Student Recital (May 2, 2014)

Etude No. 62 / Mitchell Peters Nicole Desmarais, timpani Malagueña from Spanish Dances, Op. 21 / Pablo de Sarasate Carla Mason, violin Valse Venezolano No. 2 / Antonio Lauro Michael Cirino, guitar Ballade / Albert Périlhou Nicole Mount, flute Etude No. 8 / Heitor Villa-Lobos Dylan Mowry, guitar Sicilienne and Rigaudon / Fritz Kreisler Tempo di Allegretto and Allegro Megan Polk, violin Cavatine, Op. 144 / Camile Saint-Saëns Cody O’Toole, trombone Concerto No. 1 in A minor / Jean Baptiste Accolaÿ Gail Colombo, violin Das Wohltemperierte Klavier II, BWV 886 / Johann Sebastian Bach Prelude and Fugue in Ab Major Jiaying Zhu, piano Cello Suite No. 1, BWV 1007 / J. S. Bach Prelude Killian Kerrigan, guitar El Colibri / Julio S. Sagreras Brian Picher, guitar Maria Wiegenlied / Max Reger Se Tu M’ami / Giovanni Battista Pergolesi Brooke Speigel, soprano Nocturnal After John Dowland / Benjamin Britten Passacaglia and Theme Jim Davidson, guitar Spring / Ivor Gurney Lied Der Mignon, D. 877, No. 3 / Franz Schubert Mackenzie Leahy, soprano Ma Mère L’oye (Mother Goose Suite) / Maurice Ravel Pavane de la Belle au bois dormant (Lent) Petit Poucet. (Très modéré) Laideronnette, Impératrice des pagodes ( Mouvement de marche) Jiaying Zhu, piano Alexander Heinrich, piano Waltz in Db Major, Op. 64, No. 1 / Frederic Chopin Brenner Campos, piano Three Songs Without Words / Paul Ben-Haim Arioso Ballad Shepardic Melody Colby DeWitt, alto saxophone For You There is No Song / Leslie Adams Deborah / Gene Bone Justine Smigel, sopranohttps://vc.bridgew.edu/student_concerts/1065/thumbnail.jp

Inhibition of myocardial cathepsin-L release during reperfusion following myocardial infarction improves cardiac function and reduces infarct size

Aims: Identifying novel mediators of lethal myocardial reperfusion injury that can be targeted during primary percutaneous coronary intervention (PPCI) is key to limiting the progression of patients with ST-elevated myocardial infarction (STEMI) to heart failure. Here we show through parallel clinical and integrative preclinical studies the significance of the protease cathepsin-L on cardiac function during reperfusion injury. Methods and Results: We found that direct cardiac release of cathepsin-L in STEMI patients (n = 76) immediately post-PPCI leads to elevated serum cathepsin-L levels and that serum levels of cathepsin-L in the first 24 hour post-reperfusion are associated with reduced cardiac contractile function and increased infarct size. Preclinical studies, demonstrate that inhibition of cathepsin-L release following reperfusion injury with CAA0225 reduces infarct size and improves cardiac contractile function by limiting abnormal cardiomyocyte calcium handling and apoptosis. Conclusion: Our findings suggest that cathepsin-L is a novel therapeutic target that could be exploited clinically to counteract the deleterious effects of acute reperfusion injury after an acute STEMI. Translational perspective: New therapeutic targets are urgently required to limit myocardial damage after reperfusion injury. We identified cardiac release of the protease cathepsin-L among patients following primary percutaneous coronary intervention (PPCI). Elevated serum levels of cathepsin-L were associated with reduced contractile function and increased infarct size at 24 hour and 6 months post-PPCI. Work conducted using animal models indicated that cardiac release of cathepsin-L mediated cardiac dysfunction following reperfusion injury. Specific inhibition of cathepsin-L prevented abnormal calcium handling, reduced infarct size and improved contractile function. These novel findings offer the prospect of targeting cathepsin-L-mediated cardiac dysfunction after PPCI