Fornoni Laboratory

    General information

    Alessia Fornoni M.D., Ph.D., FASN
    Assistant Professor of Clinical Medicine
    Division of Nephrology and Hypertension and Diabetes Research Institute
    University of Miami Miller School of Medicine

     

    Research Interests

    • Biology of the podocyte
    • Biology of pancreatic beta cells in diabetes

    Keywords and Phrases

    • Stress activated protein kinases and insulin resistance in diabetes
    • Role of nephrin in insulin production and function
    • Podocytes biology in diabetes
    • Podocyte dysfunction in recurrent focal segmental glomerulosclerosis
     

    Contact Information

    • Office location: Diabetes Research Institute
      1045 MW 10th Ave, Room 5010
      Miami, FL 33136
    • Tel: (305) 243-9945
    • Fax: (305) 243-4404
    • Lab Location: Diabetes Research Institute
      1045 MW 10th Ave, Room 5009
      Miami, FL 33136


     

    Members

    Member Position / Title Email
    Alessia Fornoni, M.D., Ph.D. Assistant Professor, Principal Investigator AFornoni@med.miami.edu
    Maria Saenz Laboratory Manager  
    Alexandra Jauregui, M.D. Visiting Scientist  


     

    Research

    Biology of the podocyte and the pancreatic beta cell in diabetes
    Our research stems from the idea that podocytes are insulin sensitive cells and by our evidence that podocytes may become insulin resistant in the very early phases of diabetic nephropathy. We are particularly interested in analyzing c-jun N terminal kinase (JNK) as mediator and novel therapeutic target to facilitate insulin signaling in diabetic nephropathy. We are also interested in the identification of biomarkers for diabetic nephropathy that may precede the development of diabetic nephropathy. We are studying the podocyte response to insulin and susceptibility to cell death in both experimental models of diabetic nephropathy and in human with and without nephropathy.

    We are also investigating the role of JNK inhibition in the improvement of pancreatic beta cell function. Since insulin signaling is an essential autocrine signal for proper beta cell function, we are investigating the role of JNK inhibition in the improvement of beta cell function. We have utilized JNK inhibitors developed with protein transduction domain technology to investigate the role of JNK in rodent and human islet cells viability and function. We have found and reported that JNK inhibitors improve pancreatic beta cell function, protect beta cells from apoptosis, improve islet cell recovery during human islet isolation and facilitate graft performance after transplantation into diabetic mice. We are now in the process of characterizing the specific role of JNK isoforms in islet function.

    A novel line of interest in our laboratory, together with Dr. J. Reiser and Dr. P. Mundel and in collaboration with Dr Per-Olof Berggren (Director of the Cell Biology laboratory at the Diabetes Research Institute) is the investigation of the role of slit diaphragm proteins (such as nephrin), in pancreatic beta cell function.

    We have also initiated a collaboration with Dr. George Burke III (Director of Pancreas and Kidney Transplant at the University of Miami) to investigate podocyte biology in the early phases of recurrent focal segmental glomerulosclerosis after kidney transplantation.

    Selected Publications

    • Cobianchi, L, Fornoni, A, Pileggi A, Molano, R.D., Sanabria, N.Y., Gonzalez-Quintana, J., Bocca, N., Marzorati, S., Zahr, E., Hogan, A.R., Ricordi, C., Inverardi, L. Riboflavin Inhibits IL-6 Expression and p-38 Activation in Islet Cells. Cell Transplantation, 2008, in press.
    • Yamamoto T, Ricordi C, Mita A, Miki A, Sakuma Y, Molano RD, Fornoni A, Pileggi A, Inverardi L, Ichii H. beta-Cell Specific Cytoprotection by Prolactin on Human Islets. Transplant Proc 40:382, 2008.
    • Tejada, T, Adeel I, Catanuto P, Varona-Santos J, Xia X, Sanchez P, Sanabria N, Lenz O, Elliot SJ, Fornoni, A. Failure to phosphorylate AKT in podocytes from diabetic mice with early nephropathy promotes cell death. Kidney International, 2008, E-pub
    • Fornoni A, Pileggi A, Molano RD, Sanabria N, Tejada T, Gonzalez-Quintana J, Ichii H, Inverardi L, Ricordi C, Pastori RL. Inhibition of c-jun N terminal kinase (JNK) improves functional beta cell mass in human islets and leads to AKT and glycogen synthase kinase-3 (GSK-3) phosphorylation. Diabetologia, 51:298-308, 2008
    • Fornoni A, Cobianchi L, Sanabria NY, Pileggi A, Molano DR, Ichii H, Rosero S, Inverardi L, Ricordi C, Pastori RL. The L-isoform but not D-isoform of a JNK inhibitory peptide protects pancreatic  b-cells. Biochemical and Biophysical Research Communications, 354:227-33, 2007
    • Fornoni A, Rosenzweig SA, Lenz O, Rivera A, Striker GE, Elliot SJ. Low IGFBP-2 expression is responsible for increased IRS-1 phosphorylation in mesangial cells from mice susceptible to glomerulosclerosis. Endocrinology 147:3547-54, 2006