Geneviève Jourdain : Sa carrière et son oeuvre

Geneviève Jourdain, comment décrire simplement et complètement sa carrière et son œuvre si riches, si larges et si diverses? Chercheur de renom, elle a bâti une œuvre considérable et diverse. Enseignante de talent et de conviction, elle a formé plusieurs générations d'ingénieurs. Femme de communication et d'action, elle a marqué de son empreinte la communauté de recherche en lui apportant sa connaissance du terrain et sa vision prospective de l'évolution de la recherche et de l'enseignement. Guide sûr et bienveillant, elle a été un maître au sens classique. Elle a formé de nombreux élèves, stagiaires, thésards, qu'elle a pris sous son aile et qui lui ont été chers. Elle les a guidés, conseillés, leur a ouvert des portes. Ils sont venus enrichir la famille, selon la belle image du Professeur Blanc-Lapierre, du GRETSI, contribuant ainsi à la vie de l'École française de traitement du signal

Apolipoprotein F is reduced in humans with steatosis and controls plasma triglyceride-rich lipoprotein metabolism

BACKGROUND: NAFLD affects nearly 25% of the global population. Cardiovascular disease (CVD) is the most common cause of death among patients with NAFLD, in line with highly prevalent dyslipidemia in this population. Increased plasma triglyceride (TG)-rich lipoprotein (TRL) concentrations, an important risk factor for CVD, are closely linked with hepatic TG content. Therefore, it is of great interest to identify regulatory mechanisms of hepatic TRL production and remnant uptake in the setting of hepatic steatosis. APPROACH AND RESULTS: To identify liver-regulated pathways linking intrahepatic and plasma TG metabolism, we performed transcriptomic analysis of liver biopsies from two independent cohorts of obese patients. Hepatic encoding apolipoprotein F (APOF) expression showed the fourth-strongest negatively correlation with hepatic steatosis and the strongest negative correlation with plasma TG levels. The effects of adenoviral-mediated human ApoF (hApoF) overexpression on plasma and hepatic TG were assessed in C57BL6/J mice. Surprisingly, hApoF overexpression increased both hepatic very low density lipoprotein (VLDL)-TG secretion and hepatic lipoprotein remnant clearance, associated a ~25% reduction in plasma TG levels. Conversely, reducing endogenous ApoF expression reduced VLDL secretion in vivo, and reduced hepatocyte VLDL uptake by ~15% in vitro. Transcriptomic analysis of APOF-overexpressing mouse livers revealed a gene signature related to enhanced ApoB-lipoprotein clearance, including increased expression of Ldlr and Lrp1, among others. CONCLUSION: These data reveal a previously undescribed role for ApoF in the control of plasma and hepatic lipoprotein metabolism by favoring VLDL-TG secretion and hepatic lipoprotein remnant particle clearance