Endothelial cells require functional FLVCR1a during developmental and adult angiogenesis

• DOI: 10.1007/s10456-023-09865-w
• Publication Date: 2023-01-11T17:02:54Z
• Authors: Sara Petrillo; F. De Giorgio; F. Bertino; F. Garello; V. Bitonto; D. L. Longo; S. Mercurio; G. Ammirata; A. L. Allocco; V. Fiorito; D. Chiabrando; F. Altruda; E. Terreno; P. Provero; L. Munaron; T. Genova; A. Nóvoa; A. R. Carlos; S. Cardoso; M. Mallo; M. P. Soares; E. Tolosano
• Keywords: Adult; 0301 basic medicine; Original Paper; Angiogenesis; Endothelial cell; FLVCR1; Tumor endothelial cell; Neovascularization, Pathologic; Endothelial Cells; Neovascularization, Physiologic; 3. Good health; Mice; 03 medical and health sciences; Neoplasms; Animals; Humans; Zebrafish

Abstract The Feline Leukemia Virus Subgroup C Receptor 1a (FLVCR1a) is a transmembrane heme exporter essential for embryonic vascular development. However, the exact role of FLVCR1a during blood vessel development remains largely undefined. Here, we show that highly expressed in angiogenic endothelial cells (ECs) compared to quiescent ECs. Consistently, ECs lacking give rise structurally and functionally abnormal networks multiple models developmental pathologic angiogenesis. Firstly, zebrafish embryos without displayed defective intersegmental vessels formation. Furthermore, endothelial-specific Flvcr1a targeting mice led reduced radial expansion retinal vasculature associated decreased EC proliferation. Moreover, null retinas showed organization loose attachment pericytes. Finally, adult neo-angiogenesis severely affected murine tumor Tumor were disorganized dysfunctional. Collectively, our results demonstrate critical as regulator pathological angiogenesis identifying potential therapeutic target human diseases characterized by aberrant neovascularization.