Carlson Lab

                                                       Professor                Post Docs               Fellows          

Deborah L. Carlson, PhD

Assistant Professor of Pediatrics

Office:  (214) 648-6873

Fax :  (214) 648-0432

Building: F3 Room 324

Email:  Deborah.Carlson@UTSouthwestern.edu

Each year in the United States there are approximately 2.5 million burn injures requiring medical intervention.  These injuries are not limited to adults, but also result in a significant morbidity and mortality in children. Thermal injury remains among the top 5 causes of serious injury in children.  While death and morbidity result from thermal injury itself, thermal injury is then very often complicated by superimposed infection.

Numerous studies, including those from our laboratory, have documented in both humans and in rodent models that burn patients experience marked cardiac dysfunction.    Both burn injury and burn complicated by sepsis (burn/sepsis) have been shown to severely compromise left ventricular function (LV).

 We have demonstrated that LV is associated with apoptosis.  Apoptosis, or programmed cell death, is the result of a complex cascade of cellular events culminating in chromatin condensation, DNA fragmentation, mitochondrial and ribosomal aggregation, cytoplasmice membrane blebbing, and cell shrinkage.  The regulation of apoptosis is complex, evolutionarily conserved, and culminates in the activation of a family of cysteine proteases termed caspases. While we were able to confirm apoptotic cells in the hearts of burned animals, we observed that there was a very mild degree of myocyte apoptosis, and concluded that the amount of apoptotic myocytes was not commensurate with the amount of LV dysfunction observed.  Despite the low level of apoptosis, we did demonstrate that broad spectrum pharmacologic blockage of caspases significantly blunted LV dysfunction associated with either burn or sepsis.  Our laboratory is now investigating the hypothesis that the LV dysfunction associated with burn and sepsis is a consequence of caspase activation, independent of the effects of caspases on apoptosis.  The proposed mechanisms of possible caspase involvement with LV function include effects on cardiac myofilaments, influence on matrix metalloproteinase activity and regulation of the inflammatory cascade.

Awards and Honors

Research Citation Finalist, 2007.  Society for Critical Care Medicine 36th Annual Congress.

Most Outstanding Presentation Award, 2005.  Shock Society 28th Annual Conference.

Outstanding Young Investigator Award, 2001.  James Carrico Research Forum, The University of Texas Southwestern Medical Center at Dallas.

Member since 2005 of the International Shock Society Presidential Committee for Publications.

Selected References

Carlson DL, Horton JW.  2006.  Cardiac Molecular Signaling after Burn Trauma.  J. Burn Care Research, Sept. - Oct.; 27(5):669-75.

Carlson D., Maas DL., White DJ., Tan J., Horton JW.  2006.  Antioxidant vitamin therapy alters sepsis-related apoptotic myocardial activity and inflammatory responses.  Am J Physiol Heart Circ Physiol. Dec;291(6):H2779-H2789.

Carlson DL, Willis MS, White DJ, Horton JW, Giroir BP. 2005. TNF-alpha Induced Caspase Activation Mediates Endotoxin Related Cardiac Dysfunction. Critical Care Medicine, 33(5): 1021-8.

Willis MS, Carlson DL, DiMiao JM, White MD, White DJ, Horton JW, Giroir BP. 2005. Macrophage Migration Inhibitory Factor (MIF) is a Burn Trauma Induced Cardiac Depressant.  AJP Heart and Circ., 288(2):H795-804.

Ballard-Croft C, Carlson DL, Maass DL, Horton JW.  2004.  Burn Trauma Alters Calcium Transporter Protein Expression in the Heart.  Journal of Applied Physiology, 97(4): 1470-1476.