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For More Information Contact:
Tara A. Snethen, CAE, CMP

The ASIP SROPP Award is supported byICPI MARC

ASIP Summer Research Opportunity Program in Pathology (SROPP)

Georges E. Haddad, PhD

Contact Information

Georges E. Haddad, Ph.D.
Associate Professor and Director of Graduate Studies
Dept. Physiology & Biophysics
Howard University
Office: 202-806 6305
Lab: 202-806 9788
Fax: 202-806 6344

Member of the Following FASEB Societies:

The American Physiological Society
American Society for Investigative Pathology

Program Description

Research Project

Dr. Haddad is investigating the molecular and electrical alteration that lead to cardiac hypertrophy and heart failure.

Research Interest and Approach

The Cardiovascular Laboratory in the College of Medicine at Howard University is interested in the studying the regulation of ion channels by extracellular peptides and their intracellular related signaling pathways in relation to the development of volume-overload cardiac hypertrophy and its progression into heart failure. We take multiple approaches to specifically identify the mechanisms by which cascades of intracellular signaling affect the physiological functioning of the organ. These techniques available in the laboratory enable us to research the issues of interest from the animal model to the gene level. In that regard, the following techniques are in practice in the laboratory: Patch-clamp (voltage and current clamp) to study ion channel activities on single freshly isolated or cultured cardiocytes, Fura-II and confocal Imaging to study intracellular calcium homeostasis, tissue contraction and single cellular contraction measurements, western blot and RT-PCR techniques to measure protein activation and relative gene expressions respectively, kinase assays to study kinase activity, apoptotic assays (DNA laddering, BrdU incorporation and flow-cytometry), adenoviral transfection that enables us to modulate the expression of a specific gene of interest. We are particularly interested in the regulation of potassium and calcium channels by mitogen-activated protein kinases and Akt, known to be activated during growth and hypertrophy. There altered function can have a major effect on the channels and therefore the contractile activity of the heart, and on the cellular survival through activation of apoptosis. Such effects can present the scheme leading to heart failure. Studying these pathways may lead to the development of new treatment strategy and new drug therapy. One of the heralding approaches that we are testing in the laboratory is the adenoviral gene therapy to prevent the progression of cardiac hypertrophy into heart failure.
Our studies clearly identify PI 3K and MAPK as key elements in the development of cardiac hypertrophy and directly contribute to the establishment of related cardiac dysfunction. It is our goal now to understand the biological role of these specific downstream signaling in controlling apoptosis and hypertrophy, and delineate the contribution of apoptosis to the ensuing development of heart failure.

Sponsor Selected Related Publications

Reports from Previous Students:

Bezawit Berhaneselassie, 2011
Sylvia Eberhardt, 2010

Summer Research Opportunity Program Criteria:

This Project is Suitable for all Undergraduate Students and Post-Bacs.

Application Requirements:



1. Student Resume or CV.
2. Personal statement is desirable.
3. Copy of student transcript.
4. Recommendation letters from TWO of the student's faculty mentors/advisers at the student's home institution.

Interested students should contact:
Georges E. Haddad, PhD, Office: 202-806 6305; Lab: 202-806 9788; email: