@article{WernoWilhelmiKuropkaetal.2018,
  author    = {Werno, Martin Witold and Wilhelmi, Ilka and Kuropka, Benno and Ebert, Franziska and Freund, Christian and Sch{\"u}rmann, Annette},
  title     = {The GTPase ARFRP1 affects lipid droplet protein composition and triglyceride release from intracellular storage of intestinal Caco-2 cells},
  series = {Biochemical and biophysical research communications},
  volume    = {506},
  journal   = {Biochemical and biophysical research communications},
  number    = {1},
  publisher = {Elsevier},
  address   = {San Diego},
  issn      = {0006-291X},
  doi       = {10.1016/j.bbrc.2018.10.092},
  pages     = {259 -- 265},
  year      = {2018},
  abstract  = {Intestinal release of dietary triglycerides via chylomicrons is the major contributor to elevated postprandial triglyceride levels. Dietary lipids can be transiently stored in cytosolic lipid droplets (LDs) located in intestinal enterocytes for later release. ADP ribosylation factor-related protein 1 (ARFRP1) participates in processes of LD growth in adipocytes and in lipidation of lipoproteins in liver and intestine. This study aims to explore the impact of ARFRP1 on LD organization and its interplay with chylomicron-mediated triglyceride release in intestinal-like Caco-2 cells. Suppression of Arfrp1 reduced release of intracellularly derived triglycerides (0.69-fold) and increased the abundance of transitional endoplasmic reticulum ATPase TERA/VCP, fatty acid synthase-associated factor 2 (FAF2) and perilipin 2 (Plin2) at the LD surface. Furthermore, TERA/VCP and FAF2 co-occurred more frequently with ATGL at LDs, suggesting a reduced adipocyte triglyceride lipase (ATGL)-mediated lipolysis. Accordingly, inhibition of lipolysis reduced lipid release from intracellular storage pools by the same magnitude as Arfrp1 depletion. Thus, the lack of Arfrp1 increases the abundance of lipolysis-modulating enzymes TERA/VCP, FAF2 and Plin2 at LDs, which might decrease lipolysis and reduce availability of fatty acids for triglyceride synthesis and their release via chylomicrons. (C) 2018 The Authors. Published by Elsevier Inc.},
  language  = {en}
}
@article{RoedelOttenDonatetal.2019,
  author    = {R{\"o}del, Claudia Jasmin and Otten, Cecile and Donat, Stefan and Louren{\c{c}}o, Marta Sofia Rocha and Fischer, Dorothea and Kuropka, Benno and Paolini, Alessio and Freund, Christian and Abdelilah-Seyfried, Salim},
  title     = {Blood Flow Suppresses Vascular Anomalies in a Zebrafish Model of Cerebral Cavernous Malformations},
  series = {Circulation Research},
  volume    = {125},
  journal   = {Circulation Research},
  number    = {10},
  publisher = {Lippincott Williams \& Wilkins},
  address   = {Philadelphia},
  issn      = {0009-7330},
  doi       = {10.1161/CIRCRESAHA.119.315076},
  pages     = {E43 -- E54},
  year      = {2019},
  abstract  = {RATIONALE: Pathological biomechanical signaling induces vascular anomalies including cerebral cavernous malformations (CCM), which are caused by a clonal loss of CCM1/KRIT1 (Krev interaction trapped protein 1), CCM2/MGC4607, or CCM3/PDCD10. Why patients typically experience lesions only in lowly perfused venous capillaries of the cerebrovasculature is completely unknown. OBJECTIVE: In contrast, animal models with a complete loss of CCM proteins lack a functional heart and blood flow and exhibit vascular anomalies within major blood vessels as well. This finding raises the possibility that hemodynamics may play a role in the context of this vascular pathology. METHODS AND RESULTS: Here, we used a genetic approach to restore cardiac function and blood flow in a zebrafish model of CCM1. We find that blood flow prevents cardiovascular anomalies including a hyperplastic expansion within a large Ccm1-deficient vascular bed, the lateral dorsal aorta. CONCLUSIONS: This study identifies blood flow as an important physiological factor that is protective in the cause of this devastating vascular pathology.},
  language  = {en}
}