0307 : QSOX1 has a protective role in the myocardium face to acute stress

IntroductionQSOX1 was identified as a plasma biomarker of acute heart failure (AHF). QSOX1 being a sulfhydryl oxidase, our aim was to decipher the role of QSOX1 in the heart face to an AHF event.MethodsAHF was provoked by IP injections of Isoproterenol (ISO, 300mg/kg/12h) for 2 days in mice (C57Bl/6 J) whereas control (C) received NaCl 9‰. Mice were killed at day 3, after echocardiography. QSOX1 KO (C57Bl/6 J) mice were generated using a QSOX1tm1a embryonic stem cell clone (KOMP). The KO construct contains a promoter-less lacZ gene under the control of the QSOX1 regulatory sequences. The mRNA levels were analyzed by RT-qPCR. The cellular level of oxidative stress was detected by using DHE. Fibrosis was analysed by Sirius red and collagen mRNA.ResultsAt baseline QSOX1-/- adult mice did not display any cardiac or vascular phenotype. After ISO, lacZ expression dramatically increased in QSOX1+/- hearts with the strongest β-galactosidase staining in the atria. In mice receiving ISO, a pulmonary congestion, BNP (x2 p<0.001) and CD68 (x3, p<0.001) increases were observed only in QSOX1-/-, whereas Galectin 3 increased in both groups. After ISO, the severe cardiac dysfunction in QSOX1-/- mice was associated with signs of enhanced oxidative stress (DHE staining p<0.0001). An early fibrosis was observed by Sirius red analysis and associated with an increase of collagen 1 and 3 mRNAs without difference between WT and QSOX1-/- mice.ConclusionWe provided evidence that the absence of QSOX1 leads to a more serious cardiac dysfunction in response to acute cardiac stress by ISO than in WT counterparts. Hence, our data indicated that QSOX1 protects the heart in response to acute stress

Prognostic Value of Iodine-123-Metaiodobenzylguanidine Scintigraphy in Light-Chain Amyloidosis

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