Kaie Ojamaa, PhD

Investigator, The Feinstein Institute for Medical Research

Associate Professor, Molecular Medicine, Hofstra Northwell School of Medicine

Phone: (516) 562-1591
Email: kojamaa@northwell.edu

About the Investigator

Dr. Ojamaa is an associate investigator for the Lab for Molecular Cardiovascular Research at the Feinstein Institute for Medical Research and an associate professor of Molecular Medicine at Hofstra Northwell School of Medicine and Pediaric Cardiology at Steven & Alexandra Cohen Medical Center.

Dr. Ojamaa’s laboratory has been studying cardiac growth regulation, intracellular signaling and gene expression, and has focused recently on the role of innate immunity and inflammatory responses in heart and lung in response to infections and ischemia/hypoxia. This research effort grew from a working collaboration with several investigators at the Feinstein Institute whose expertise in inflammation, endothelial reactivity, autoimmunity, have added immeasurably to the studies centered on the ischemic heart as well as cardiac hypertrophy and failure.

Research Focus

Dr. Ojamaa’s laboratory focuses on understanding the causes of heart disease in both the young and the adult patient with the goal of developing novel therapeutics for these disorders. Specifically, their studies address the role of inflammation and neuro-hormones in the response of the heart to the damaging effects of myocardial ischemia during a heart attack, and why the heart often fails in the long term. In the newborn patient, they aim to understand how increased inflammation may affect neurodevelopment.

Cardiac hypertrophy and heart failure

One in five Americans over age 40 will develop heart failure resulting in a poor quality of life and increased mortality, which comes with an increased cost to society. Pathologic growth of the human heart is a clinical diagnosis defined by an increase in the mass of the heart that is an important risk factor for increased mortality. The lab’s research focuses on potential targets for therapeutics in this complex disease such as anti-oxidants and hormones (thyroid hormones) that are naturally present in the heart and circulation. Their experimental preclinical studies have found that these molecules can reduce oxidative stress within the hypertrophied heart leading to improved function and overall survival.

Acute myocardial infarction

Coronary artery disease is the primary cause of heart disease in the US with more than one million people experiencing a heart attack each year. Although non-invasive intervention such as catheterization or coronary artery bypass graft surgery has saved lives, many survivors go on to develop heart failure and arrhythmias with a diminished quality of life. The lab is studying ways to minimize damage to the heart tissue after an ischemic event by targeting cellular repair and survival mechanisms, thereby improving cardiac tissue remodeling and contractile function. Specifically, targeting the inflammatory responses after cardiac ischemia may improve cardiac function and long term heart health.

Pediatric congenital heart disease

Congenital heart disease affects one in 120 live births. Surgical correction of the heart defect often occurs within the particularly vulnerable newborn period within one month of life. The lab is studying the effects of inflammation and immune mechanisms on the brain and neurocognitive development of these neonates, and specifically, the effects of surgically-induced inflammation on the brain, heart and lung functions. Their studies aim to find ways to lessen the damaging effects of inflammatory molecules and to reduce innate immune activation so that the brain can be protected.

Lab Members

Nyaab Khan
Postdoctoral research trainee
Email: Nkhan5@northwell.edu

Spyros Mavropoulos
Hofstra Northwell School of Medicine MD/PhD student

Lindsey McPhillips, DO
Pediatric Cardiology fellow

Education

McGill University, Canada
Degree: BSc
1975
Field of Study: Biochemistry

McGill University, Canada
Degree: MSc
1979
Field of Study: Biochemistry

Pennsylvania State University, PA
Degree: PhD
1985
Field of Study: Physiology

Awards & Honors

1970-1975 JW McConnell Memorial Scholarship; and Margaret E. Wilson Bursary; and J. Lellepi Scholarship at McGill University
1977-1979 Walter M. Stewart Postgraduate Scholarship at McGill University
1979-1985 Post-graduate Stipend at Pennsylvania State University
1985-1987 NIH Fogarty Fellowship
1994-1998 American Heart Association – NY State Affiliate peer review cmte. member
1997 American Heart Association – Award for Excellence in Cardiovascular Research
1998-2003 Independent Scientist Award, National Heart, Lung and Blood Institute, NIH
1998-2002 NIH Cardiovascular A Study Section regular member
1999-2000 American Heart Association – NE Consortium peer review cmte chairperson
2005 NIH Cardiac Contractility, Hypertrophy & Failure Study Section, Ad Hoc reviewer
2005 NIH MABS (Modeling & Analysis of Biological Systems) study section, Ad Hoc reviewer
2005 Philip Morris External Research Program, Ad Hoc reviewer
2002-2006 AHA-Heritage Research Cmte. Co-chairperson
2006 AHA NE consortium peer review cmte member
2007 AHA Heritage
2008 peer review cmte Chairperson, Clinically Applied Research Applications AHA National peer review cmte member
2010 NIH Cardiac Contractility, Hypertrophy & Heart Failure study section, Ad Hoc reviewer
2011 NIH Cardiovascular Sciences, Ad Hoc reviewer
2011 American Heart Association – Rock Star of Research Recognition Award
2012 Robin & Jack Ross Faculty Mentorship Award
2014 Dvora Horvitz Segal Memorial Research-in-Training Award
2015 Meadowbrook Initiative Grant for Educational Advancement

Publications
  1. “Age influences inflammatory responses, hemodynamics, and cardiac proteasome activation during acute lung injury.” Linge HM, Lee JY, Ochani K, Koga K, Kohn N, Ojamaa K, Powell SR, Miller EJ. Exp Lung Res. 2015 41(4):216-27.
  2. “Low-dose T₃ replacement restores depressed cardiac T₃ levels, preserves coronary microvasculature and attenuates cardiac dysfunction in experimental diabetes mellitus.” Weltman NY, Ojamaa K, Schlenker EH, Chen YF, Zucchi R, Saba A, Colligiani D, Rajagopalan V, Pol CJ, Gerdes AM. Mol Med. 2014; 20:302-12
  3. “Restoration of cardiac tissue thyroid hormone status in experimental hypothyroidism: a dose-response study in female rats.” Weltman NY, Ojamaa K, Savinova OV, Chen YF, Schlenker EH, Zucchi R, Saba A, Colligiani D, Pol CJ, Gerdes AM. Endocrinology. 2013 Jul;154(7):2542-52
  4. “Macrophage migration inhibitory factor antagonizes pressure overload-induced cardiac hypertrophy.” Koga K, Kenessey A, Ojamaa KAm J Physiol Heart Circ Physiol. 2013;304(2):H282-93
  5. Koga K, Kenessey A, Powell SR, Sison CP, Miller EJ, Ojamaa K. “Macrophage migration inhibitory factor provides cardioprotection during ischemia/reperfusion by reducing oxidative stress.” Antioxid Redox Signal. 2011; 14(7):1191-202
  6. Ojamaa K. “Signaling mechanisms in thyroid hormone-induced cardiac hypertrophy.” Vascul Pharmacol. 2010; 52(3-4):113-9.
  7. Takahashi K, Koga K, Linge HM, Zhang Y, Lin X, Metz CN, Al-Abed Y, Ojamaa K, Miller EJ. “Macrophage CD74 contributes to MIF-induced pulmonary inflammation.” Respir Res. 2009;10:33
  8. Dhanantwari P, Nadaraj S, Kenessey A, Chowdhury D, Al-Abed Y, Miller EJ, Ojamaa K. “Macrophage migration inhibitory factor induces cardiomyocyte apoptosis.” Biochem Biophys Res Commun. 2008; 371(2):298-303.
  9. Walsh R, Boyer C, LaCorte J, Parnell V, Sison C, Chowdhury D, Ojamaa K. “N-terminal B-type natriuretic peptide levels in pediatric patients with congestive heart failure undergoing cardiac surgery.” J Thorac Cardiovasc Surg. 2008; 135(1):98-105.
  10. Merchant S, Nadaraj S, Chowdhury D, Parnell VA, Sison C, Miller EJ, Ojamaa K. “Macrophage migration inhibitory factor in pediatric patients undergoing surgery for congenital heart repair.” Mol Med. 2008; 14(3-4):124-30
  11. Madhok AB, Ojamaa K, Haridas V, Parnell VA, Pahwa S, Chowdhury D. “Cytokine response in children undergoing surgery for congenital heart disease.” Pediatr Cardiol. 2006; 27(4):408-13.
  12. Kenessey A, Ojamaa K. “Thyroid hormone stimulates protein synthesis in the cardiomyocyte by activating the Akt-mTOR and p70S6K pathways.” J Biol Chem. 2006; 281(30):20666-72.

View more at PubMed