Diego F. Alvarez, M.D., Ph.D.

 

 

M.D.: Universidad Libre de Colombia, Cali, Colombia
Ph.D.: University of South Alabama
Post-doctoral: University of South Alabama
Current Position: Associate Professor
Phone: (251) 460-6392
Email: dalvarez@southalabama.edu

 

 

Research Interests

Stem cells constitute an important source for the treatment of a panoply of diseases and a variety of other clinical conditions. A main focus of interest is how stem cells can be differentiated (committed) into particular lineages such that the derived progeny can accomplish specific functions. Stem cells with a range of potentials for the generation of specific, mature-differentiated adult cells have been isolated from the inner cell mass of embryos, placenta, amniotic fluid, cord blood and even from adult tissues themselves. Importantly, stem cells that resemble those isolated from embryos can now be generated from mature-differentiated adult cells by introducing into the cells a cocktail of limited transcription factors (2 to 4). I am interested in understanding the regulatory mechanisms that dictate the plasticity, or the ability, of the aforementioned stem cells to generate differentiated progeny in a directed and controlled manner. In addition, we seek to understand the molecular mechanisms that dictate the progenitor capacity of these cells and in such the role of Nucleosome Assembly Protein 1 (NAP1) is examined. Specifically the generation of endothelial progenitor cells, precursors of endothelial cells, is an ultimate goal in my Lab as those cells can be utilized as a cell based therapy to restore disrupted endothelial barriers.

Acute Lung Injury (ALI) or its more severe form the Acute Respiratory Distress Syndrome (ARDS) is a leading cause of mortality in critical care units throughout the world. Endothelial barrier disruption is a hallmark of ALI. Mortality occurs in approximately 40% of the patients and typically occurs 10 to 30 days following the onset of injury. Moreover, surviving patients may experience limited respiratory function up to one year after being released from the hospital. While the pathophysiology of ALI during this late stage of the syndrome (e.g. 10 to 30 days following onset) has germane seminal contributions leading to the development of pharmacological targets, none of them have resulted in definitive reduction of the associated morbidity-mortality. Thus, a second major focus of interest is to examine the capacity of endothelial progenitor cells (both native and exogenous) to repair the endothelial barrier and its ability to improve the outcome in an in vivo model by inflicting lung injury in rodents with Pseudomonas aeruginosa. A translational aim is also considered where the number and function of endothelial progenitor cells in patients with ALI is studied.

Chronic lung diseases such as emphysema constitute the fourth leading cause of mortality among all causes of deaths in the US. While cigarette smoking is the major cause of emphysema, strategies directed to modify smoking behavior among the population have been successful.  Similar to ALI, there are no current therapeutic interventions directed to restore the lost parenchyma seen during emphysema. Considering that blood supply is necessary for tissue maintenance and repair, it is plausible that a mechanism of emphysema occurs after lack of repair or injured endothelial barriers, leading to blood vessel loss and lung parenchymal destruction.  Therefore, we seek to study the ability of endogenous and exogenous endothelial progenitor cells to maintain the endothelial barrier and the parenchymal structure by using in vitro and in vivo models of smoking.

 

Representative Publications

 

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