A Mattiazzi

Summary

Affiliation: Universidad Nacional de La Plata
Country: Argentina

Publications

  1. ncbi request reprint The importance of the Thr17 residue of phospholamban as a phosphorylation site under physiological and pathological conditions
    A Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Medicina, La Plata, Argentina
    Braz J Med Biol Res 39:563-72. 2006
  2. ncbi request reprint Ca2+/calmodulin-dependent protein kinase: a key component in the contractile recovery from acidosis
    Alicia Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120 1900 La Plata, Argentina
    Cardiovasc Res 73:648-56. 2007
  3. ncbi request reprint Role of phospholamban phosphorylation on Thr17 in cardiac physiological and pathological conditions
    Alicia Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas Medicina, 60 y 120, 1900, La Plata, Argentina
    Cardiovasc Res 68:366-75. 2005
  4. ncbi request reprint Role of dual-site phospholamban phosphorylation in the stunned heart: insights from phospholamban site-specific mutants
    M Said
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas 60 y 120, 1900 La Plata, Argentina
    Am J Physiol Heart Circ Physiol 285:H1198-205. 2003
  5. ncbi request reprint Phosphorylation of phospholamban in ischemia-reperfusion injury: functional role of Thr17 residue
    A Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, La Plata, Argentina
    Mol Cell Biochem 263:131-6. 2004
  6. pmc Calcium-calmodulin dependent protein kinase II (CaMKII): a main signal responsible for early reperfusion arrhythmias
    M Said
    Centro de Investigaciones Cardiovasculares, CONICET La Plata, Facultad de Ciencias Medicas, UNLP, La Plata, Argentina
    J Mol Cell Cardiol 51:936-44. 2011
  7. pmc Increased intracellular Ca2+ and SR Ca2+ load contribute to arrhythmias after acidosis in rat heart. Role of Ca2+/calmodulin-dependent protein kinase II
    M Said
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, La Plata, Argentina
    Am J Physiol Heart Circ Physiol 295:H1669-83. 2008
  8. ncbi request reprint Time course and mechanisms of phosphorylation of phospholamban residues in ischemia-reperfused rat hearts. Dissociation of phospholamban phosphorylation pathways
    Leticia Vittone
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, La Plata, Argentina
    J Mol Cell Cardiol 34:39-50. 2002
  9. ncbi request reprint Immunodetection of phosphorylation sites gives new insights into the mechanisms underlying phospholamban phosphorylation in the intact heart
    C Mundina-Weilenmann
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina
    J Biol Chem 271:33561-7. 1996
  10. ncbi request reprint Role of phosphorylation of Thr(17) residue of phospholamban in mechanical recovery during hypercapnic acidosis
    Cecilia Mundina-Weilenmann
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, 60 y 120, 1900 La Plata, Argentina
    Cardiovasc Res 66:114-22. 2005

Collaborators

Detail Information

Publications28

  1. ncbi request reprint The importance of the Thr17 residue of phospholamban as a phosphorylation site under physiological and pathological conditions
    A Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Medicina, La Plata, Argentina
    Braz J Med Biol Res 39:563-72. 2006
    ..Thus, phosphorylation of the Thr17 residue of PLN probably participates in a protective mechanism that favors Ca2+ handling and limits intracellular Ca2+ overload in pathological situations...
  2. ncbi request reprint Ca2+/calmodulin-dependent protein kinase: a key component in the contractile recovery from acidosis
    Alicia Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120 1900 La Plata, Argentina
    Cardiovasc Res 73:648-56. 2007
    ..In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery...
  3. ncbi request reprint Role of phospholamban phosphorylation on Thr17 in cardiac physiological and pathological conditions
    Alicia Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas Medicina, 60 y 120, 1900, La Plata, Argentina
    Cardiovasc Res 68:366-75. 2005
    ..In this review, we attempt to highlight the signaling cascade and the physiological relevance of the phosphorylation of this residue in the heart under both physiological and pathological situations...
  4. ncbi request reprint Role of dual-site phospholamban phosphorylation in the stunned heart: insights from phospholamban site-specific mutants
    M Said
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas 60 y 120, 1900 La Plata, Argentina
    Am J Physiol Heart Circ Physiol 285:H1198-205. 2003
    ..These findings indicate that, although both PLB phosphorylation sites are involved in the mechanical recovery after ischemia, Thr17 appears to play a major role...
  5. ncbi request reprint Phosphorylation of phospholamban in ischemia-reperfusion injury: functional role of Thr17 residue
    A Mattiazzi
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, La Plata, Argentina
    Mol Cell Biochem 263:131-6. 2004
    ..This decrease was associated with an impairment of myocardial relaxation. The present study suggests that the phosphorylation of Thr17 of PLB upon reflow, may favor the full recovery of relaxation after ischemia...
  6. pmc Calcium-calmodulin dependent protein kinase II (CaMKII): a main signal responsible for early reperfusion arrhythmias
    M Said
    Centro de Investigaciones Cardiovasculares, CONICET La Plata, Facultad de Ciencias Medicas, UNLP, La Plata, Argentina
    J Mol Cell Cardiol 51:936-44. 2011
    ..Moreover, phosphorylation of PLN-Thr17 and L-type Ca(2+) channels might contribute to reperfusion-induced PBs, by increasing SR Ca(2+) content and Ca(2+) influx...
  7. pmc Increased intracellular Ca2+ and SR Ca2+ load contribute to arrhythmias after acidosis in rat heart. Role of Ca2+/calmodulin-dependent protein kinase II
    M Said
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, La Plata, Argentina
    Am J Physiol Heart Circ Physiol 295:H1669-83. 2008
    ..The results reveal that arrhythmias after acidosis are dependent on CaMKII activation and are associated with an increase in SR Ca(2+) load, which appears to be mainly due to the increase in PT-PLN...
  8. ncbi request reprint Time course and mechanisms of phosphorylation of phospholamban residues in ischemia-reperfused rat hearts. Dissociation of phospholamban phosphorylation pathways
    Leticia Vittone
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, La Plata, Argentina
    J Mol Cell Cardiol 34:39-50. 2002
    ..Phosphorylation of Thr(17)at the onset of reflow may provide the cell a mechanism to cope with Ca(2+)overload, transiently favoring the recovery of relaxation during early reperfusion...
  9. ncbi request reprint Immunodetection of phosphorylation sites gives new insights into the mechanisms underlying phospholamban phosphorylation in the intact heart
    C Mundina-Weilenmann
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina
    J Biol Chem 271:33561-7. 1996
    ..It is suggested that under physiological conditions, this requisite is only filled by cAMP-dependent mechanisms...
  10. ncbi request reprint Role of phosphorylation of Thr(17) residue of phospholamban in mechanical recovery during hypercapnic acidosis
    Cecilia Mundina-Weilenmann
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, 60 y 120, 1900 La Plata, Argentina
    Cardiovasc Res 66:114-22. 2005
    ..To assess the time course of phosphorylation of phospholamban residues, the underlying mechanisms determining these phosphorylations, and their functional impact on the mechanical recovery during acidosis...
  11. pmc Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
    Carlos A Valverde
    Facultad de Cs Médicas, Centro de Investigaciones Cardiovasculares, UNLP, CONICET, La Plata, Argentina
    Cardiovasc Res 85:671-80. 2010
    ..Substantial evidence supports that this dysfunction is triggered by Ca2+ overload during reperfusion. The aim of the present manuscript is to define the origin of this Ca2+ increase in the intact heart...
  12. ncbi request reprint The relative relevance of phosphorylation of the Thr(17) residue of phospholamban is different at different levels of beta-adrenergic stimulation
    Matilde Said
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina
    Pflugers Arch 444:801-9. 2002
    ..phosphorylation at low isoproterenol concentrations might therefore be attributed to a level of PKA activity insufficient to increase [Ca](i) to activate the CaMKII system and/or to inhibit the phosphatase that dephosphorylates PLB..
  13. ncbi request reprint Phospholamban phosphorylation in ischemia-reperfused heart. Effect of pacing during ischemia and response to a beta-adrenergic challenge
    Cecilia Mundina-Weilenmann
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, La Plata, Argentina
    Mol Cell Biochem 252:239-46. 2003
    ..However, the phosphorylation, inotropic and lusitropic response to beta-adrenergic stimulation was significantly decreased both in P and NP hearts...
  14. ncbi request reprint CaMKII inhibition protects against necrosis and apoptosis in irreversible ischemia-reperfusion injury
    Martin Vila-Petroff
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, 60 y 120, 1900 La Plata, Argentina
    Cardiovasc Res 73:689-98. 2007
    ..The goal of the present study is to investigate the role of CaMKII in irreversible ischemia and reperfusion (I/R) injury...
  15. ncbi request reprint Positive inotropic and negative lusitropic effect of angiotensin II: intracellular mechanisms and second messengers
    M A Salas
    Centro de Investigaciones Cardiovasculares, , La Plata, 1900, Argentina
    J Mol Cell Cardiol 33:1957-71. 2001
    ..The results suggest that the antirelaxant effect of angiotensin II might be determined by the decrease in Ca2+ efflux through the Na+/Ca2+ exchanger produced by the angiotensin II-induced prolongation of the action potential duration...
  16. ncbi request reprint beta 2-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
    Leticia Vittone
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900, La Plata, Argentina
    Naunyn Schmiedebergs Arch Pharmacol 373:60-70. 2006
    ..Neither the depression nor the enhancement of the post-ischemic contractile recovery were related with the increase in ROS formation induced by endogenous catecholamines...
  17. pmc Ca(2+)/calmodulin-dependent protein kinase II contributes to intracellular pH recovery from acidosis via Na(+)/H(+) exchanger activation
    Martin Vila-Petroff
    Centro de Investigaciones Cardiovasculares, CCT La Plata CONICET, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120 1900 La Plata, Argentina
    J Mol Cell Cardiol 49:106-12. 2010
    ..They also prove clinically important in multiple disorders which, like ischemia/reperfusion injury or hypertrophy, are associated with increased NHE-1 and CaMKII...
  18. ncbi request reprint Angiotensin II-induced negative inotropy in rat ventricular myocytes: role of reactive oxygen species and p38 MAPK
    Julieta Palomeque
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, La Plata 1900, Argentina
    Am J Physiol Heart Circ Physiol 290:H96-106. 2006
    ..Furthermore, they reveal p38 MAPK as the putative effector of the reduction in myofilament responsiveness to Ca2+ and the decrease in contractility induced by the peptide...
  19. ncbi request reprint Phospholamban phosphorylation by CaMKII under pathophysiological conditions
    Leticia Vittone
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina
    Front Biosci 13:5988-6005. 2008
    ..Phosphorylation of Thr17 residue of PLN and CaMKII activity vary in the different models of HF. The possible role of these changes in the depressed cardiac function of HF will be discussed...
  20. pmc Ca2+/calmodulin kinase II increases ryanodine binding and Ca2+-induced sarcoplasmic reticulum Ca2+ release kinetics during beta-adrenergic stimulation
    Paola Ferrero
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina
    J Mol Cell Cardiol 43:281-91. 2007
    ....
  21. ncbi request reprint Contractile recovery from acidosis in toad ventricle is independent of intracellular pH and relies upon Ca2+ influx
    Margarita A Salas
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina
    J Exp Biol 209:916-26. 2006
    ..The results further indicate that both the reverse mode NCX and the L-type Ca2+ channels, appear to be involved in the increase in intracellular Ca2+ concentration that mediates the contractile recovery from acidosis...
  22. ncbi request reprint Phospholamban phosphorylation sites enhance the recovery of intracellular Ca2+ after perfusion arrest in isolated, perfused mouse heart
    Carlos A Valverde
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, 60 y 120, 1900 La Plata, Argentina
    Cardiovasc Res 70:335-45. 2006
    ..To investigate the importance of the phosphorylation of Ser16 and Thr17 sites of phospholamban (PLN) on intracellular Ca2+ (Cai2+) handling and contractile recovery of the stunned myocardium...
  23. ncbi request reprint Multiple alterations in Ca2+ handling determine the negative staircase in a cellular heart failure model
    Julieta Palomeque
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, La Plata 1900, Argentina
    J Card Fail 13:143-54. 2007
    ..Either decreases in SERCA2a expression, increases in Na(+)/Ca(2+) exchanger (NCX) expression or elevated Na(+)(i) have been independently proposed as mediators of the negative FFR...
  24. doi request reprint Angiotensin II-induced oxidative stress resets the Ca2+ dependence of Ca2+-calmodulin protein kinase II and promotes a death pathway conserved across different species
    Julieta Palomeque
    Centro de Investigaciones Cardiovasculares, Facultad de Medicina, Universidad Nacional de La Plata, Centro Científico Tecnológico CONICET, La Plata, Argentina
    Circ Res 105:1204-12. 2009
    ..Whether these molecules are either interconnected in a single pathway or constitute different and alternative cascades by which Ang II exerts its apoptotic action, is not known...
  25. pmc The signalling pathway of CaMKII-mediated apoptosis and necrosis in the ischemia/reperfusion injury
    Margarita A Salas
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, 60 y 120, 1900 La Plata, Argentina
    J Mol Cell Cardiol 48:1298-306. 2010
    ..The results reveal an apoptotic-necrotic pathway mediated by CaMKII-dependent phosphorylations at the SR, which involves the reverse NCX mode and the mitochondria as trigger and end effectors, respectively, of the cascade...
  26. doi request reprint Na+/K+-ATPase inhibition by ouabain induces CaMKII-dependent apoptosis in adult rat cardiac myocytes
    Luciana Sapia
    Centro de Investigaciones Cardiovasculares, CONICET La Plata, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, La Plata 1900, Argentina
    J Mol Cell Cardiol 49:459-68. 2010
    ..The finding that KN93 prevents ouabain-induced apoptosis without affecting inotropy suggests the potential use of CaMKII inhibitors as an adjunct to digitalis treatment for cardiovascular disease...
  27. pmc Frequency-dependent acceleration of relaxation in mammalian heart: a property not relying on phospholamban and SERCA2a phosphorylation
    Carlos A Valverde
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina
    J Physiol 562:801-13. 2005
    ..More likely, a CaMKII-independent mechanism could be involved, whereby increasing stimulation frequency would disrupt the SERCA2a-PLN interaction, leading to an increase in SR Ca(2+) uptake and myocardial relaxation...
  28. doi request reprint Ca2+-calmodulin-dependent protein kinase phosphorylation of ryanodine receptor may contribute to the beta-adrenergic regulation of myocardial contractility independently of increases in heart rate
    Alicia Mattiazzi
    Circ Res 103:e10-1; author reply e12. 2008