Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from MSC-treated monocytes


ABSTRACT: Chronic inflammation leading to pro-inflammatory macrophage infiltration contributes to the pathogenesis of type 2 diabetes and subsequently the development of diabetic nephropathy. Mesenchymal stem cells (MSCs) possess unique immunomodulatory and cytoprotective properties making them an ideal candidate for therapeutic intervention We used microarrays to detail changes in the gene expression profile of monocytes isolated from type 2 diabetic patients with end-stage renal disease and non-diabetic control subjects following co-culture with MSCs. Control blood samples were obtained from 4 donors from the Australian Red Cross Blood Service. Blood was also obtained from 5 diabetic patients with end-stage renal disease receiving haemodialysis at the Monash Medial Centre. CD14+ monocytes were isolated from blood using microbeads and co-cultured for 48 hours with and without human bone marrow-derived MSCs using an in vitro transwell system. An Affymetrix GeneChip Human Gene 2.0 ST array was used.

ORGANISM(S): Homo sapiens

SUBMITTER: Tyrone Chen 

PROVIDER: E-GEOD-65561 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Human mesenchymal stem cells alter the gene profile of monocytes from patients with Type 2 diabetes and end-stage renal disease.

Wise Andrea F AF   Williams Timothy M TM   Rudd Stephen S   Wells Christine A CA   Kerr Peter G PG   Ricardo Sharon D SD  

Regenerative medicine 20151106 2


<h4>Aim</h4>Macrophage infiltration contributes to the pathogenesis of Type 2 diabetes. Mesenchymal stem cells (MSCs) possess immunomodulatory properties, making them an ideal candidate for therapeutic intervention. This study investigated whether MSCs can modulate the phenotype of monocytes isolated from Type 2 diabetic patients with end-stage renal disease.<h4>Materials & methods</h4>Monocytes from control (n = 4) and Type 2 diabetic patients with end-stage renal disease (n = 5) were assessed  ...[more]

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