Deb Laboratory


Stem Cells and Regeneration

Our laboratory is broadly interested in understanding the biology of adult stem cells and specifically how they can be targeted to enhance organ regeneration and repair. We are investigating repair and regeneration in the heart, that represents a terminally differentiated organ and possesses a minimal ability to regenerate itself following injury. We are studying signaling systems in the injured heart that regulate a regenerative response to tissue injury in contrast to a fibrotic one. The specific projects in this regard are as follows:

1)Cardiac progenitors in cardiac repair and regeneration following injury

Heart disease remains a leading cause of mortality and morbidity in the developed world and is an emerging public health problem in the developing world. The heart is unable to efficiently replace myocytes lost secondary to injury or a heart attack and heals itself by fibrosis. Ultimately this non-functioning scar leads to worsening cardiac performance and heart failure. We have identified several members of the Wnt signaling system that appear to regulate vital components of the response to injury of heart tissue. Using mouse models that we possess in our laboratory, we are currently investigating how the Wnt signaling system can be manipulated after cardiac injury to minimize scarring and enhance regeneration.

2)Regulation of the cardiac stem cell niche

Using novel isolation and culture techniques, we have isolated “cardiospheres” from the adult mouse and rat heart. Cardiospheres are spherical clusters of cells, contain a mixture of undifferentiated progenitors and somatic cells and have the ability to differentiate into multiple cell lineages. We are studying this cardiac progenitor niche and determining signaling mechanisms that regulate cardiac progenitor differentiation and self-renewal particularly after acute cardiac injury. 

3)To study the regulation of vascular progenitors in diseased states

Patients with cardiovascular disease have decreased numbers as well impaired function of circulating endothelial progenitors. We have isolated both human and murine endothelial and smooth muscle vascular progenitors from peripheral blood and studying signaling systems that are dysregulated in diseased conditions. Using a combination of transgenic reporter as well as SCID mice, we are investigating how certain signaling patterns can be manipulated to enhance function of vascular progenitors isolated from patients with vascular disease.