Project description:Diabetic kidney disease is the leading cause of end-stage renal disease worldwide. Our understanding of the early kidney response to chronic hyperglycemia remains incomplete. In this study, we aimed to uncover the early, dysregulated pathways in the diabetic kidney before the onset of microalbuminuria by analysing the urinary proteomes of otherwise healthy youths with and without type 1 diabetes. Our study population included two cohorts for the discovery (N = 30) and validation (N = 30) of differentially excreted proteins. Of the 2451 proteins identified, 576 were quantified in all samples from the discovery cohort, and 34 comprised the urinary signature for early type 1 diabetes after Benjamini-Hochberg adjustment (Q < 0.05). The top pathways associated with this signature included lysosome, glycosaminoglycan degradation, and innate immune system (Q < 0.01). Notably, all enzymes involved in keratan sulfate degradation were significantly elevated in urines from youths with type 1 diabetes (fold change > 1.6). Increased urinary excretion of monocyte differentiation antigen CD14, hexosaminidase A, and lumican was also observed in the validation cohort (P < 0.05). Our findings draw attention to novel pathways such as keratan sulfate degradation in the early kidney response to hyperglycemia.

2020-06-01 | PXD017213 | Pride

HLA sequencing in type 1 diabetes

Project description:NGS sequencing of HLA region in type 1 diabetes

| PRJEB76550 | ENA

Environmental Arsenic and Diabetes Mellitus (the Chihuahua Cohort)

Project description:Environmental Arsenic and Diabetes Mellitus (the Chihuahua Cohort)

| PRJNA671487 | ENA

Environmental Arsenic and Diabetes Mellitus (the Chihuahua Cohort)

Project description:Environmental Arsenic and Diabetes Mellitus (the Chihuahua Cohort)

| PRJNA671488 | ENA

Small RNA-sequencing of plasma exosome-enriched extracellular vesicles derived miRNAs from lactating mothers with type 1 diabetes and lactating healthy mothers

Project description:Previous studies have shown that the circulating miRNA signatures are altered in plasma-derived extracellular vesicles of individuals with type 1 diabetes. These alterations in the miRNA profile could serve as a potential biomarker applicable in clinical practice for monitoring disease status in lactating mothers with type 1 diabetes during the postpartum period. In the present study, we investigate the profiles of extracellular vesicle-derived miRNAs in circulation in a cohort of lactating mothers with and without type 1 diabetes.

2021-09-23 | E-MTAB-10458 | biostudies-arrayexpress

Diabetes Mellitus Type 1 miRnome

Project description:Diabetes Mellitus Type 1 miRnome

| PRJEB51173 | ENA

Urinary peptidomics in youths with and without type 1 diabetes

Project description:Although the early mechanisms responsible for diabetic kidney disease remain unclear, it is widely believed that chronic hyperglycemia disrupts the proteolytic milieu in the diabetic kidney and may contribute to early kidney injury. We thus performed mechanistic peptidomics in type 1 diabetes before the onset of microalbuminuria. In the discovery cohort of 30 participants, we identified 6550 peptides from 753 proteins. After removing false hits and potential contaminants, there were 6323 quantified peptides: 5708 peptides can be found in youths with type 1 diabetes, 5011 in healthy controls, and 4396 common to both groups. After applying a cut-off of 100%, there were 162 peptides found in each and every urine sample. From this subset, fifteen peptides were differentially excreted between youths with type 1 diabetes and their non-diabetic peers (P < 0.05, t-test); five remained significant after Benjamini-Hochberg adjustment (Q < 0.05). Excretion rates of six peptides were validated in a second cohort of thirty participants using parallel reaction monitoring (separate PRIDE file). Interestingly, these peptides originated from a small region near the C-terminus of uromodulin, a kidney-specific protein. In silico analyses of cleavage sites implicated several metallo and serine proteases involved in wound healing. Two of the uromodulin peptides activated NFκB in a TLR4-dependent manner in cultured kidney tubular cells and also promoted neutrophil migration in vitro. In summary, the differential excretion of uromodulin peptides may shed light onto early inflammatory processes in the diabetic kidney.

2020-01-20 | PXD012210 | Pride

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