Anti-apoptotic Effects of Bone Marrow on Human Islets: A Preliminary ReportLu-Guang Luo1* and John ZQ Luo2
- *Corresponding Author:
- Dr. LuGuang Luo
Roger Williams Hospital
Boston University School of Medicine
825 Chalkstone Avenue, Providence, RI 02908, USA
Tel: +1 401 456 5344
Fax: +1 401 456 5759
E-mail: [email protected]
Received date: January 20, 2015; Accepted date: April 07, 2015; Published date: April 09, 2015
Citation: Luo LG, Luo JZQ (2015) Anti-apoptotic Effects of Bone Marrow on Human Islets: A Preliminary Report. J Stem Cell Res Ther 5:274. doi:10.4172/2157-7633.1000274
Copyright: © 2015 Luo LG, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Apoptosis is one of the major factors contributing to the failure of human islet transplantation. Contributors to islet apoptosis exist in both the pre-transplantation and post transplantation stages. Factors include the islet isolation process, deterioration in vitro prior to transplantation, and immune rejection post transplantation. Previous studies have demonstrated that co-cultured bone marrow cells with human islets not only significantly enhanced the longevity of human islets but also maintained function. We hypothesized that the protective effects of bone marrow cells on human islets are through mechanisms related to preventing apoptosis. This study observed the levels of inflammatory factors such as interleukin-1β (IL-1β), the release of extracellular ATP in vitro, and expression levels of P2X7 ATP receptor (P2X7R), all of which lead to the occurrence of apoptosis in human islets. When human islets were cocultured with human bone marrow, there was a reduction in the rate of apoptosis correlated with the reduction in inflammatory factors, extra cellular ATP accumulation, and ATP receptor P2X7R expression versus human islets cultured alone. These results suggest that co-culturing bone marrow cells with human islets inhibits inflammation and reduces apoptosis, thus protecting islets from self-deterioration.