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Agnieszka Swiatecka-Urban, MD

Job Title Assistant Professor, Department of Nephrology, Children's Hospital of Pittsburgh of UPMC
Job Title Assistant Professor, Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine
4401 Penn Avenue, Suite Floor 3
Pittsburgh, PA 15224
412-692-5182 Phone
412-692-7443 Fax

Education and Training

Medical School:

1991 Academia Medica Gedanensis, Gdansk, Poland

Residency:

1998 Department of Pediatrics, St. Vincent’s Hospital, Manhattan, NY

Fellowship:

2001 Department of Pediatrics, Division of Nephrology, Montefiore Medical Center, Bronx, NY
2003 Department of Physiology, Dartmouth Medical School, Hanover, NH

Memberships

  • American Society of Nephrology
  • International Pediatric Nephrology Association 
  • American Society of Pediatric Nephrology, Member of the ASPN mentoring task force
  • Women in Nephrology

Board Certifications

  • FMGEMS Part 1 and 2
  • ECFMG Certificate
  • USMLE Step 1-3
  • American Board of Pediatrics
  • American Board of Pediatric Nephrology

Awards

  • Graduated with the Highest Honors in Biology and Chemistry, Lyceum of Copernicus, Gdansk, Poland
  • The First National Prize for achievements in biology for a graduating student, the Polish Ministry of Education, Warsaw, Poland
  • Travel Award, The 10th Annual North American Cystic Fibrosis Conference
  • Dr. Fernando Moreno Award for the Graduating Pediatric Resident, St. Vincent’s Hospital
  • Award in Recognition of Dedication to Patient Care, St. Vincent’s Hospital
  • Travel Award, The American Society of Transplantation Symposium
  • Travel Award, The American Society of Transplantation and American Society of Transplant Surgery Joined National Meeting
  • Travel Award, Professional Development Seminar, Sponsored by Women in Nephrology and the American Society of Nephrology
  • Young Investigator Research Symposium Award, Montefiore Medical Center, Albert Einstein College of Medicine
  • Certificate of Achievement in Recognition of Completion of the Covelli Family Fellowship for Research, Albert Einstein College of Medicine
  • Travel Award, The 56th Annual Meeting and Symposium of the Society of General Physiologists
  • Fellow of the American Society of Nephrology since 2005
  • Member of the Salt and Water Club since 2007

Publications

  • Swiatecka-Urban A, Boyd C, Coutermarsh B, Karlson KH, Barnaby R, Aschenbrenner L, Langford GM, Hasson T, Stanton BA (2004) Myosin VI Regulates Endocytosis of the Cystic Fibrosis Transmembrane Conductance Regulator. J Biol Chem 279(36):38025-31.
  • Swiatecka-Urban A, Brown A, Moreau-Marquis S, Renuka BJ, Coutermarsh B, Barnaby R, Karlson KH, Flotte TR, Fukuda M, Langford GM, Stanton BA (2005) The Short Apical Membrane Half-life of Rescued ∆F508-CFTR Results from Accelerated Endocytosis of ∆F508-CFTR in Polarized Human Airway Epithelial Cells. J Biol Chem 280(44):36762-72.
  • Swiatecka-Urban A, Talebian L, Kanno E, Moreau-Marquis S, Coutermarsh B, Hansen K, Barnaby R, Karlson KH, Barnaby R, Cheney RE, Langford GM, Fukuda M, Stanton BA (2007) Myosin Vb is Required for Trafficking of CFTR in Rab11a-specific Apical Recycling Endosomes in Polarized Human Airway Epithelial Cells. J Biol Chem 282(32):23725-36.

    View Dr. Swiatecka-Urban's full list of publications from PubMed.

Research Interests

The role of Rab GTPases in regulating the plasma membrane half-life of CFTR. The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated chloride channel that is expressed in the apical plasma membrane in many epithelial tissues. Cystic fibrosis (CF) is caused by mutations in the CFTR gene and is one of the most common lethal inherited disorders in Caucasians (1 in 3,200 live births affected in the US). The most common CF mutation, ∆F508 causes: (1) retention of CFTR in the endoplasmic reticulum (ER), (2) reduced open probability of the CFTR chloride channel, and (3) decreased plasma membrane half-life of CFTR. Thus, correction of the defects caused by the ∆F508 mutation will require a combined therapy that includes increased exit from the ER, increased chloride channel activity, and increased plasma membrane half-life. Of these points, particularly little is known about the mechanisms that regulate the plasma membrane half-life of ∆508-CFTR. The biochemical plasma membrane half-life of CFTR is at least in part determined by the relative rates of CFTR endocytosis, recycling, and degradation. Rab proteins, a large family of small GTPases, facilitate a variety of trafficking events, including endocytosis and sorting to a recycling or a degradative pathway. The role of Rab GTPases in regulating CFTR trafficking is not completely understood. In particular, little is known about the role of Rab GTPases in sorting CFTR between the recycling and degradative compartments. Thus, my long-term goal is to elucidate these mechanisms in order to develop a strategy to increase the expression of ∆F508-CFTR in the plasma membrane.

The role of nephrin trafficking in maintaining the dynamic structure of the glomerular slit diaphragm (pathomechanisms of nephrotic syndrome). Nephrin, a cell adhesion molecule of the immunoglobulin (IgCAM) superfamily is a transmembrane protein expressed in the podocyte foot processes. Podocytes, the visceral glomerular epithelial cells, form a close-fitting network of interdigitating cellular extensions – foot processes – linked by modified tight junctions, called slit diaphragms. The slit diaphragm is a dynamic structure and a crucial component of the filtration barrier that plays a major role in the size selectivity, preventing passage of proteins and other molecules larger than albumin into the glomerular filtrate, and ultimately into the urine. Nephrotic syndrome is a very common kidney disease in children and adults. The pathomechanism of nephrotic syndrome is not well understood and remains one of the most important questions in nephrology today. The characteristic ultrastructural changes observed during the development of nephrotic syndrome – retraction and effacement of the podocyte foot processes – lead to disruption of the slit diaphragm and proteinuria. These morphological changes are closely associated with altered expression of nephrin. Mutations in the nephrin gene are responsible for many forms of congenital nephrotic syndrome and downregulation of nephrin expression correlates with the degree of proteinuria in diabetic nephropathy.  Although nephrin is critically important for the integrity of the slit diaphragm, the exact mechanisms are not well understood. In particular, very little is known about the role of nephrin trafficking in maintaining the dynamic structure of the filtration barrier. Thus, my long-term goal is to elucidate these mechanisms in order to develop strategies to prevent nephrotic syndrome.


Active Research Projects / Grants

  • Cell Biology of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)
  • Regulation of the Endocytic Trafficking of CFTR
  • Regulation of Endocytic Trafficking of Nephrin
Last Update
February 19, 2009
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Last Update
February 19, 2009
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