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A high glycemic burden drives functional and metabolic alterations of human monocytes in patients with type 1 diabetes

ABSTRACT: A high glycemic burden drives functional and metabolic alterations of human monocytes in patients with type 1 diabetes

PROVIDER: PRJNA646775 | ENA |

REPOSITORIES: ENA

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A high glycemic burden drives functional and metabolic alterations of human monocytes in patients with type 1 diabetes

Project description:Diabetes mellitus is associated with serious long-term complications, including increased cardiovascular risk and a higher occurrence of infections. These diabetes-related complications are suggestive of altered responses of the innate immune system. Recent studies have shown that energy metabolism of monocytes is a crucial determinant of their functionality. Here we investigate whether metabolism and function of monocytes are changed in patients with diabetes and aim to identify diabetes-associated factors driving these alterations. Patients with type 1 diabetes (T1D) and healthy age-, sex- and BMI-matched nondiabetic controls were recruited and detailed characteristics related to disease status including diabetes duration and glycemic burden (HbA1c levels) were collected. Monocytes were isolated from peripheral blood to determine immune functionality, metabolic responses and to perform transcriptome analyses. Upon ex vivo stimulation with TLR-4 agonist LPS or TLR-2 agonist P3C, monocytes of patients with T1D secreted lower levels of various cytokines (TNFα, IL-1β and IL-1Ra) and had lower glycolytic rates in comparison to monocytes isolated from matched controls. Stratification based on HbA1c levels revealed that a lower cytokine secretion was coupled to a higher glycolytic rate of monocytes in patients with a higher glycemic burden. Gene expression signatures of circulating monocytes displayed an enhanced inflammatory expression pattern that was associated with this high glycemic burden. A high glycemic burden in patients with T1D promotes expression of inflammatory genes of monocytes in vivo and is coupled to an impaired relationship between metabolism and inflammatory function upon activation ex vivo.

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Monocytes release pro-cathepsin D to drive blood-to-brain transcytosis in diabetes

Project description:Microvascular complications are the major outcome of type 2 diabetes mellitus progression and the underlying mechanism remains to be determined. To explore the contribution of circulating monocytes to the microvascular lesions, high-throughput RNA sequencing was conducted and we found high-level expression of cathepsin D (CTSD) in the monocytes of type 2 diabetes mellitus patients. The transgenic mice expressing human CTSD in the monocytes showed increased brain microvascular permeability resembling the diabetic microvascular phenotype, accompanied with cognitive deficit. Mechanistically, we found the monocytes release non-enzymatic pro-CTSD to upregulate caveolin expression in brain endothelium triggering caveolae-mediated transcytosis, without affecting the paracellular route of brain microvasculature. The circulating pro-CTSD activated the caveolae-mediated transcytosis in brain endothelial cells via its binding with low density lipoprotein receptor-related protein 1 (LRP1). Importantly, genetic ablation of CTSD in the monocytes exhibited protective effect against the diabetes-enhanced brain microvascular transcytosis and the diabetes-induced cognitive impairment. Our findings thus uncover the novel role of circulatory pro-CTSD from monocytes in the pathogenesis of cerebral microvascular lesions in diabetes. The circulatory pro-CTSD is thus a potential target for the intervention of microvascular complications in diabetes.

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Project description:We identified a novel lncRNA DRAIR that is downregulated in CD14+ monocytes from type 2 diabetes relative to controls. Functional studies showed that DRAIR regulates anti-inflammatory genes and its knockdown enhances proinflammatoory phentype of monocytes. To examine mechanisms of DRAIR actions, we performed Chromatin isolation by RNA purification (ChIRP) assays using DRAIR biotinylated tiling oligonucleotides to identify chromatin inding sites in THP-1 monocytes.

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Profiling of CD14+ monocytes from humans with Type diabetes and without diabetes

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RNA-sequencing of IRF5+ and IRF5- circulating monocytes from patients with Type-2 Diabetes

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Profiling of CD14+ monocytes from humans with Type diabetes and without diabetes [RNA-Seq]

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