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Your search keyword '"Solinhac, Romain"' showing total 15 results
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15 results on '"Solinhac, Romain"'

4. Mutation of Arginine 264 on ERα (Estrogen Receptor Alpha) Selectively Abrogates the Rapid Signaling of Estradiol in the Endothelium Without Altering Fertility

Author

Adlanmerini, Marine, Fébrissy, Chanaelle, Zahreddine, Rana, Vessières, Emilie, Buscato, Mélissa, Solinhac, Romain, Favre, Julie, Anquetil, Typhaine, Guihot, Anne-Laure, Boudou, Frederic, Raymond-Letron, Isabelle, Chambon, Pierre, Gourdy, Pierre, Ohlsson, Claes, Laurell, Henrik, Fontaine, Coralie, Metivier, Raphaël, Le Romancer, Muriel, Henrion, Daniel, Arnal, Jean-Francois, and Lenfant, Francoise

Published
2020
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11. Additional file 2 of Integrative mapping analysis of chicken microchromosome 16 organization

Author

Solinhac, Romain, Leroux, Sophie, Galkina, Svetlana, Chazara, Olympe, Feve, Katia, Vignoles, Florence, Morisson, Mireille, Derjusheva, Svetlana, Bed'hom, Bertrand, Vignal, Alain, Fillon, Valérie, and Pitel, Frédérique

Abstract

Additional File 2:454 contigs distribution on the chicken sequence assembly. The 454 contigs ( http://genome.wustl.edu/genomes/view/gallus_gallus/ ) were aligned to the available chicken sequence assembly (galGal 3, http://genome.ucsc.edu/index.html ). The 7 matching contigs are represented along the GGA16 sequence. File format: PowerPoint (PPT 42 KB)

Published
2021
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13. Smooth muscle cells-derived CXCL10 prevents endothelial healing through PI3Kγ-dependent T cells response

Author

Lupieri, Adrien, primary, Smirnova, Natalia F, additional, Solinhac, Romain, additional, Malet, Nicole, additional, Benamar, Mehdi, additional, Saoudi, Abdel, additional, Santos-Zas, Icia, additional, Zeboudj, Lynda, additional, Ait-Oufella, Hafid, additional, Hirsch, Emilio, additional, Ohayon, Paul, additional, Lhermusier, Thibault, additional, Carrié, Didier, additional, Arnal, Jean-François, additional, Ramel, Damien, additional, Gayral, Stephanie, additional, and Laffargue, Muriel, additional

Published
2019
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14. Smooth muscle cells-derived CXCL10 prevents endothelial healing through PI3Kγ-dependent T cells response.

Author

Lupieri, Adrien, Smirnova, Natalia F, Solinhac, Romain, Malet, Nicole, Benamar, Mehdi, Saoudi, Abdel, Santos-Zas, Icia, Zeboudj, Lynda, Ait-Oufella, Hafid, Hirsch, Emilio, Ohayon, Paul, Lhermusier, Thibault, Carrié, Didier, Arnal, Jean-François, Ramel, Damien, Gayral, Stephanie, and Laffargue, Muriel

Subjects
SMOOTH muscle, T cells, HEALING, MUSCLE cells, SECRETION, FRACTURE healing, DELETION mutation
Abstract

Aims Defects in efficient endothelial healing have been associated with complication of atherosclerosis such as post-angioplasty neoatherosclerosis and plaque erosion leading to thrombus formation. However, current preventive strategies do not consider re-endothelialization in their design. Here, we investigate mechanisms linking immune processes and defect in re-endothelialization. We especially evaluate if targeting phosphoinositide 3-kinase γ immune processes could restore endothelial healing and identify immune mediators responsible for these defects. Methods and results Using in vivo model of endovascular injury, we showed that both ubiquitous genetic inactivation of PI3Kγ and hematopoietic cell-specific PI3Kγ deletion improved re-endothelialization and that CD4+ T-cell population drives this effect. Accordingly, absence of PI3Kγ activity correlates with a decrease in local IFNγ secretion and its downstream interferon-inducible chemokine CXCL10. CXCL10 neutralization promoted re-endothelialization in vivo as the same level than those observed in absence of PI3Kγ suggesting a role of CXCL10 in re-endothelialization defect. Using a new established ex vivo model of carotid re-endothelialization, we showed that blocking CXCL10 restore the IFNγ-induced inhibition of endothelial healing and identify smooth muscle cells as the source of CXCL10 secretion in response to Th1 cytokine. Conclusion Altogether, these findings expose an unforeseen cellular cross-talk within the arterial wall whereby a PI3Kγ-dependent T-cell response leads to CXCL10 production by smooth muscle cells which in turn inhibits endothelial healing. Therefore, both PI3Kγ and the IFNγ/CXCL10 axis provide novel strategies to promote endothelial healing. [ABSTRACT FROM AUTHOR]

Published
2020
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