MicroRNA-224 is Readily Detectable in Urine of Individuals with Diabetes Mellitus and is a Potential Indicator of Beta-Cell Demise

Genes

Siobhán Bacon²  Britta Engelbrecht¹  Jasmin Schmid¹  Shona Pfeiffer¹  Ross Gallagher¹  Ailbhe McCarthy²  Marie Burke²  Caoimhín Concannon¹  Jochen H. M. Prehn¹  Maria M. Byrne² 

[1] Departments of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St Stephen’s Green, Dublin 2, Ireland; E-Mails:;Department of Endocrinology, Mater Misericordiae University Hospital, Eccles Street, Dublin 7, Ireland; E-Mails:

关键词: diabetes associated microRNA;    miR-103;    miR-224;    urinary biomarker;    insulin secretion;   

DOI  :  10.3390/genes6020399

来源: mdpi

【 摘 要 】

MicroRNA (miRNA) are a class of non-coding, 19–25 nucleotide RNA critical for network-level regulation of gene expression. miRNA serve as paracrine signaling molecules. Using an unbiased array approach, we previously identified elevated levels of miR-224 and miR-103 to be associated with a monogenic form of diabetes; HNF1A-MODY. miR-224 is a novel miRNA in the field of diabetes. We sought to explore the role of miR-224 as a potential biomarker in diabetes, and whether such diabetes-associated-miRNA can also be detected in the urine of patients. Absolute levels of miR-224 and miR-103 were determined in the urine of n = 144 individuals including carriers of a HNF1A mutation, participants with type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM) and normal controls. Expression levels were correlated with clinical and biochemical parameters. miR-224 was significantly elevated in the urine of carriers of a HNF1A mutation and participants with T1DM. miR-103 was highly expressed in urine across all diabetes cohorts when compared to controls. For both miR-224 and-103, we found a significant correlation between serum and urine levels (p < 0.01). We demonstrate that miRNA can be readily detected in the urine independent of clinical indices of renal dysfunction. We surmise that the differential expression levels of miR-224 in both HNF1A-MODY mutation carriers and T1DM may be an attempt to compensate for beta-cell demise.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.