Journal article
Circulating high-molecular-weight RAGE ligands activate pathways implicated in the development of diabetic nephropathy
SA Penfold, MT Coughlan, SK Patel, PM Srivastava, KC Sourris, D Steer, DE Webster, MC Thomas, RJ MacIsaac, G Jerums, LM Burrell, ME Cooper, JM Forbes
Kidney International | Published : 2010
DOI: 10.1038/ki.2010.134
Abstract
The accumulation of advanced glycation end products is thought to be a key factor in the initiation and progression of diabetic nephropathy. Here we determined whether the size of the ligands for the receptor for advanced glycation end products (RAGEs) that were present in the serum of patients with type 2 diabetes modulates their pathogenic potential. Serum was collected from control subjects and patients with type 2 diabetes with varying degrees of renal disease (normo-, micro-, or macroalbuminuria). The titers of the RAGE ligands N-carboxymethyllysine (CML), S100A, S100B, and high-mobility group box 1 (HMGB1) were measured by enzyme-linked immunosorbent assay in serum as well as in pooled..
View full abstractGrants
Funding Acknowledgements
We thank the following people: Sianna Panagiotopoulos, Trudy Smith, and Aysel Akdeniz for the collection of the serum samples; Andrew Carey for the HRP-conjugated Protein G; and Amy Morley, Anna Gasser, and Felicia Yap for their technical assistance. This research was funded by the Juvenile Diabetes Research Foundation (JDRF) (JMF, MEC), the NIH (MCT, DEW), and Diabetes Australia. JMF is a recipient of a JDRF career development award and MEC holds an NHRMC Australian Fellowship and a JDRF Scholars Award. MTC holds an Australian Diabetes Society Early Career Fellowship. MCT is funded by the NHMRC and Kidney Health Australia by the Bootle bequest. SKP, LMB, and PMS are supported by the NHMRC.