@article{JonasSchwerbelZellneretal.2022,
  author    = {Jonas, Wenke and Schwerbel, Kristin and Zellner, Lisa and J{\"a}hnert, Markus and Gottmann, Pascal and Sch{\"u}rmann, Annette},
  title     = {Alterations of lipid profile in livers with impaired lipophagy},
  series = {International journal of molecular sciences},
  volume    = {23},
  journal   = {International journal of molecular sciences},
  number    = {19},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {1422-0067},
  doi       = {10.3390/ijms231911863},
  pages     = {12},
  year      = {2022},
  abstract  = {Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Various mechanisms such as an increased uptake in fatty acids or de novo synthesis contribute to the development of steatosis and progression to more severe stages. Furthermore, it has been shown that impaired lipophagy, the degradation of lipids by autophagic processes, contributes to NAFLD. Through an unbiased lipidome analysis of mouse livers in a genetic model of impaired lipophagy, we aimed to determine the resulting alterations in the lipidome. Observed changes overlap with those of the human disease. Overall, the entire lipid content and in particular the triacylglycerol concentration increased under conditions of impaired lipophagy. In addition, we detected a reduction in long-chain polyunsaturated fatty acids (PUFAs) and an increased ratio of n-6 PUFAs to n-3 PUFAs, which was due to the depletion of n-3 PUFAs. Although the abundance of major phospholipid classes was reduced, the ratio of phosphatidylcholines to phosphatidylethanolamines was not affected. In conclusion, this study demonstrates that impaired lipophagy contributes to the pathology of NAFLD and is associated with an altered lipid profile. However, the lipid pattern does not appear to be specific for lipophagic alterations, as it resembles mainly that described in relation to fatty liver disease.},
  language  = {en}
}
@article{JueppnerMubeenLeisseetal.2017,
  author    = {J{\"u}ppner, Jessica and Mubeen, Umarah and Leisse, Andrea and Caldana, Camila and Brust, Henrike and Steup, Martin and Herrmann, Marion and Steinhauser, Dirk and Giavalisco, Patrick},
  title     = {Dynamics of lipids and metabolites during the cell cycle of Chlamydomonas reinhardtii},
  series = {The plant journal},
  volume    = {92},
  journal   = {The plant journal},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0960-7412},
  doi       = {10.1111/tpj.13642},
  pages     = {331 -- 343},
  year      = {2017},
  abstract  = {Metabolites and lipids are the final products of enzymatic processes, distinguishing the different cellular functions and activities of single cells or whole tissues. Understanding these cellular functions within a well-established model system requires a systemic collection of molecular and physiological information. In the current report, the green alga Chlamydomonas reinhardtii was selected to establish a comprehensive workflow for the detailed multi-omics analysis of a synchronously growing cell culture system. After implementation and benchmarking of the synchronous cell culture, a two-phase extraction method was adopted for the analysis of proteins, lipids, metabolites and starch from a single sample aliquot of as little as 10-15million Chlamydomonas cells. In a proof of concept study, primary metabolites and lipids were sampled throughout the diurnal cell cycle. The results of these time-resolved measurements showed that single compounds were not only coordinated with each other in different pathways, but that these complex metabolic signatures have the potential to be used as biomarkers of various cellular processes. Taken together, the developed workflow, including the synchronized growth of the photoautotrophic cell culture, in combination with comprehensive extraction methods and detailed metabolic phenotyping has the potential for use in in-depth analysis of complex cellular processes, providing essential information for the understanding of complex biological systems.},
  language  = {en}
}
@article{TentschertDraudeJungnickeletal.2013,
  author    = {Tentschert, J. and Draude, F. and Jungnickel, H. and Haase, A. and Mantion, Alexandre and Galla, S. and Thuenemann, Andreas F. and Taubert, Andreas and Luch, A. and Arlinghaus, H. F.},
  title     = {TOF-SIMS analysis of cell membrane changes in functional impaired human macrophages upon nanosilver treatment},
  series = {Surface and interface analysis : an international journal devoted to the development and application of techniques for the analysis surfaces, interfaces and thin films},
  volume    = {45},
  journal   = {Surface and interface analysis : an international journal devoted to the development and application of techniques for the analysis surfaces, interfaces and thin films},
  number    = {1},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {0142-2421},
  doi       = {10.1002/sia.5155},
  pages     = {483 -- 485},
  year      = {2013},
  abstract  = {Silver nanoparticles (SNP) are among the most commercialized nanoparticles. Here, we show that peptide-coated SNP cause functional impairment of human macrophages. A dose-dependent inhibition of phagocytosis is observed after nanoparticle treatment, and pretreatment of cells with N-acetyl cysteine (NAC) can counteract the phagocytosis disturbances caused by SNP. Using the surface-sensitive mode of time-of-flight secondary ion mass spectrometry, in combination with multivariate statistical methods, we studied the composition of cell membranes in human macrophages upon exposure to SNP with and without NAC preconditioning. This method revealed characteristic changes in the lipid pattern of the cellular membrane outer leaflet in those cells challenged by SNP. Statistical analyses resulted in 19 characteristic ions, which can be used to distinguish between NAC pretreated and untreated macrophages. The present study discusses the assignments of surface cell membrane phospholipids for the identified ions and the resulting changes in the phospholipid pattern of treated cells. We conclude that the adverse effects in human macrophages caused by SNP can be partially reversed through NAC administration. Some alterations, however, remained.},
  language  = {en}
}