@article{539af933b3014d3b95368f520c6d300d,
title = "Vasohibin1, a new mouse cardiomyocyte ires trans-acting factor that regulates translation in early hypoxia",
abstract = "Hypoxia, a major inducer of angiogenesis, triggers 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 mouse cardiomyocytes: most genes are induced at the translatome level, including all IRES-containing mRNAs. Our data reveal activation of (lymph)angiogenic factor mRNA IRESs in early hypoxia. We identify vasohibin1 (VASH1) as an IRES trans-acting factor (ITAF) able to bind RNA and to activate the FGF1 IRES in hypoxia while it tends to inhibit several IRESs in normoxia. VASH1 depletion has also a wide impact on the translatome of (lymph)angiogenesis genes, suggesting that this protein can regulate translation positively or negatively in early hypoxia. Translational control thus appears as a pivotal process to trigger new vessel formation in ischemic heart.",
keywords = "Cardiomyocyte, Hypoxia, IRES, Translational control, Vasohibin",
author = "Fransky Hantelys and Godet, {Anne Claire} and Florian David and Florence Tatin and Edith Renaud-Gabardos and Fran{\c c}oise Pujol and Leila Diallo and Isabelle Ader and Laetitia Ligat and Henras, {Anthony K.} and Yasufumi Sato and Angelo Parini and Eric Lacazette and Barbara Garmy-Susini and Prats, {Anne Catherine}",
note = "Funding Information: Our thanks go to J.J. Maoret and F. Martins from the Inserm UMR1048 GeT-TQ plateau of the GeT plateform Genotoul (Toulouse), F. Lopez and L. Tonini from the proteomic platform genotoul (Toulouse), J. Iacovoni from the Inserm UMR 1048 bioinformatics plateau, as well as L. van den Berghe and C. Segura from the Inserm UMR1037 vectorology plateau (Toulouse) and A. Lucas from the We-Met Functional Biochemistry Facility (Toulouse). We also thank V. Poinsot for helpful discussion and W. Claycomb for providing HL-1 cells. This work was supported by R{\'e}gion Midi-Pyr{\'e}n{\'e}es, Association Fran{\c c}aise contre les Myopathies (AFM-T{\'e}l{\'e}thon), Association pour la Recherche sur le Cancer (ARC), European funding (REFBIO), Fondation Toulouse Cancer Sant{\'e} and Agence Nationale de la Recherche ANR-18-CE11-0020-RIBOCARD. F.H. had fellowships from the R{\'e}gion Midi-Pyr{\'e}n{\'e}es and from the Ligue Nationale Contre le Cancer (LNCC). E.R.G. had a fellowship from AFM-Telethon. A.C. Godet had a fellowship from LNCC. Funding Information: This work was supported by R{\'e}gion Midi-Pyr{\'e}n{\'e}es, Association Fran{\c c}aise contre les Myopathies (AFM-T{\'e}l{\'e}thon), Association pour la Recherche sur le Cancer (ARC), European funding (REFBIO), Fondation Toulouse Cancer Sant{\'e} and Agence Nationale de la Recherche ANR-18-CE11-0020-RIBOCARD. F.H. had fellowships from the R{\'e}gion Midi-Pyr{\'e}n{\'e}es and from the Ligue Nationale Contre le Cancer (LNCC). E.R.G. had a fellowship from AFM-Telethon. A.C. Godet had a fellowship from LNCC. Publisher Copyright: {\textcopyright} 2019, eLife Sciences Publications Ltd. All rights reserved.",
year = "2019",
month = dec,
doi = "10.7554/eLife.50094",
language = "English",
volume = "8",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications",
}