promoted senescence.
Yasuo Okamoto - One of the best experts on this subject based on the ideXlab platform.
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sphingosine kinase 2 prevents macrophage cholesterol accumulation and atherosclerosis by stimulating autophagic Lipid Degradation
Scientific Reports, 2019Co-Authors: Kazuhiro Ishimaru, Kazuaki Yoshioka, Kuniyuki Kano, Makoto Kurano, Daisuke Saigusa, Junken Aoki, Yutaka Yatomi, Noriko Takuwa, Yasuo OkamotoAbstract:Atherosclerosis is the major cause of ischemic coronary heart diseases and characterized by the infiltration of cholesterol-accumulating macrophages in the vascular wall. Although sphingoLipids are implicated in atherosclerosis as both membrane components and Lipid mediators, the precise role of sphingoLipids in atherosclerosis remains elusive. Here, we found that genetic deficiency of sphingosine kinase-2 (SphK2) but not SphK1 aggravates the formation of atherosclerotic lesions in mice with ApoE deficiency. Bone marrow chimaera experiments show the involvement of SphK2 expressed in bone marrow-derived cells. In macrophages, deficiency of SphK2, a major SphK isoform in this cell type, results in increases in cellular sphingosine and ceramides. SphK2-deficient macrophages have increases in Lipid droplet-containing autophagosomes and autolysosomes and defective lysosomal Degradation of Lipid droplets via autophagy with an impaired luminal acidic environment and proteolytic activity in the lysosomes. Transgenic overexpression of SphK1 in SphK2-deficient mice rescued aggravation of atherosclerosis and abnormalities of autophagosomes and lysosomes in macrophages with reductions of sphingosine, suggesting at least partial overlapping actions of two SphKs. Taken together, these results indicate that SphK2 is required for autophagosome- and lysosome-mediated catabolism of intracellular Lipid droplets to impede the development of atherosclerosis; therefore, SphK2 may be a novel target for treating atherosclerosis.
Noriko Takuwa - One of the best experts on this subject based on the ideXlab platform.
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sphingosine kinase 2 prevents macrophage cholesterol accumulation and atherosclerosis by stimulating autophagic Lipid Degradation
Scientific Reports, 2019Co-Authors: Kazuhiro Ishimaru, Kazuaki Yoshioka, Kuniyuki Kano, Makoto Kurano, Daisuke Saigusa, Junken Aoki, Yutaka Yatomi, Noriko Takuwa, Yasuo OkamotoAbstract:Atherosclerosis is the major cause of ischemic coronary heart diseases and characterized by the infiltration of cholesterol-accumulating macrophages in the vascular wall. Although sphingoLipids are implicated in atherosclerosis as both membrane components and Lipid mediators, the precise role of sphingoLipids in atherosclerosis remains elusive. Here, we found that genetic deficiency of sphingosine kinase-2 (SphK2) but not SphK1 aggravates the formation of atherosclerotic lesions in mice with ApoE deficiency. Bone marrow chimaera experiments show the involvement of SphK2 expressed in bone marrow-derived cells. In macrophages, deficiency of SphK2, a major SphK isoform in this cell type, results in increases in cellular sphingosine and ceramides. SphK2-deficient macrophages have increases in Lipid droplet-containing autophagosomes and autolysosomes and defective lysosomal Degradation of Lipid droplets via autophagy with an impaired luminal acidic environment and proteolytic activity in the lysosomes. Transgenic overexpression of SphK1 in SphK2-deficient mice rescued aggravation of atherosclerosis and abnormalities of autophagosomes and lysosomes in macrophages with reductions of sphingosine, suggesting at least partial overlapping actions of two SphKs. Taken together, these results indicate that SphK2 is required for autophagosome- and lysosome-mediated catabolism of intracellular Lipid droplets to impede the development of atherosclerosis; therefore, SphK2 may be a novel target for treating atherosclerosis.
Sylvie Derenne - One of the best experts on this subject based on the ideXlab platform.
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Leaf Lipid Degradation in soils and surface sediments: A litterbag experiment
Organic Geochemistry, 2016Co-Authors: Thanh Thuy Nguyen Tu, Céline Egasse, Christelle Anquetil, Florent Zanetti, Bernd Zeller, Sylvain Huon, Sylvie DerenneAbstract:The fate of leaf Lipids upon early diagenesis was monitored in a two year litterbag experiment in a soil and at the water-sediment interface of an adjacent pond. The biomarker content of degrading leaves exhibited substantial variability among litterbags, even for a given time step within a given environmental condition, likely reflecting natural microenvironmental variability. Due to this variability and the oxic conditions in the pond, no substantial difference between the soil and the pond could be evidenced in the biomarker Degradation pattern. An occasional increase in the abundance of several biomarkers (β- sitosterol, oleanolic acid, C16 phytyl ester, C27n-alkane) was also noted during the experiment, which was attributed to release of bound compounds and/or an external contribution. Nevertheless, absolute quantification showed that the concentration of all Lipid constituents was reduced, but they exhibited different decay profiles: (i) rapid extensive Degradation (phytyl ester), (ii) exponential-like decrease (fatty Lipids) and (iii) variable Degradation profile (polycyclic triterpenoids). However, all the main constituents initially present in the senescent leaves were still detected after two years of Degradation in both environments. Fatty Lipid abundance generally decreased to < 10% of the initial content but their main distribution features (carbon number maximum and predominance) remained unchanged. The results thus tend to validate their use as proxy for source and environment in ancient organic matter. They also suggest that, on a mid-term basis, a plant biomarker signature is not substantially affected by differential Degradation in soil and at the water-sediment interface, at least for a qualitative approach.