A5091240818- Angiogenesis and VEGF in Cancer
- Barrier Structure and Function Studies
- PI3K/AKT/mTOR signaling in cancer
- Cell Adhesion Molecules Research
- Vascular Malformations and Hemangiomas
- Vascular Tumors and Angiosarcomas
- Kruppel-like factors research
- Cellular Mechanics and Interactions
- Axon Guidance and Neuronal Signaling
- Islanding Detection in Power Systems
- Vascular Anomalies and Treatments
- Neurological Disease Mechanisms and Treatments
- Renal Diseases and Glomerulopathies
- Hippo pathway signaling and YAP/TAZ
- Vascular Malformations Diagnosis and Treatment
Goethe University Frankfurt
2024
Josep Carreras Leukaemia Research Institute
2021-2023
Institut d'Investigació Biomédica de Bellvitge
2018-2020
Instituto de Salud Carlos III
2019
Angiogenesis is a dynamic process relying on endothelial cell rearrangements within vascular tubes, yet the underlying mechanisms and functional relevance are poorly understood. Here we show that PI3Kα regulates using combination of PI3Kα-selective inhibitor endothelial-specific genetic deletion to abrogate activity during vessel development. Quantitative phosphoproteomics together with detailed biology analyses in vivo vitro reveal PI3K signalling prevents NUAK1-dependent phosphorylation...
Pericytes regulate vessel stabilization and function, their loss is associated with diseases such as diabetic retinopathy or cancer. Despite physiological importance, pericyte function molecular regulation during angiogenesis remain poorly understood.To decipher the transcriptomic programs of pericytes angiogenesis, we crossed Pdgfrb(BAC)-CreERT2 mice into RiboTagflox/flox mice. Pericyte morphological changes were assessed in mural cell-specific R26-mTmG reporter mice, which low doses...
Phosphoinositide 3-kinases (PI3Ks) phosphorylate intracellular inositol lipids to regulate signaling and vesicular trafficking. Mammals have eight PI3K isoforms, of which class I PI3Kα II PI3K-C2α are essential for vascular development. The PI3K-C2β is also abundant in endothelial cells. Using vivo vitro approaches, we found that was a critical regulator blood vessel growth by restricting mTORC1 signaling. Mice expressing kinase-inactive form displayed enlarged vessels without corresponding...
ABSTRACT Low-flow vascular malformations are congenital overgrowths composed by abnormal blood vessels potentially causing pain, bleeding, and obstruction of different organs. These diseases caused oncogenic mutations in the endothelium which result overactivation PI3K/AKT pathway. Lack robust vivo preclinical data has prevented development translation into clinical trials specific molecular therapies for these diseases. Here, we describe a new reproducible model PI3K-driven using postnatal...
Abstract Veins have emerged as the origin of all other endothelial cell subtypes needed to expand vascular networks during developmental and pathological neoangiogenesis. Here, we uncover significant role angioneurin Fibronectin Leucine Rich Transmembrane protein (FLRT) 2 in central nervous system (CNS) development mouse. Early postnatal FLRT2 deletion reveals specific defects retinal veins, impacting proliferation, sprouting polarity that result reduced tip cells at front. interacts with...
Abstract Veins have emerged as the origin of all other endothelial cell subtypes needed to expand vascular networks during developmental and pathological neoangiogenesis. Here, we uncover role angioneurin Fibronectin Leucine Rich Transmembrane protein (FLRT) 2 in central nervous system (CNS) development mouse. Early postnatal FLRT2 deletion reveals specific defects retinal veins, impacting proliferation, sprouting polarity that result reduced tip cells at front. interacts with VE-cadherin...