Philip J diIorio PhD
|Title||Research Assistant Professor|
|Institution||University of Massachusetts Medical School|
|Department||Program in Molecular Medicine|
|Address||University of Massachusetts Medical School|
368 Plantation Street, AS7-2043
Worcester MA 01605
|Institution||UMMS - Graduate School of Biomedical Sciences|
|Department||Interdisciplinary Graduate Program|
|The Iacocca Foundation||2002
||2004||Islet development in zebrafish|
|Worcester Foundation for Biomedical Research||2005
||2005||Zebrafish islet development: An in vivo model of beta-cell apoptosis|
|Diabetes Action Research and Education Foundation (DAREF)||2005
||2005||Matrix and Adhesive Influences During Pancreatic Islet Development in Zebrafish|
|National Institutes of Health/Diabetes and Endocrinology Research Center (DERC)||2007
||2008||Insulin Expression and Signaling During Pre-pancreatic Embryogenesis|
Cell-based therapies hold great promisefor diabetes treatment. However, human islet supplies cannot meet current, norprojected, annual need for transplants. Efforts to re-establish functional betacell mass in patients through in situregeneration/proliferation or transplantation of beta cells generated in vitro through trans-differentiation; replication;or directed differentiation from pluripotent precursors have had limitedsuccess. We hypothesize that the efficacy of these approaches is constrained byincomplete understanding of functional human beta cell development.
We focus on microRNAs (miRs) tounderstand human beta cell development because they 1) have important roles inorgan formation and tissue function 2) individual miRs coordinate cellularresponses (like migration, adhesion, differentiation, and metabolism) todevelopmental signals by interacting with numerous, functionally integrated mRNAs.Identifying these mRNAs, the ultimate goal of this proposal, allows us toreconstruct pathways of beta cell development.
Our workflow employs Next GenerationSequencing to "discover" miRNAs expressed in FACS purified humanfetal beta cells. We have generatedunique libraries of human, fetal microRNAs (miRs) and identified thirty-six miRs not previously studied in beta cells. Wecarry out mechanistic analyses of miRs in i) lentivirus-transduced fetalpancreas ii) zebrafish embryos and iii) the novel, glucose-responsive humanbeta cell line, EndoC-ßH1a. Using multiple models that provide insight into miR-dependentbeta cell differentiation, islet formation, and insulin secretion, we willidentify target genes and signaling pathways important for human beta celldevelopment and function. We anticipateour studies will enhance clinically-oriented efforts to expand beta cell massfor the treatment of diabetes.
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