Research Topics
Genomes and Genes
| Zamaneh KassiriSummaryAffiliation: University of Alberta Country: Canada Publications
| Collaborators
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Detail Information
Publications
Loss of PI3Kγ enhances cAMP-dependent MMP remodeling of the myocardial N-cadherin adhesion complexes and extracellular matrix in response to early biomechanical stressDanny Guo
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Canada
Circ Res 107:1275-89. 2010..Loss of phosphoinositide 3-kinase (PI3K)γ, the isoform linked to G protein-coupled receptor signaling, results in increased myocardial contractility, but the response to pressure overload is controversial...
Loss of TIMP3 selectively exacerbates diabetic nephropathyRatnadeep Basu
Dept of Physiology, Univ of Alberta, Edmonton, Alberta, Canada T6G 2S2
Am J Physiol Renal Physiol 303:F1341-52. 2012..Our data provide definitive evidence for a critical and selective role of TIMP3 in diabetic renal injury consistent with gene expression findings from human diabetic kidneys...- Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart diseaseDong Fan
Department of Physiology, University of Alberta, Edmonton, AB, T6G 2S2, Canada
Fibrogenesis Tissue Repair 5:15. 2012..We will further provide an overview of what we have learned from experimental animal models and genetically modified mice with altered expression of ECM regulatory proteins, MMPs and TIMPs... - Loss of TIMP3 enhances interstitial nephritis and fibrosisZamaneh Kassiri
Department of Physiology, Cardiovascular Research Group, Room 474, Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta, T6G 2S2 Canada
J Am Soc Nephrol 20:1223-35. 2009..Taken together, these results provide evidence that TIMP3 is an important mediator of kidney injury, and regulating its activity may have therapeutic benefit for patients with kidney disease... - Cardioprotective effects mediated by angiotensin II type 1 receptor blockade and enhancing angiotensin 1-7 in experimental heart failure in angiotensin-converting enzyme 2-null miceVaibhav B Patel
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
Hypertension 59:1195-203. 2012.... - Enhanced susceptibility to biomechanical stress in ACE2 null mice is prevented by loss of the p47(phox) NADPH oxidase subunitSreedhar Bodiga
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada T6G 2S2
Cardiovasc Res 91:151-61. 2011..Loss of ACE2 enhances the susceptibility to heart disease but the mechanism remains elusive. We hypothesized that ACE2 deficiency activates the NADPH oxidase system in pressure overload-induced heart failure... - Early activation of matrix metalloproteinases underlies the exacerbated systolic and diastolic dysfunction in mice lacking TIMP3 following myocardial infarctionVijay Kandalam
Department of Physiology, University of Alberta, Edmonton, Alberta
Am J Physiol Heart Circ Physiol 299:H1012-23. 2010..Hence, timing of treatments to improve cardiac response to MI may be critical in producing favorable outcome... - Prevention of angiotensin II-mediated renal oxidative stress, inflammation, and fibrosis by angiotensin-converting enzyme 2Jiuchang Zhong
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
Hypertension 57:314-22. 2011..ACE2 is an important negative regulator of Ang II-induced renal disease and enhancing ACE2 action may have therapeutic potential for patients with kidney disease... - Angiotensin-converting enzyme 2 suppresses pathological hypertrophy, myocardial fibrosis, and cardiac dysfunctionJiuchang Zhong
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada
Circulation 122:717-28, 18 p following 728. 2010..We hypothesized that ACE2 is a negative regulator of angiotensin II (Ang II)-mediated signaling and its adverse effects on the cardiovascular system... - Loss of angiotensin-converting enzyme-2 exacerbates diabetic cardiovascular complications and leads to systolic and vascular dysfunction: a critical role of the angiotensin II/AT1 receptor axisVaibhav B Patel
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Alberta, Edmonton, Canada
Circ Res 110:1322-35. 2012..Angiotensin-converting enzyme-2 (ACE2) is a negative regulator of the renin-angiotensin system. We hypothesize that loss of ACE2 exacerbates cardiovascular complications induced by diabetes... - TIMP2 deficiency accelerates adverse post-myocardial infarction remodeling because of enhanced MT1-MMP activity despite lack of MMP2 activationVijay Kandalam
Department of Physiology, Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta, Canada
Circ Res 106:796-808. 2010..Hence, it is difficult to predict the function of TIMP2 as protective (MMP-inhibiting) or harmful (MMP-activating) in heart disease... - Tumor necrosis factor induces matrix metalloproteinases in cardiomyocytes and cardiofibroblasts differentially via superoxide production in a PI3Kgamma-dependent mannerAhmed E Awad
Dept of Physiology, Univ of Alberta, 474 HMRC, Edmonton, AB T6G 2S2, Canada
Am J Physiol Cell Physiol 298:C679-92. 2010.... - Type 1 diabetic cardiomyopathy in the Akita (Ins2WT/C96Y) mouse model is characterized by lipotoxicity and diastolic dysfunction with preserved systolic functionRatnadeep Basu
Department of Physiology, Rm 474, Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
Am J Physiol Heart Circ Physiol 297:H2096-108. 2009..We conclude that early type 1 diabetic cardiomyopathy is characterized by diastolic dysfunction associated with lipotoxic cardiomyopathy with preserved systolic function in the absence of interstitial fibrosis and hypertrophy... - Lack of tissue inhibitor of metalloproteinases 2 leads to exacerbated left ventricular dysfunction and adverse extracellular matrix remodeling in response to biomechanical stressVijay Kandalam
Assistant Professor, Department of Physiology, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, Canada
Circulation 124:2094-105. 2011..Tissue inhibitor of metalloproteinases 2 is unique among TIMPs in activating pro-MMP2 in addition to inhibiting a number of MMPs. Given this dual role of TIMP2, we investigated whether TIMP2 serves a critical role in heart disease... - Human recombinant ACE2 reduces the progression of diabetic nephropathyGavin Y Oudit
Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
Diabetes 59:529-38. 2010..Inhibition of ACE2 function accelerates diabetic kidney injury, whereas renal ACE2 is downregulated in diabetic nephropathy. We examined the ability of human recombinant ACE2 (hrACE2) to slow the progression of diabetic kidney injury... - Agonist-induced hypertrophy and diastolic dysfunction are associated with selective reduction in glucose oxidation: a metabolic contribution to heart failure with normal ejection fractionJun Mori
Department of Pediatrics and Pharmacology, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, Canada
Circ Heart Fail 5:493-503. 2012.... - Loss of angiotensin-converting enzyme 2 accelerates maladaptive left ventricular remodeling in response to myocardial infarctionZamaneh Kassiri
Department of Physiology, University of Alberta, Edmonton, Canada
Circ Heart Fail 2:446-55. 2009..We hypothesized that ACE2 deficiency may compromise the cardiac response to myocardial infarction (MI)... - MMP-2 mediates angiotensin II-induced hypertension under the transcriptional control of MMP-7 and TACEJeffrey Odenbach
Department of Biochemistry, School of Molecular and Systems Medicine, University of Alberta, Edmonton, Alberta, Canada
Hypertension 57:123-30. 2011..This suggests a functional specialization of MMP-2 in agonist-induced cardiovascular disease development that has potential implications for the design of metalloproteinase-based therapeutic strategies... - Matrix metalloproteinase-7 and ADAM-12 (a disintegrin and metalloproteinase-12) define a signaling axis in agonist-induced hypertension and cardiac hypertrophyXiang Wang
Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada
Circulation 119:2480-9. 2009..Here, we report that matrix metalloproteinase-7 (MMP-7) and a disintegrin and metalloproteinase-12 (ADAM-12) form a novel signaling axis in these processes... - Tissue inhibitor of metalloproteinases (TIMPs) in heart failureLinn Moore
Department of Physiology, Cardiovascular Research Centre, Mazankowski Alberta Heart Institute, University of Alberta, Heritage Medical Research Centre, Edmonton, AB, Canada
Heart Fail Rev 17:693-706. 2012..We will further discuss how ECM molecules and regulatory genes can be used as biomarkers of disease in heart failure patients... - Titin is a target of matrix metalloproteinase-2: implications in myocardial ischemia/reperfusion injuryMohammad A M Ali
Department of Pharmacology, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
Circulation 122:2039-47. 2010..Here we determine whether titin is an intracellular substrate for MMP-2 and if its degradation during ischemia/reperfusion contributes to cardiac contractile dysfunction... - Uncoupling between enhanced excitation-contraction coupling and the response to heart disease: lessons from the PI3Kγ knockout murine modelDanny Guo
Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Canada
J Mol Cell Cardiol 50:606-12. 2011.... - Tumor necrosis factor-alpha-converting enzyme is a key regulator of agonist-induced cardiac hypertrophy and fibrosisXiang Wang
Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada
Hypertension 54:575-82. 2009..Targeting TACE has potential therapeutic importance for modulating agonist-induced cardiac remodeling... - Antenatal sildenafil treatment attenuates pulmonary hypertension in experimental congenital diaphragmatic herniaChristina Luong
Department of Pediatrics, Women and Children Health Research Institute, Cardiovascular Research Group, University of Alberta, Edmonton, Canada
Circulation 123:2120-31. 2011..Because of the limited success in postnatal management of CDH, we hypothesized that antenatal PDE5 inhibition would attenuate pulmonary artery remodeling in experimental nitrofen-induced CDH... 
Reduction of I(to) causes hypertrophy in neonatal rat ventricular myocytesZamaneh Kassiri
Department of Physiology, Heart and Stroke/Richard Lewar Center, University of Toronto, Toronto, Canada
Circ Res 90:578-85. 2002..2)N infection were prevented by blocking Ca2+ entry and excitability with verapamil or high [K+]o. Our studies suggest that reductions of K(v4.2/3)-based I(to) play a role in hypertrophy signaling by activation of calcineurin...- Role of PI3 kinase gamma in excitation-contraction coupling and heart diseaseGavin Y Oudit
Department of Medicine, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada
Cardiovasc Hematol Disord Drug Targets 7:295-304. 2007..In this review article, we discuss the key role of PI3Kgamma gamma in regulating cAMP, Ca(2+) cycling, beta-adrenergic signaling and myocardial structure and function in heart disease...