Directed differentiation into insulin-producing cells using microRNA manipulation
Williams Michael D.,
Joglekar Mugdha V.,
Hardikar Anandwardhan A.,
Wong Wilson K. M.
Affiliations
Williams Michael D.
Diabetes and Islet biology Group, NHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Level 6, Medical Foundation Building, 92-94 Parramatta Road, Camperdown, NSW 2050, Australia
Joglekar Mugdha V.
Diabetes and Islet biology Group, NHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Level 6, Medical Foundation Building, 92-94 Parramatta Road, Camperdown, NSW 2050, Australia
Hardikar Anandwardhan A.
Diabetes and Islet biology Group, NHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Level 6, Medical Foundation Building, 92-94 Parramatta Road, Camperdown, NSW 2050, Australia
Wong Wilson K. M.
Diabetes and Islet biology Group, NHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Level 6, Medical Foundation Building, 92-94 Parramatta Road, Camperdown, NSW 2050, Australia
Our commentary is focused on three studies that used microRNA overexpression methods for directed differentiation of stem cells into insulin-producing cells. Islet transplantation is the only cell-based therapy used to treat type 1 diabetes mellitus. However, due to the scarcity of cadaveric donors and limited availability of good quality and quantity of islets for transplant, alternate sources of insulin-producing cells are being studied and used by researchers. This commentary provides an overview of distinct studies focused on manipulating microRNA expression to optimize differentiation of embryonic stem cells or induced pluripotent stem cells into insulin-producing cells. These studies have used different approaches to overexpress microRNAs that are highly abundant in human islets (such as miR-375 and miR-7) in their differentiation protocol to achieve better differentiation into functional islet beta (β)-cells.