Dataset Information

Urinary proteome of dogs with kidney injury during babesiosis.

ABSTRACT: BACKGROUND:Acute kidney injury is the most frequent complication of babesiosis in dogs and may provide a natural model for identifying early and specific markers of kidney injury in this species. There are limited data on urine proteomics in dogs, and none of the effect of babesiosis on the urine proteome. This study aimed to identify urinary proteins of dogs with kidney injury during the natural course of babesiosis caused by Babesia canis, and to compare them with proteins in a control group to reveal any potential biomarkers predicting renal injury before the presence of azotemia. Urine samples were collected from 10 dogs of various breeds and sex with naturally occurring babesiosis, and 10 healthy dogs. Pooled urine samples from both groups were separated by 2D (two-dimensional) electrophoresis, followed by protein identification using MALDI-TOF (matrix-assisted laser desorption ionization time of flight) mass spectrometry. RESULTS:In total, 176 proteins were identified in the urine samples from healthy dogs, and 403 proteins were identified in the urine samples from dogs with babesiosis. Of the 176 proteins, 146 were assigned exclusively to healthy dogs, and 373 of the 403 proteins were assigned exclusively to dogs with babesiosis; 30 proteins were common for both groups. Characteristic analysis of 373 proteins found in dogs with babesiosis led to the isolation of 8 proteins associated with 10 metabolic pathways involved in immune and inflammatory responses. CONCLUSIONS:It was hypothesized that epithelial-mesenchymal transition might play an important role in the mechanisms underlying pathological changes in renal tissue during babesiosis, as indicated by a causal relationship network built by combining 5 of the 10 selected metabolic pathways, and 4 of the 8 proteins associated with these pathways; this network included cadherins, gonadotropin releasing hormone receptors, inflammatory responses mediated by chemokine and cytokine signalling pathways, integrins, interleukins, and TGF-? (transforming growth factor ?) pathways. Those pathways were linked by interleukin-13, bone morphogenetic protein 7, ?2(1) collagen, and tyrosine protein kinase Fer, which are potential biomarkers of damage during babesiosis in dogs, that might indicate early renal injury.

SUBMITTER: Winiarczyk D

PROVIDER: S-EPMC6894246 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Urinary proteome of dogs with kidney injury during babesiosis.

Winiarczyk D D Michalak K K Adaszek L L Winiarczyk M M Winiarczyk S S

BMC veterinary research 20191204 1

<h4>Background</h4>Acute kidney injury is the most frequent complication of babesiosis in dogs and may provide a natural model for identifying early and specific markers of kidney injury in this species. There are limited data on urine proteomics in dogs, and none of the effect of babesiosis on the urine proteome. This study aimed to identify urinary proteins of dogs with kidney injury during the natural course of babesiosis caused by Babesia canis, and to compare them with proteins in a control ...[more]

PMID: 31801572

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Project description:Urinary tract infections (UTIs) caused by uropathogenic Escherichia coli (UPEC) can lead to severe kidney injury. However, the molecular mechanisms underlying the pathological process of kidney injury are still incompletely understood. In the present study, we demonstrate that microRNA-146b (miR-146b) deficiency aggravates kidney injury during UTIs caused by UPEC. In a mouse kidney infection model utilizing urosepsis isolate CFT073, we found that miR-146b expression significantly increased in the early stages of UPEC infection. Also, miR-146b-deficient mice displayed exacerbated inflammation in the kidney injury with severe M1 macrophage infiltration. Additionally, the results showed that miR-146b targeted interferon regulatory factor 5-regulated M1 macrophage polarization during UTIs. The results suggested that miR-146b contributed significantly to the control of kidney damage during UTIs, highlighting that miR-146b might be used as a novel therapeutic target for treating kidney injury during UTIs. IMPORTANCE Kidney injury during acute urinary tract infections (UTIs) caused by uropathogenic Escherichia coli (UPEC) is an important public health problem. However, how kidney injury develops during UPEC infection is still unclear. Although antibiotic therapy is currently an effective treatment for UTI, it cannot avoid kidney injury. MicroRNAs have gained extensive attention as essential molecules capable of regulating the autoimmune response. Among these, microRNA-146b (miR-146b) is involved in regulating inflammatory responses. In the present study, we demonstrated that miR-146b played an essential role in the development of kidney injury during UTIs caused by UPEC. The results showed that miR-146b may suppress M1 macrophage polarization and alleviate acute kidney injury. Furthermore, the miR-146b activator, agomir, in order to upregulate miR-146b, was effective in treating kidney damage by inhibiting the activation of M1 macrophages. In conclusion, our findings elucidated the mechanisms by which miR-146b alleviated kidney injury induced by UTIs, shed new light on the relationship between microRNA and bacterial infection, and provided a novel therapeutic target for treating this common bacterial infection.

Project description:BackgroundAcute kidney injury (AKI) is associated with high morbidity and mortality in dogs, but diagnosis may be impaired due the insensitivity of routine renal function biomarkers to detect earlier or milder forms of injury. Snake envenomation is one of several causes of AKI in dogs and humans. Dogs are commonly envenomated by the European adder (Vipera berus) between April and October each year, but few studies exist examining serial serum creatinine (sCr) and symmetric dimethylarginine (SDMA) measurements and AKI biomarkers in these dogs. Novel urinary biomarkers could improve clinical outcome by allowing earlier diagnosis of and intervention in AKI. The aim of this study was to assess the presence of AKI in dogs envenomated by V. berus at 12, 24 and 36 h after bite, as well as 14 days later, using sCr, SDMA and a panel of urinary AKI biomarkers normalised to urine creatinine (uCr), compared to a group of healthy control dogs.ResultsThirty-five envenomated dogs and 35 control dogs were included. Serum creatinine did not exceed the upper reference limit at any time point in any dog after envenomation. Serum SDMA did not exceed 0.89 μmol/L in any dog. Compared to controls, urinary albumin/uCr, neutrophil gelatinase-associated lipocalin/uCr and monocyte chemotactic protein-1/uCr were significantly elevated 12 h (P < 0.0001, P < 0.0001, P = 0.01), 24 h (P < 0.001, P < 0.001, P = 0.002) and 36 h (P < 0.001, P < 0.001, P = 0.0008) after bite. Osteopontin/uCr was higher 24 and 36 h after bite (P < 0.0001), kidney injury molecule-1/uCr, interleukin-8/uCr and γ- glutamyl transferase/uCr were significantly higher 36 h after bite (P = 0.003, P = 0.0005, P = 0.001). Urinary cystatin C/uCr was not significantly different to controls at any timepoint. Biomarker/uCr ratios were not significantly different 14 days after envenomation compared to controls.ConclusionUrinary biomarker/Cr ratios are indicative of mild transient, non-azotaemic AKI in dogs envenomated by V. berus.

Project description:Background: Cardiac surgery-associated acute kidney injury (CSA-AKI) may increase the mortality and incidence rates of chronic kidney disease in critically ill patients. This study aimed to investigate the underlying correlations between urinary proteomic changes and CSA-AKI. Methods: Nontargeted proteomics was performed using nano liquid chromatography coupled with Orbitrap Exploris mass spectrometry (MS) on urinary samples preoperatively and postoperatively collected from patients with CSA-AKI. Gemini C18 silica microspheres were used to separate and enrich trypsin-hydrolysed peptides under basic mobile phase conditions. Differential analysis was conducted to screen out urinary differential expressed proteins (DEPs) among patients with CSA-AKI for bioinformatics. Kyoto Encyclopedia of Genes and Genomes (KEGG) database analysis was adopted to identify the altered signal pathways associated with CSA-AKI. Results: Approximately 2000 urinary proteins were identified and quantified through data-independent acquisition MS, and 324 DEPs associated with AKI were screened by univariate statistics. According to KEGG enrichment analysis, the signal pathway of protein processing in the endoplasmic reticulum was enriched as the most up-regulated DEPs, and cell adhesion molecules were enriched as the most down-regulated DEPs. In protein-protein interaction analysis, the three hub targets in the up-regulated DEPs were α-1-antitrypsin, β-2-microglobulin and angiotensinogen, and the three key down-regulated DEPs were growth arrest-specific protein 6, matrix metalloproteinase-9 and urokinase-type plasminogen activator. Conclusion: Urinary protein disorder was observed in CSA-AKI due to ischaemia and reperfusion. The application of Gemini C18 silica microspheres can improve the protein identification rate to obtain highly valuable resources for the urinary DEPs of AKI. This work provides valuable knowledge about urinary proteome biomarkers and essential resources for further research on AKI.

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Urinary proteome of dogs with kidney injury during babesiosis.

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Urinary proteome of dogs with kidney injury during babesiosis.

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