Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 419, Issue C, Pages 83-91Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2015.10.002
Keywords
ERBB3; CTCF; IncRNAs; Type 1 diabetes; Beta cell; Apoptosis
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Funding
- University of Copenhagen
- Danish Council for Strategic Research Center for non-coding RNA in Technology and Health [09-067036/DSF]
- European Foundation for the Study of Diabetes
- National Institute of Health [1 DP3 DK085678]
- Poul and Erna Sehested Hansen Foundation
- Novo Nordisk
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The study aimed to explore the role of ERBB3 in type 1 diabetes (T1D). We examined whether genetic variation of ERBB3 (rs2292239) affects residual beta-cell function in T1D cases. Furthermore, we examined the expression of ERBB3 in human islets, the effect of ERBB3 knockdown on apoptosis in insulin producing INS-1E cells and the genetic and regulatory architecture of the ERBB3 locus to provide insights to how rs2292239 may confer disease susceptibility. rs2292239 strongly correlated with residual beta-cell function and metabolic control in children with T1D. ERBB3 locus associated lncRNA (NON-HSAG011351) was found to be expressed in human islets. ERBB3 was expressed and down-regulated by pro-inflammatory cytokines in human islets and INS-1E cells; knockdown of ERBB3 in INS-1E cells decreased basal and cytokine-induced apoptosis. Our data suggests an important functional role of ERBB3 and its potential regulators in the beta-cells and may constitute novel targets to prevent beta-cell destruction in T1D. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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