Back to Main

Faculty Detail    
Campus Address LHRB 431B Zip 0007
Phone  205-996-2184
Other websites

Undergraduate  University of Florida    1988  BS, Microbiology and Cell Science 
Undergraduate  Unviersity of Florida    1990  BS, Chemistry 
Graduate  University of Florida    2001  PhD, Anatomy and Cell Biology 

Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Medicine  Med - Nephrology Assistant Professor
Center  Biomedical Engineering  Biomatrix Eng Regen Med (BERM) Ctr Assistant Professor
Center  General Clinical Research Center  Nephrology Research & Training Center Assistant Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 

Biographical Sketch 
Dr. Curtis received her formal education at the University of Florida (UF). Between her undergraduate and graduate studies, she worked as a Biological Scientist in the laboratories of Dr. Kyle Rarey at UF where she conducted research on the physiology of non-sensory tissues of the inner ear.

Following receipt of her doctoral degree, Dr. Curtis held a postdoctoral training position with Dr. Edward Scott at UF, studying the role of selectins on retinal neovascularization. Upon moving to Birmingham, Dr. Curtis began a second postdoctoral position in the laboratory of Dr. Chris Klug at UAB, where she studied bone marrow stem cells in renal repair. A final postdoctoral training position was in the laboratories of Dr. Paul W. Sanders in Nephrology, where she continued her study of renal repair in acute kidney injury with a focus on renal-derived sources of repair.

During her postdoctoral training, Dr. Curtis was funded by two Institutional T32 training grants and was fortunate to receive a Frederick Gardner Cottrell Postdoctoral Enhancement Award from UAB, an award that was established to foster the training and advancement of individuals interested in academic research. Dr. Curtis is currently an Assistant Professor of Medicine where she is continuing her efforts to identify the source of reparative cells in acute kidney injury and the role of a stress enzyme, heme oxygenase-1 in acute kidney injury, particularly in the setting of aging in females.

Society Memberships
Organization Name Position Held Org Link
American Heart Association  member   
American Physiological Society  member   
American Society of Cell Biology  member 
American Society of Nephrology  member 
Association for Women in Science  member 
National Kidney Foundation  member 
National Postdoctoral Association  current member; past member of Board of Directors 
The Gerontological Society of America  member   
Women in Nephrology  member of Exective Council 

Research/Clinical Interest
Aging and gender in acute kidney injury
The ability of the kidney to repair itself in response to acute kidney injury (AKI) or after transplantation has long been appreciated however the source of cells that contribute to this process and the signaling mechanisms that are involved have not been clearly defined. My laboratory has two lines of investigation to better understand the epithelial biology of AKI: (1) to understand which cells may contribute to the cellular reconstitution of the nephron and (2) how aging and gender influence the protective actions of a stress enzyme, heme oxygenase-1 (HO-1). Cellular repair in the kidney has been suggested to occur by adult epithelia that de-differentiate, divide and then re-differentiate, or by renal stem cell-derived cellular repair. Data in the literature support both of these mechanisms of cellular repair and it is possible that that they each contribute to repair with the predominant mechanism dependent on the degree or type of injury. We developed a novel methodology for the study of cellular repair in a model of AKI that does not bias toward either mode of repair. Using this model system, we have demonstrated that reparative cells may derive from all gross regions of the kidney which may suggest more than one type of reparative cell or more than one niche of a single reparative cell population. In this focus, our current research efforts are directed toward examining the following questions: (1) what is the identity of the reparative cells?; (2) where is the niche from which these reparative cells derive?; (3) what signaling induces the migration and epithelial incorporation of these renal reparative cells?. In a second line of investigation, we are interested to know how HO-1 effects in AKI are modulated with age and with gender. Clinically and in animal models, females show greater resistance to AKI, and age is an independent predictor of worse outcomes in AKI. HO-1 is a stress enzyme which is induced in AKI and provides protective effects both in kidney cells and in cells outside the kidney. Our current efforts are directed at understanding how HO-1 expression in AKI is modulated by gender and age and determining a novel role for HO-1 in the serum of patients and animal models. Specific questions under investigation are (1) what is the effect of aging on this repair response?, and (2) Does HO-1 play a critical role in the protective mechanisms in females that are lost with aging? A greater understanding of the epithelial cell biology of repair in AKI will provide further insight into the design of novel therapies.

Selected Publications 
Publication PUBMEDID
Boddu R, Hull TD, Bolisetty S, Hu X, Meohle MS, Daher JP, Kamal AI, Joseph R, George JF, Agarwal A, Curtis LM, West AB. Leucinie-rich repeat kinase 2 deficiency is protective in rhabdomyolysis-induced kidney injury. Hum Mol Genet 2015 Apr 22 [Epub ahead of print]   In process 
Hull TD, Kamal AI, Boddu R, Bolisetty S, Guo L, Tisher CC, Rangarajan S, Chen B, Curtis LM, George JF, Agarwal A. Heme oxygenase-1 regulates myeloid cell trafficking in AKI. J Am Soc Nephrol 2015 Feb 12. [Epub ahead of print]   In process 
Rangarajan S, Sunil B, Fan C, Wang PX, Cutter G, Sanders PW, Curtis LM. Distinct populations of label-retaining cells in the adult kidney are defined temporally and exhibit divergent regional distributions. Am J Physiol Renal Physiol. 2014 Sep 18:ajprenal.00213.2014.   25234315 
Rangarajan S, Sunil B, Curtis LM (2014) Ascorbic Acid in Cancer: A Renewed Hope? J Cancer Sci Ther 6:323-336. doi: 10.4172/1948-5956.1000291   
Ying W, Allen C, Curtis LM, Aaron K, Sanders PW. Mechanism and Prevention of Acute Kidney Injury from Cast Nephropathy in a Rodent Model. J Clin Invest 2012 May 1;122(5):1777-85.  22484815 
Zarjou A, Kim J, Traylor AM, Sanders PW, Balla J, Agarwal A, Curtis LM. Paracrine effects of mesenchymal stem cells in cisplatin-induced renal injury require heme oxygenase-1. Am J Physiol: Renal Physiol 2011 Jan; 300(1):F254-62.  21048024 
Curtis LM, Chen S, Chen B, Agarwal A, Klug CA, Sanders PW. Contribution of intrarenal cells to cellular repair after acute kidney injury: subcapsular implantation technique. Am J Physiol Renal Physiol. 2008 Jul;295(1):F310-4.   18448588 
Curtis LM and Agarwal A. HOpe for contrast-induced acute kidney injury. Kidney Int. 2007 Oct;72(8):907-9.  17914415 
Roberts J, Chen B, Curtis LM, Sanders PW, Agarwal A, Zinn KR. Detection of early changes in renal function using Tc-99m-Mag3 imaging in a murine model of ischemia-reperfusion injury. Am J Physiol Renal Physiol. 2007 Oct;293(4):F1408-12.  17634403 
Shiraishi F, Curtis LM, Truong L, Poss K, Visner GA, Madsen K, Nick HS, Agarwal A. Heme oxygenase-1 gene ablation or expression modulates cisplatin-induced renal tubular apoptosis. Am J Physiol Renal Physiol. 2000 May; 278(5): F726-36.  10807584 

acute kidney injury, aging, stem cells, heme oxygenase-1, gender