PT  - JOURNAL ARTICLE
AU  - Fransky Hantelys
AU  - Anne-Claire Godet
AU  - Florian David
AU  - Florence Tatin
AU  - Edith Renaud-Gabardos
AU  - Françoise Pujol
AU  - Leila Diallo
AU  - Isabelle Ader
AU  - Laetitia Ligat
AU  - Anthony K. Henras
AU  - Yasufumi Sato
AU  - Angelo Parini
AU  - Eric Lacazette
AU  - Barbara Garmy-Susini
AU  - Anne-Catherine Prats
TI  - Vasohibin1, a new IRES trans-acting factor for induction of (lymph)angiogenic factors in early hypoxia
AID  - 10.1101/260364
DP  - 2019 Jan 01
TA  - bioRxiv
PG  - 260364
4099  - http://biorxiv.org/content/early/2019/07/11/260364.short
4100  - http://biorxiv.org/content/early/2019/07/11/260364.full
AB  - Hypoxia, a major inducer of angiogenesis, is known to trigger major changes of gene expression at the transcriptional level. Furthermore, global protein synthesis is blocked while internal ribosome entry sites (IRES) allow specific mRNAs to be translated. Here we report the transcriptome and translatome signatures of (lymph)angiogenic genes in hypoxic HL-1 cardiomyocytes: most genes are not induced at the transcriptome-, but at the translatome level, including all IRES-containing mRNAs. Our data reveal activation of (lymph)angiogenic mRNA IRESs in early hypoxia. We identify vasohibin1 (VASH1) as an IRES trans-acting factor (ITAF) able to activate FGF1 and VEGFD IRESs in hypoxia while it inhibits several IRESs in normoxia. Thus this new ITAF may have opposite effects on IRES activities. These data suggest a generalized process of IRES-dependent translational induction of (lymph)angiogenic growth factors expression in early hypoxia, whose pathophysiological relevance is to trigger formation of new functional vessels in ischemic heart. VASH1 is not always required, indicating that the IRESome composition is variable, thus allowing subgroups of IRESs to be activated under the control of different ITAFs.